Category Archives: Testosterone Replacement Therapy

By John Vandermosten, CFA

NASDAQ:LPCN

READ THE FULL LPCN RESEARCH REPORT

On May 9, 2022 Lipocine LPCN filed its Form 10-Q and posted its earnings release for the quarter ending March 31, 2022.

Highlights for the first quarter 2022 and to-date include:

TLANDO US commercialization licensing agreement with Antares Pharma - October 2021

FDA grants Fast Track Designation to LPCN 1144 - November 2021

First patient dosed in Phase II, LPCN 1148 in liver cirrhosis - December 2021

Presentations at 2022 NASH-TAG Conference - January 2022

Publication of Phase III results for TLANDO - January 2022

Licensee Antares TLANDO NDA resubmission accepted - February 2022

Regulatory guidance on LPCN 1144 in non-cirrhotic NASH - March 2022

Lipocine generated no revenues in the first quarter. It reported net loss of ($3.5) million, or ($0.04) per diluted share.

For the quarter ending March 31, 2022 and versus the same ending March 31, 2021:

Revenues were zero in both periods;

Research & Development expense totaled $1.9 million, up 19% from $1.6 million, driven by higher contract research organization (CRO) expenses for LPCN 1148, pharmacokinetic and food effect studies for LPCN 1107 and 1154, greater manufacturing scale-up costs for LPCN 1111 and higher personnel expenses;

General & Administrative expenses were $1.2 million, falling 19% from $1.5 million primarily due to lower legal costs relating to the Clarus lawsuit, and lower personnel costs, partially offset by higher professional fees, consulting fees, proxy solicitation expenses and corporate insurance costs;

Total other net expense was ($0.4) million, compared to ($0.3) million, as increases in interest and investment income were more than offset by an increase in unrealized loss on the warrant liability;

Net loss was ($3.5) million or ($0.04) per share compared with net loss of ($3.4) million or ($0.04) per share, respectively.

At quarter's end, marketable securities, cash and equivalents totaled $42.0 million. Cash burn for 1Q:22 was ($3.9) million, compared with ($4.1) million in 1Q:21. During the three month period, Lipocine repaid $0.8 million of debt and received $0.2 million from option exercises for a net cash change vs. year end 2021 of ($2.8) million.

TLANDO Licensing Agreement with Antares Pharma

On October 18th of last year Lipocine announced that it had entered into a licensing agreement with Antares Pharma. The agreement is for commercialization of TLANDO in the US and includes the following terms:

Up to $21 million in licensing fees;

$11 million payable immediately;

$10 million in future payments subject to certain conditions;

Commercial sales payments based on milestones up to $160 million;

Tiered royalties on net sales from mid-teens up to 20%;

Antares responsible for all commercialization, post-marketing studies, and sourcing of TLANDO in US;

Also included is Antares option to license TLANDO XR; if exercised

Antares gains license to develop and commercialize TLANDO XR in the US;

Lipocine would receive $4 million in license fees;

Up to $35 million in clinical and regulatory milestone payments;

Tiered royalties on net sales from mid-teens to 20%

Antares responsible for all clinical development costs, regulatory filings, commercialization and post-marketing activities.

On April 1, 2022, Lipocine and Antares amended the Tlando XR option agreement, extending it by three months to June 30, 2022 from the original March 31 date. Tlando XR is the next generation of Tlando which allows for once daily dosing for the TRT therapy. In return for the extension, Antares paid Lipocine $500,000 which will be credited towards the $4 million license fee required if Antares wishes to execute the license.

Lipocine retains all rights to rest of world and non-testosterone replacement therapy indications for both TLANDO and TLANDO XR. We update our model to reflect the terms of this arrangement and assume that Antares will exercise its option to advance TLANDO XR.

LPCN 1144 for Treatment of Non-Cirrhotic NASH

With the commercialization of TLANDO underway with Antares, LPCN 1144 moves into pole position at Lipocine. The company will shift its primary attention towards LPCN 1144 and an upcoming End of Phase II (EoP2) meeting with the FDA to determine trial design. We anticipate that a clear path forward for LPCN 1144 will be provided to stakeholders later this year.

Regulatory Guidance on LPCN 1144

On March 1, 2022, Lipocine provided an update on its Type C meeting with the FDA regarding LPCN 1144's development. The FDA provided written response acknowledging that LPCN 1144's NDA would be submitted via 505(b)(2) regulatory pathway, that no additional nonclinical studies are needed to support the submission, and that Lipocine's Phase II LiFT study's multicomponent primary surrogate endpoint is acceptable for seeking approval under accelerated approval. The FDA recommended Lipocine either conduct a separate dose-ranging study prior to Phase III or evaluate multiple doses in the Phase III study and that the aforementioned multicomponent primary surrogate endpoint is acceptable. The FDA recommended Phase III study duration of 72 weeks. The FDA also recommended that Lipocine submit an updated Phase III protocol and discuss details further in an EoP2 which is expected to take place in 3Q:22.

Next Steps

Now that selected 36-week biopsy data has been presented to stakeholders and with the Fast Track Designation in its back pocket, Lipocine's next steps are to prepare a presentation for a scientific and medical conference and complete the extension study. With feedback from its Type C meeting with the FDA, Lipocine is now charged with redesigning and submitting an updated Phase III protocol to the FDA, and scheduling an EoP2 meeting with the FDA. In response to FDA guidance, Lipocine must decide whether it wishes to conduct a preliminary dose-ranging study, or to incorporate dose-ranging into the design of its Phase III trial. Management has voiced its desire to seek a partner to advance LPCN 1144 into a registrational study.

Clarus Settlement

In mid-2021, Lipocine settled its claims related to the patent infringement litigation with Clarus for $4.0 million as described in our August 6, 2021 report. $2.5 million was paid immediately, followed by a promised $1.0 million payment in July 2022 and $500,000 in July 2023. On April 29, 2022, Lipocine modified the agreement in its favor by consenting to pay Clarus $1.25 million in May 2022, with no additional payments required thereafter. This provides non-discounted savings of $250,000 over the original agreement and settles the financial aspect of this matter.

Milestones

TLANDO

NDA filed for TLANDO - February 2020

Tentative approval of TLANDO - December 2020

TLANDO licensing agreement with Antares - October 2021

TLANDO full approval - March 28, 2022

First sales late 2Q:22

LPCN 1144

Presentation of 36-week LiFT study, biopsy data to investors - August 2021

End of Phase II meeting with FDA - 2H:21

Grant of Fast Track Designation for LPCN 1144 - November 2021

Type C meeting results for LPCN 1144 - March 2022

LPCN 1144 End-of-Phase II meeting request - April 2022

Open Label Extension (OLE) topline results May 2022

LPCN 1144 End-of-Phase II meeting - 3Q:22

Explore business development partnering 2022/2023

LPCN 1148

IND clearance for Phase II study of LPCN 1148 - May 2020

Male cirrhosis trial first subject dosed for LPCN 1148 - 4Q:21

Enrollment completion - 3Q:22

Topline 24-week results - 1Q:23

LPCN 2101 IND in epilepsy - 2022

Topline announcement for PK study for LPCN 1154 - 4Q:21/1Q:22

Launch Phase IIa proof of concept Post-Partum Depression (PPD) trial - 4Q:21

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1. Lipocine Corporate Presentation January 2022

Read this article:
LPCN: First Quarter 2022 Financial and Operational Results - Benzinga

The following discussion of our financial condition and results of operationsshould be read in conjunction with our unaudited condensed consolidatedfinancial statements and the related notes thereto and other financialinformation included elsewhere in this report. For additional context with whichto understand our financial condition and results of operations, see themanagement's discussion and analysis included in our Form 10-K, filed with theSEC on March 9, 2022 as well as the financial statements and related notescontained therein.

As used in the discussion below, "we," "our," and "us" refers to Lipocine.

This section and other parts of this report contain forward-looking statementswithin the meaning of Section 27A of the Securities Act of 1933, as amended, andSection 21E of the Securities Exchange Act of 1934, as amended, that involverisks and uncertainties. Forward-looking statements provide current expectationsof future events based on certain assumptions and include any statement thatdoes not directly relate to any historical or current fact. Forward-lookingstatements may refer to such matters as products, product benefits, pre-clinicaland clinical development timelines, clinical and regulatory expectations andplans, expected responses to regulatory actions, anticipated financialperformance, future revenues or earnings, business prospects, projectedventures, new products and services, anticipated market performance, expectedresearch and development and other expenses, future expectations for liquidityand capital resources needs and similar matters. Such words as "may", "will","expect", "continue", "estimate", "project", and "intend" and similar terms andexpressions are intended to identify forward looking statements. Forward-lookingstatements are not guarantees of future performance and our actual results maydiffer significantly from the results discussed in the forward-lookingstatements. Factors that might cause such differences include, but are notlimited to, those discussed in Part II, Item 1A (Risk Factors) of this Form10-Q, or in Part I, Item 1A (Risk Factors) of our Form 10-K filed with the SECon March 9, 2022. Except as required by applicable law, we assume no obligationto revise or update any forward-looking statements for any reason.

We are a clinical-stage biopharmaceutical company focused on neuroendocrine andmetabolic disorders using our proprietary oral drug delivery technology. Ourproprietary delivery technologies are designed to improve patient compliance andsafety through orally available treatment options. Our primary developmentprograms are based on oral delivery solutions for poorly bioavailable drugs. Wehave a portfolio of differentiated innovative product candidates that targethigh unmet needs for neurological and psychiatric CNS disorders, liver diseases,and hormone supplementation for men and women.

We entered into a license agreement for the development and commercializationour product candidate, TLANDO, an oral testosterone replacement therapy ("TRT")comprised of testosterone undecanoate ("TU"). TLANDO is a registered trademarkassigned to Antares. On October 14, 2021, we entered into a license agreement(the "Antares License Agreement") with Antares Pharma, Inc. ("Antares" or our"Licensee"), pursuant to which we granted to Antares an exclusive,royalty-bearing, sublicensable right and license to develop and commercialize,upon final approval of TLANDO from the United States Food and DrugAdministration ("FDA"), the TLANDO product for TRT in the U.S. Any FDA requiredpost-marketing studies will also be the responsibility of our licensee, Antares.On March 28, 2022, Antares received approval from the FDA for TLANDO as a TRT inadult males for conditions associated with a deficiency of endogenoustestosterone, also known as hypogonadism.

Additional pipeline candidates include: LPCN 1148 comprising a novel prodrug oftestosterone, testosterone laurate ("TL"), for the management of decompensatedcirrhosis; LPCN 1144, an oral prodrug of androgen receptor modulator for thetreatment of non-cirrhotic non-alcoholic steatohepatitis ("NASH") which hascompleted phase 2 testing; LPCN 1111 (TLANDO XR), a next generation oral TRTproduct comprised of testosterone tridecanoate ("TT") with the potential foronce daily dosing which has completed Phase 2 testing; ; LPCN 1107, potentiallythe first oral hydroxy progesterone caproate ("HPC") product indicated for theprevention of recurrent preterm birth ("PTB"), which has completed a dosefinding clinical study in pregnant women and has been granted orphan drugdesignation by the FDA; and neuroactive steroids (NAS) including LPCN 1154 forpostpartum depression (PPD) and LPCN 2101 for epilepsy.

The following chart summarizes the status of our product candidate developmentprograms:

To date, we have funded our operations primarily through the sale of equitysecurities, debt and convertible debt and through up-front payments, researchfunding and royalty and milestone payments from our license and collaborationarrangements. We have not generated any revenues from product sales and we donot expect to generate revenue other than TLANDO royalties and license fees fromproduct sales by Antares unless and until we obtain regulatory approval of ourproduct candidates.

We have incurred losses in most years since our inception. As of March 31, 2022,we had an accumulated deficit of $176.2 million. Income and losses fluctuateyear to year, primarily depending on the nature and timing of research anddevelopment occurring on our product candidates. Our net loss was $3.5 millionfor the three months ended March 31, 2022, compared to $3.4 million for thethree months ended March 31, 2021. Substantially all of our operating lossesresulted from expenses incurred in connection with our product candidatedevelopment programs, our research activities and general and administrativecosts associated with our operations.

We expect to continue to incur significant expenses and operating losses for theforeseeable future as we:

To fund future long-term operations, including the potential commercializationof any of our product candidates, we will need to raise additional capital. Theamount and timing of future funding requirements will depend on many factors,including capital market conditions, the commercial success of TLANDO,regulatory requirements related to our other product development programs, thetiming and results of our ongoing development efforts, the potential expansionof our current development programs, potential new development programs, ourability to license our products to third parties, the pursuit of variouspotential commercial activities and strategies associated with our developmentprograms and related general and administrative support. We anticipate that wewill seek to fund our operations through public or private equity or debtfinancings or other sources, such as potential license, partnering andcollaboration agreements. We cannot be certain that anticipated additionalfinancing will be available to us on favorable terms, in amounts sufficient tofund our operations, or at all. Although we have previously been successful inobtaining financing through public and private equity securities offerings andour license and collaboration agreements, there can be no assurance that we willbe able to do so in the future.

Our goal is to become a leading biopharmaceutical company focused on applyingour proprietary drug delivery technology for the development of pharmaceuticalproducts focusing on neuroendocrine and metabolic disorders. The key componentsof our strategy are to:

Build a diversified multi-asset pipeline of novel therapies. We intend to employa value-driven strategy based on our proprietary technology platform to identifyand develop product candidates for neuroendocrine and metabolic disordersincluding Central Nervous System (CNS) disorders and end stage diseases such asdecompensated cirrhosis. We intend to focus on product candidates that webelieve are differentiated, have attractive profiles, and address a clear unmetmedical need that we can advance quickly and efficiently into late-stagedevelopment.

Advance LPCN 1148, a unique prodrug of androgen receptor agonist to manage endstage (decompensated) liver cirrhosis disease. We believe LPCN 1148, a novelprodrug of testosterone, could address a significant unmet medical need inpatients with decompensated liver cirrhosis accompanied with muscle disordersuch as secondary sarcopenia. Sarcopenia in male cirrhotic patients is known tobe independently associated with poor outcomes including quality of life,increased decompensation events such as hepatic encephalopathy, increasedhospital admissions, and increased mortality rate. We believe LPCN 1148 may beeligible for an orphan drug designation. Enrollment in a multi-centerplacebo-controlled phase 2 trial is currently ongoing.

Support our licensee in commercialization of our licensed oral TRT option. Webelieve the TRT market needs a differentiated, convenient oral option. We haveexclusively licensed rights to TLANDO to Antares for commercialization of TLANDOin the US. We plan to support our licensee's efforts to effectively enable theavailability of TLANDO to patients in a timely manner, in addition to receivingmilestone and royalty payments associated with TLANDO commercialization asagreed to in the Antares License Agreement.

Develop partnership(s) to continue the advancement of pipeline assets. Wecontinuously strive to prioritize our resources in seeking co-developmentpartnerships of our pipeline assets. We currently plan to explore partnering ofLPCN 1144, our candidate for treatment of non-cirrhotic NASH, LPCN 1107, ourcandidate for prevention of pre-term birth, and LPCN 1111, a once-a-day therapycandidate for TRT.

Our pipeline of clinical candidates including LPCN 1148, an androgen therapy forthe management of cirrhosis, LPCN 1144, an oral androgen therapy for thetreatment of non-cirrhotic NASH, LPCN 1111, a next-generation potential oncedaily oral TRT, LPCN 1107, an oral therapy for the prevention of PTB, and NASincluding LPCN 1154 for postpartum depression (PPD) and LPCN 2101 for epilepsy.We will continue to explore other product candidates targeting indications witha significant unmet need.

Our products are based on our proprietary Lip'ral drug delivery technologyplatform. Lip'ral based TLANDO was approved in March 2022. Lip'ral technology isa patented technology based on lipidic compositions which form an optimaldispersed phase in the gastrointestinal environment for improved absorption ofinsoluble drugs. The drug loaded dispersed phase presents the solubilized drugefficiently at the absorption site (gastrointestinal tract membrane) thusimproving the absorption process and making the drug less dependent onphysiological variables such as dilution, gastro-intestinal pH, and food effectsfor absorption. Lip'ral based formulation enables improved solubilization andhigher drug-loading capacity, which can lead to improved bioavailability,reduced dose, faster and more consistent absorption, reduced variability,reduced sensitivity to food effects, improved patient compliance, and targetedlymphatic delivery where appropriate.

LPCN 1148: Oral Product Candidate for the Management of Decompensated Cirrhosis

We are currently evaluating LPCN 1148 comprising testosterone laurate (TL) forthe management of decompensated cirrhosis. We believe LPCN 1148 targets unmetneeds for cirrhosis subjects including improvement in the quality of life ofpatients while on the liver transplant waiting list, prevention or reduction inthe occurrence of new decompensation events, and improvement in post livertransplant survival, including outcomes and costs.

We are currently conducting a Phase 2 POC study (NCT04874350) in male cirrhoticsubjects to evaluate the therapeutic potential of LPCN 1148 for the managementof sarcopenia. The ongoing Phase 2 POC study is a prospective, multi-center,randomized, placebo-controlled study in male sarcopenic cirrhotic patients.Subjects will be randomized 1:1 to one of two arms. The treatment arm is an oraldose of LPCN 1148, and the second arm is a matching placebo. The primaryendpoint is change in skeletal muscle index at week 24 with key secondaryendpoints including change in liver frailty index, rates of breakthrough hepaticencephalopathy, and number of waitlist events, including all-cause mortality.Total treatment is expected to be 52 weeks. We currently expect enrollment inthe Phase 2 study to be complete by the end of the third quarter of 2022 andtop-line 24-week results by the end of the first quarter of 2023.

Possible outcomes of interest from the Phase 2 study include clinical outcomessuch as overall survival and new decompensation events (including hepaticencephalopathy and/or ascites occurrences), rates of survival to transplant,rates of hospitalizations, infections, etc., muscle changes such as muscle mass,body composition, myosteatosis (muscle fat), functional capacity changes such asliver frailty index (LFI), patient reported outcomes (PROs), and biochemicalmarkers including hematocrit for anemia status, albumin, creatinine/kidneyfunction, etc.

Disease Overview - Cirrhosis

There are over 2 million cases of cirrhosis worldwide, with over 500,000 peopleliving with decompensated cirrhosis in the U.S. and nonalcoholic fatty liverdisease is the most rapidly increasing indication for liver transplant. 62% ofthose on the liver transplant ("LT") waitlist are male. The economic burden(approximately $812,500/transplant) is high and continues to increase. Each yearabout half of the approximately 17,000 people in U.S. on the LT waitlist undergotransplant, while nearly 3,000 patients either die or are removed from the listbecause they were "too sick to transplant."

Liver cirrhosis is defined as the histological development of regenerativenodules surrounded by fibrous bands. Cirrhotic patients typically have ayears-long silent, asymptomatic phase (compensated cirrhosis) until decreasingliver function and increasing portal pressure move the patient into thesymptomatic phase (decompensated cirrhosis). Transition to decompensatedcirrhosis is marked by clinical events including ascites, encephalopathy,jaundice, and/or variceal hemorrhage. Decompensated subjects survive on averageless than 2 years. Common causes of liver cirrhosis include alcoholic liverdisease, nonalcoholic fatty liver disease (NAFLD), chronic hepatitis B and C,primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) andcryptogenic.

Common complications in cirrhotic patients may include: compromised liverfunction, portal hypertension, varices in GI tract with internal bleeding,edema, ascites, hepatic encephalopathy, compromised immunity withpost-transplant acute rejection risk, high sodium levels, increased bilirubin,low albumin level, insulin resistance with impaired peripheral uptake ofglucose, depression, accelerated muscle disorder in the form of sarcopenia,myosteotosis, and frailty with compromised energetics, bone diseases (e.g.,osteoporosis), high alkaline phosphatase (ALP), cachexia, malnutrition, weightloss (>5%), symptoms of hypogonadism such as abnormal hair distribution, anemia,sexual dysfunction, testicular atrophy, muscle wasting, fatigue, osteoporosis,gynecomastia, inflammation with elevated cytokines, and infection risk leadingto hospital admissions and possibly death.

Hepatic encephalopathy ("HE"), a significant decompensation event in patientwith cirrhosis, is a brain dysfunction caused by liver insufficiency and/orportal systemic shunting. Because the damaged liver cannot function normally (asin cirrhosis), neurotoxins such as ammonia are inadequately removed fromsystemic circulation and travel to the brain, where they affectneurotransmission. This can cause episodes of HE, which may present asalterations in consciousness, cognition, and behavior that range from minimal tosevere. Overt HE occurs in 30% to 40% of patients with cirrhosis at some pointduring the clinical course of their disease. As the burden of chronic liverdisease and cirrhosis is increasing, the frequency of HE is also increasing.

Muscle Disorders and Cirrhosis

Muscle disorders secondary to cirrhosis could be manifested in the form ofseveral inter-related characteristics such as sarcopenia, myosteotosis, andfrailty impacting muscle mass, strength, quality, and function. Chronicinflammation and oxidative stress have also been reported to accelerate musclewasting. Muscle also plays a significant compensatory role in detoxifyingammonia, a neurotoxin and a myotoxin implicated in precipitation of HE incirrhosis patients.

Sarcopenia and associated frailty affect up to 70% of cirrhotic men and are aleading cause of patients being removed from the LT wait list. Due to the lackof available organs and aging demographics of those on the waitlist, patientsthat do receive a transplant are "increasingly being described as frail". Thepresence of sarcopenia or frailty is associated with increased risk ofhospitalization and hepatic decompensation, a two-fold increase in waitlistmortality, poor post-transplant outcomes, and reportedly is equivalent to adding9-10 points to the Model for End-Stage Liver Disease (MELD) score.

Sarcopenia is typically associated with body composition changes with decreasedmuscle mass and/or low skeletal muscle index. Change in one or more ofappendicular lean mass, total lean mass, fat mass, high VAT (visceral adiposetissue), waist circumference, weight, and/or BMI are notable features.Myosteotosis (fat infiltration in muscles) is indicative of poor muscle quality.Frailty is a state of low energetics accompanied with low physicalperformance/mobility probably because of poor muscle strength/function and isassessed via various measures such as decreased gait speed, weak hand grip; slowrising from a chair, balance, isometric knee extension peak torque or acomposite measure such as liver frailty index (LFI).

Reportedly, as shown in the figure below, muscle disorder such as sarcopenia andmyosteotosis in cirrhosis could be a clinically meaningful predictor of survivaland mortality with lower survival in cirrhotic patients with accompanying muscledisorders.

Muscle Disorders and Mortality in Liver Cirrhosis

Sarcopenia develops in the majority of male cirrhosis patients. The mainmechanisms associated with sarcopenia and decompensated cirrhosis include acatabolic state, progressive immobility, imbalance between muscle breakdown andformation, and hormonal changes. Patients are typically diagnosed withdecompensated cirrhosis upon development of cirrhotic symptoms (e.g., jaundice,HE), and the diagnosis is confirmed via various liver function/imaging tests(e.g., MELD score, liver biopsy, CT scan). A variety of clinical evaluations formuscle mass, strength, and function are typically used to diagnose sarcopenia.Sarcopenia in cirrhosis also correlates with decompensation events, particularlyHE (sarcopenia is about 2-fold more prevalent in overt HE patients than thosewithout overt HE). Notably, low testosterone in males is associated withsarcopenia, severity of cirrhosis, and mortality.

Reportedly, as shown in figure below, sarcopenia is a predictor for increasedmortality in cirrhosis (about 2-fold higher compared to no sarcopenia).

Reportedly, as shown in figure below, pre transplant sarcopenia in livercirrhosis often produces poor post-transplant outcomes with higher mortalityrates. Longer post-transplant hospitalization and rehabilitation can bedemanding on the individual, both physically and financially.

Myosteatosis, fat infiltration in muscles, has been found in many cirrhoticpatients undergoing liver transplant evaluation, and studies have associated itwith more complications and poor survival. Myosteatosis is characteristicallyassociated with liver steatosis in NAFLD, resulting from ectopic fataccumulation in skeletal muscle. Myosteatosis may affect many individuals who donot meet the anthropometric criteria for sarcopenia or obesity. The accumulationof excess fat in extramyocellular compartments is mostly pathologic. It can bedefined as intramuscular (between muscle fibers) or intermuscular (betweenmuscle fascicles) and is associated with lower muscle function and strength,muscle atrophy, and physical disabilities.

Frailty is a state of low energetics accompanied with low physicalperformance/mobility, usually as a result of poor muscle strength/function andits presence is assessed via various measures such as decreased gait speed, weakhand grip, slow rising from a chair, poor balance, low isometric knee extensionpeak torque or a composite measure such as liver frailty index (LFI).

Reportedly, as shown in figure below, frailty predicts LT waitlist mortalityamong outpatients with cirrhosis regardless of the MELD score.

The presence of frailty is associated with increased waitlist death/delisting

Moreover, it has also been reported, as shown in figure below, that there is ahigher incidence of waitlist mortality as the frailty worsened.

Trajectory of liver frailty and mortality

Currently, there are no FDA approved drugs to treat secondary sarcopenia incirrhosis. We believe we are the only clinical-stage company pursuingdecompensation in sarcopenic cirrhotic patients, and no regulatory precedentcurrently exists for the approval of decompensation or sarcopenia-targetedtherapies. We believe LPCN 1148 has the potential to aid the management ofdecompensation events in male sarcopenic cirrhotic patients through thefollowing possible mechanisms of action: myo-augmentation (impact muscle massand/or quality and/or function) via myostatin inhibition, myosteatosisreduction, anti-catabolic effect, changes in body composition (increase leanmass and/or reduce fat mass) and slowing muscle autophagy; inducinghepato-effective actions with improved key liver injury markers; increaseprotein synthesis; improve anemia, induce immunomodulation with improvement ofimmuno-dysregulation, and lower infection rates; anti-inflammatory/antioxidanteffects by lowering undesirable cytokines such as IL-1, IL-6, and TNF-?; andimprove mitochondrial function.(1)

(1) Ref: Leise. Mayo Clin Proc. 2014.; Hudson. Eur J Gastroenterol. 2019.; Bajaj.

LPCN 1144: An Oral Prodrug of Bioidentical Testosterone Product Candidate forthe Treatment of NASH

We are currently evaluating LPCN 1144, an oral prodrug of bioidenticaltestosterone comprised of TU, for the treatment of non-cirrhotic NASH.

NASH is a more advanced state of non-alcoholic fatty liver disease ("NAFLD") andcan progress to a cirrhotic liver or liver failure, require liver transplant,and can result in hepatocellular carcinoma/ liver cancer, and death. Progressionof NASH to end stage liver disease will soon surpass all other causes of liverfailure requiring liver transplantation. Importantly, beyond these criticalconditions, NASH and NAFLD patients additionally suffer heightenedcardiovascular risk and, in fact, die more frequently from cardiovascular eventsthan from liver disease. NAFLD/NASH is becoming more common due to its strongcorrelation with obesity and metabolic syndrome, including components ofmetabolic syndrome such as diabetes, cardiovascular disease and high bloodpressure. Twenty to thirty percent of the U.S. population is estimated to sufferfrom NAFLD and fifteen to twenty percent of this group progresses to NASH, whichis a substantially large population that lacks an effective therapy. NASH is asilent killer that affects millions in the U.S. Diagnoses have been on the riseand are expected to increase dramatically in the next decade. Approximately 50%of NASH patients are in adult males. In men, especially with comorbiditiesassociated with NAFLD/NASH, testosterone deficiency has been associated with anincreased visceral adipose tissue and insulin resistance, which could be factorscontributing to NAFLD/NASH. There is currently no approved therapy for thetreatment of NASH although there are several drug candidates currently underdevelopment with many clinical failures to date.

The critical pathophysiologic mechanisms underlying the development andprogression of NASH include reduced ability to handle lipids, increased insulinresistance, injury to hepatocytes and liver fibrosis in response to hepatocyteinjury. NASH patients have an excessive accumulation of fat in the liverresulting primarily from a caloric intake above and beyond energy needs. Ahealthy liver contains less than 5% fat, but a liver in someone with NASH cancontain more than 20% fat. This abnormal liver fat contributes to theprogression to NASH, a liver necro-inflammatory state that can lead to scarring,also known as fibrosis, and, for some, can progress to cirrhosis and liverfailure.

Alanine aminotransferase ("ALT") is an enzyme that is produced in liver cellsand is naturally found in the blood of healthy individuals. In liver disease,liver cells are damaged and, as a consequence, ALT is released into the blood,increasing ALT levels above the normal range. Physicians routinely test bloodlevels of ALT to monitor the health of a patient's liver. ALT level is aclinically important biochemical marker of the severity of liver inflammationand ongoing liver disease. Elevated levels of ALT represent general markers ofliver cell death and inflammation without regard to any specific mechanism.Aspartate aminotransferase ("AST") is a second enzyme found in the blood that isproduced in the liver and routinely measured by physicians along with ALT. Aswith ALT, AST is often elevated in liver disease and, like ALT, is considered anoverall marker of liver inflammation.

Most people with NASH are asymptomatic and their disease is often discoveredincidentally following a liver imaging procedure, such as an ultrasound,prescribed for other reasons or as part of an investigation for elevated liverenzymes. Once suspected clinically, a liver biopsy is required to definitivelydiagnose NASH, which necessitates the joint presence of steatosis, ballooningand lobular inflammation. Once pathologically confirmed, the severity of NAFLDand NASH is determined using the histologically validated NAFLD activity score,which grades disease activity on a scale of 0 to 8. The NAFLD activity score isthe sum of the individual scores for steatosis (0 to 3), lobular inflammation (0to 3), and hepatocellular ballooning (0 to 2) but does not include a score forfibrosis. Fibrosis staging (F0-F4) relies on the NASH CRN classification (F0 =no fibrosis; F1 = perisinusoidal or portal/periportal fibrosis (not both); F2 =both perisinusoidal and portal/periportal fibrosis; F3 = bridging fibrosis; F4 =cirrhosis).

Histological diagnosis remains the gold standard for assessment of NASH andfibrosis. However, given that liver biopsy is associated with risks of pain,bleeding and other morbidity, as well as significant cost, the procedure is notpractical for general patient screening. Several non-invasive tools such asclinical risk scores and imaging techniques are increasingly used to assesspotential NASH patients. Clinical risk scores such as the NAFLD fibrosis score,Fibrosis-4 index, the Enhanced Liver Fibrosis score and vibration-controlledtransient elastography ("VCTE"), have been validated and are increasingly used.These tools have an excellent negative predictive value and an acceptablepositive predictive value for detection of advanced (? F3) fibrosis and areincreasingly used in clinical settings. Extensive efforts are also under way todevelop non-invasive means to identify patients with NAS ? 4 or fibrosis ? F2without a liver biopsy. In draft guidance, the FDA encouraged sponsors toidentify biochemical or noninvasive imaging biomarkers that, once characterizedand agreed by the FDA, could replace liver biopsies for patient selection andefficacy assessment in clinical trials.

We expect that the validation and subsequent adoption of these new tools willresult in an increase in the diagnosis and treatment rates for NASH in thefuture.

We have recently completed the LiFT Phase 2 clinical study in biopsy-confirmednon-cirrhotic NASH subjects. The LiFT clinical study was a prospective,multi-center, randomized, double-blind, placebo-controlled multiple-arm study inbiopsy-confirmed hypogonadal and eugonadal male NASH subjects with grade F1-F3fibrosis and a target NAFLD Activity Score ? 4 with a 36-week treatment period.The LiFT clinical study enrolled 56 biopsy confirmed NASH male subjects.Subjects were randomized 1:1:1 to one of three arms (Treatment A is a twicedaily oral dose of 142 mg testosterone equivalent, Treatment B is a twice dailyoral dose of 142 mg testosterone equivalent formulated with 217 mg of d-alphatocopherol equivalent, and the third arm is twice daily matching placebo).

The primary endpoint of the LiFT clinical study was change in hepatic fatfraction via MRI-PDFF and exploratory liver fat/marker end points post 12 weeksof treatment. Additionally, key secondary endpoints post 36 weeks of treatmentincluded assessment of histological change for NASH resolution and/or fibrosisimprovement (biopsy) as well as liver fat data (MRI-PDFF). The LiFT clinicalstudy was not powered to assess statistical significance of any of the secondaryendpoints. Other important endpoints included the following: change in liverinjury markers, anthropomorphic measurements, lipids, insulin resistance andinflammatory/fibrosis markers; as well as patient reported outcomes.

Additionally, subjects have access to LPCN 1144 through an open label extension("OLE") study. The extension study will enable the collection of additional dataon LPCN 1144 for up to a total of 72 weeks of therapy, as well as data for 36weeks of therapy for those subjects on placebo in the LiFT study. The OLE hasbeen completed and we expect topline results from the study in May 2022.

Treatments with LPCN 1144 post 12 weeks of treatment resulted in robust liverfat reduction, assessed by MRI-PDFF, and showed improvement of liver injurymarkers with no observed tolerability issues.

Liver biopsies were performed at baseline ("BL") and after 36 weeks of treatment("EOS"). Prespecified biopsy analyses included NASH Clinical Research Network("CRN") scoring as well as a continuous paired ("Paired Technique") and digitaltechnique ("Digital Technique-Fibronest"). All biopsy analyses were performed onthe same slides and the reads for the three techniques were done independently.Analysis sets included the NASH Resolution Set (all subjects that have BL andEOS biopsy with NASH at BL [NAS ?4 with lobular inflammation score ? 1 andhepatocyte ballooning score ?1 at BL] (n=37)), the Biopsy Set (all subjects withbaseline and EOS biopsies (n=44)), and the Safety Set (all randomized subjects(n=56)).

Both LPCN 1144 treatment arms met with statistical significance thepre-specified accelerated approval regulatory endpoint of NASH resolution withno worsening of fibrosis based on NASH CRN scoring. Additionally, both treatmentarms showed substantial improvement of the observed NASH activity in steatosis,inflammation, and ballooning.

Key results from the LiFT clinical study are presented in the following tablesand figures:

In both treatment arms, substantial reductions in markers of liver injurycompared to placebo were observed post four weeks of treatment and weresustained through EOS. Using all available Safety Set data, ALT decreased up toa mean of 23.4 U/L at EOS from all group mean baseline of 51.5 U/L and ASTdecreased up to a mean of 13.3 U/L at EOS from all group mean baseline of 31.9U/L.

Positive effects in appendicular lean mass and whole-body fat mass, an indicatorof overall tissue quality, based on dual-energy X-ray absorptiometry scans, werenoted in both LPCN 1144 treatment arms.

Finding on liver injury marker and positive effects on body composition can beseen in the following table:

During the 36 weeks of treatment, LPCN 1144 was well tolerated with an overallsafety profile comparable to placebo.

In November 2021, the FDA granted Fast Track Designation to LPCN 1144 as atreatment for non-cirrhotic NASH. The Fast Track program is designed toaccelerate the development and expedite the review of products, such as LPCN1144, which are intended to treat serious diseases and for which there is anunmet medical need.

We had a written only response from FDA for a LPCN 1144 Type C meeting with theFDA in January 2022 to discuss the development path forward with LPCN 1144. TheFDA acknowledged that the NDA submission of LPCN 1144 would be via 505(b)2regulatory pathway and agreed that no additional non-clinical studies are neededto support an NDA submission. The FDA recommended to request an end-of-phase 2(EOP2) meeting. The FDA acknowledged that in the LiFT study subjects achievedimprovements in key components associated with NASH histopathology after36-weeks of treatment with LPCN 1144 in adult males and agreed that the proposedmulticomponent primary surrogate endpoint is acceptable for seeking approvalunder the accelerated approval pathway. The FDA also recommended eitherconducting a separate dose-ranging study prior to phase 3 or evaluating multipledoses in phase 3. The FDA agreed that the proposed primary multicomponentsurrogate endpoint, NASH resolution with no worsening of fibrosis, is acceptablefor seeking approval under the accelerated approval pathway and the FDArecommended a phase 3 trial with a study duration of 72 weeks. The FDA hasrequested that Lipocine submit an updated Phase 3 protocol for FDA feedback onthe study design and we have requested an EOP2 meeting to discuss the phase 3and confirmatory trial designs.

We are exploring the possibility of licensing LPCN 1144 to a third party,although no licensing agreement has been entered into by the Company. Noassurance can be given that any license agreement will be completed, or, if anagreement is completed, that such an agreement would be on acceptable terms.

TLANDO: An Oral Product Candidate for Testosterone Replacement Therapy

As previously described, under the Antares License Agreement, we granted toAntares an exclusive, royalty-bearing, sublicensable right and license todevelop and commercialize, upon final approval of TLANDO from the FDA, ourTLANDO product for TRT in the U.S. On December 8, 2020, the FDA providedtentative approval for TLANDO as a TRT in adult males for conditions associatedwith a deficiency of endogenous testosterone, also known as hypogonadism. TheFDA provided final approval of TLANDO on March 28, 2022. Any FDA requirement toconduct certain post-marketing studies will be the responsibility of ourlicensee, Antares.

Proof-of-concept for TLANDO was initially established in 2006, and subsequentlyTLANDO was licensed in 2009 to Solvay Pharmaceuticals, Inc. which was thenacquired by Abbott Products, Inc. ("Abbott"). Following a portfolio reviewassociated with the spin-off of AbbVie Inc. by Abbott in 2011, the rights toTLANDO were reacquired by us. All obligations under the prior license agreementhave been completed except that Lipocine will owe Abbott a perpetual 1% royaltyon net sales. Such royalties are limited to $1 million in the first two calendaryears following product launch, after which period there is not a cap onroyalties and no maximum aggregate amount. If generic versions of any suchproduct are introduced, then royalties are reduced by 50%.

Under the Pediatric Research Equity Act ("PREA"), since TLANDO received full FDAapproval, under the Antares Licensing Agreement, Antares will need to addressthe PREA requirement to assess the safety and effectiveness of TLANDO inpediatric patients. The FDA may also require certain post-marketing studies tobe conducted which will also be the responsibility of our licensee, Antares.

Upon execution of the Antares License Agreement, Antares paid to us an initialpayment of $11.0 million. Antares will also make additional payments of $5.0million to us on each of January 1, 2025, and January 1, 2026, provided thatcertain conditions are satisfied. We are also eligible to receive milestonepayments of up to $160.0 million in the aggregate, depending on the achievementof certain sales milestones in a single calendar year with respect to allproducts licensed by Antares under the Antares License Agreement. In addition,upon commercialization, we will receive tiered royalty payments at rates rangingfrom percentages in the mid-teens to up to 20% of net sales of TLANDO in theUnited States, subject to certain minimum royalty obligations. Further, onOctober 14, 2021, we assigned our Manufacturing Agreement, dated August 27,2013, by and between the Company and Encap Drug Delivery (the "ManufacturingAgreement") to Antares as part of the Antares License Agreement.

We are exploring the possibility of licensing LPCN 1021 (known as TLANDO in theUnited States) to third parties outside the United States, although no licensingagreement has been entered into by the Company. If and when an agreement is madewith a partner, such arrangement would likely be contingent upon obtainingacceptable cost of goods by securing an agreement with a new manufacturer inaddition to obtaining local regulatory approval. No assurance can be given thatany license agreement will be completed, or, if an agreement is completed, thatsuch an agreement would be on terms favorable to us.

LPCN 1111: A Next-Generation Long-Acting Oral Product Candidate for TRT

LPCN 1111: is a next-generation, novel ester prodrug of testosterone comprisedof testosterone tridecanoate (TT) which uses the proprietary delivery technologyto enhance solubility and improve systemic absorption. We completed a Phase 2bdose finding study in hypogonadal men in the third quarter of 2016. The primaryobjectives of the Phase 2b clinical study were to determine the starting Phase 3dose of LPCN 1111 along with safety and tolerability of LPCN 1111 and itsmetabolites following oral administration of single and multiple doses inhypogonadal men. Good dose-response relationship was observed over the testeddose range in the Phase 2b study. Additionally, the target Phase 3 dose metprimary and secondary end points. Overall, LPCN 1111 was well tolerated with nodrug-related severe or serious adverse events reported in the Phase 2b study.

In February 2018 we had a meeting with the FDA to discuss these pre-clinicalresults and to discuss the Phase 3 clinical study and path forward for LPCN1111. Based on the results of the FDA meeting and additional pre-clinicalstudies conducted after the FDA meeting, we have proposed a Phase 3 protocol forLPCN 1111 and have solicited FDA feedback. Based on initial FDA feedback, weexpect the Phase 3 clinical trial design to follow the International Council forHarmonisation of Technical Requirements for Pharmaceuticals for Human Use("ICH") guidelines and we expect the trial will include at least a three-monthefficacy treatment period and a one-year safety component for approximately 100subjects. We are currently seeking further clarification from FDA with respectto the total subject LPCN 1111 exposure information needed for an NDA filing. Wecontinue to refine the Phase 3 protocol and plan to request FDA approval of theprotocol once it is finalized. Additionally, the FDA previously requested that afood effect and a phlebotomy study be completed, and that ambulatory bloodpressure monitoring ("ABPM") be included as part of the Phase 3 clinical study.We are currently transferring the manufacturing of LPCN 1111 to a third-partycontract manufacturer and scaling up the formulation after which we anticipatethe next steps in developing LPCN 1111 may be to conduct a foodeffect/phlebotomy study with LPCN 1111. Under the terms of the Antares LicenseAgreement, Antares has been granted an option to license LPCN 1111, exercisableon or before March 31, 2022, for further development and, should LPCN 1111receive FDA approval, commercialization. On April 1, 2022, the Company enteredinto the First Amendment to the License Agreement (the "Amendment"), pursuant towhich the License Agreement was amended to extend the deadline by which Antaresshall exercise its option to license LPCN 1111 to June 30, 2022. Asconsideration for the Company agreeing to enter into the Amendment, Antares paidthe Company a non-refundable cash fee of $500,000 in April 2022.If Antaresexercises its option to license LPCN 1111, we will be entitled to an additionalpayment of $3.5 million, as well as development milestone payments of up to$35.0 million in the aggregate and tiered royalty payments at rates ranging frompercentages in the mid-teens to 20% of net sales of LPCN 1111 in the UnitedStates. We are currently in the process of scaling up manufacturing productionof clinical supplies for a Phase 3 clinical trial.

LPCN 1107: An Oral Product Candidate for the Prevention of Preterm Birth

We believe LPCN 1107 has the potential to become the first oralhydroxyprogesterone caproate ("HPC") product indicated for the reduction of riskof PTB (delivery less than 37 weeks) in women with singleton pregnancy who havea history of singleton spontaneous PTB. Prevention of PTB is a significant unmetneed as approximately 11.7% of all U.S. pregnancies result in PTB, a leadingcause of neonatal mortality and morbidity.

We have completed a multi-dose PK dose selection study in pregnant women. Theobjective of the multi-dose PK selection study was to assess HPC blood levels inorder to identify the appropriate LPCN 1107 Phase 3 dose. The multi-dose PK doseselection study was an open-label, four-period, four-treatment, randomized,single and multiple dose PK study in pregnant women with three dose levels ofLPCN 1107 and the IM HPC (Makena). The study enrolled 12 healthy pregnant women(average age of 27 years) with a gestational age of approximately 16 to 19weeks. Subjects received three dose levels of LPCN 1107 (400 mg BID, 600 mg BID,or 800 mg BID) in a randomized, crossover manner during the first threetreatment periods and then received five weekly injections of HPC during thefourth treatment period. During each of the LPCN 1107 treatment periods,subjects received a single dose of LPCN 1107 on Day 1 followed by twice dailyadministration from Day 2 to Day 8. Following completion of the three LPCN 1107treatment periods and a washout period, all subjects received five weeklyinjections of HPC. Results from this study demonstrated that average steadystate HPC levels (Cavg0-24) were comparable or higher for all three LPCN 1107doses than for injectable HPC. Additionally, HPC levels as a function of dailydose were linear for the three LPCN 1107 doses. Also, unlike the injectable HPC,steady state exposure was achieved for all three LPCN 1107 doses within sevendays.

A traditional PK/PD based Phase 2 clinical study in the intended patientpopulation is not expected to be required prior to entering into Phase 3.Therefore, based on the results of our multi-dose PK study we had anEnd-of-Phase 2 meeting and subsequent guidance meetings with the FDA to define apivotal Phase 2b/3 development plan for LPCN 1107. However, these discussionswill need to be updated based on recent developments with Covis' Makena. Weplan to resume our interactions with the FDA to discuss our pivotal clinicaltrial design and better understand next steps to advance LPCN 1107

We are exploring the possibility of licensing LPCN 1107 to a third party,although no licensing agreement has been entered into by the Company. Noassurance can be given that any license agreement will be completed, or, if anagreement is completed, that such an agreement would be on acceptable terms.

The FDA has granted orphan drug designation to LPCN 1107 based on a majorcontribution to patient care. Orphan designation qualifies Lipocine for variousdevelopment incentives, including tax credits for qualified clinical testing,and a waiver of the prescription drug user fee when we file our NDA.

On October 5, 2020, the FDA's Center for Drug Evaluation and Research ("CDER")proposed that Makena be withdrawn from the market because the PROLONG trialfailed to verify the clinical benefit of Makena and concluded that the availableevidence does not show Makena is effective for its approved use.

CDER issued AMAG Pharmaceuticals, the NDA holder at the time, a Notice ofOpportunity for Hearing to withdraw approval of Makena, for which AMAGPharmaceuticals responded by requesting a hearing and providing detail on thecompany's position, recognizing clinicians' decade-long use of Makena'streatment and the public health implications of withdrawing approval. The FDACommissioner has recently granted Covis a public hearing although the date ofthat hearing is not publicly known. During this time, Makena and the approvedgenerics of Makena will remain on the market until the FDA makes a finaldecision about these products.

Currently, Makena and the approved generics of Makena are the only productsapproved for the prevention of recurrent preterm birth.

The FDA also indicated that it intends to hold a meeting with experts inobstetrics, neonatal care, and clinical trial design to discuss how tofacilitate development of effective and safe therapies to treat preterm birth.

Oral NAS Programs for CNS Disorders

Some preferred endogenous or naturally occurring NAS present in central nervoussystem (CNS) act as positive allosteric modulators (PAM) of the GABAA receptor,the major biological target of the inhibitory neurotransmitter ?-aminobutyricacid (GABAA). To improve oral delivery of these modulators, several syntheticNAS derivatives of endogenous GABAA receptor PAMs, have been developed fortherapeutic use in the past few decades.

We believe through utilization of our proprietary technology we may have theability to enable effective oral delivery of endogenous GABAA receptor PAMswhich historically had been challenging to deliver orally as they were deemed tobe not orally bioavailable. We believe these endogenous GABAA receptor PAMsprovide opportunity as a differentiated NAS for treatment of various CNSdisorders via the preferred and convenient oral route.

LPCN 1154: Product Candidate for PPD

We are currently evaluating LPCN 1154 comprising an endogenous NAS for PPD. FDAhas cleared LPCN 1154 IND (investigational new drug) application to conduct aphase 2 study in PPD. We have completed a PK study with LPCN 1154 post oraladministration in which we believe clinically relevant levels of the active wereobserved. We are currently conducting a food effect PK study.

PPD (Postpartum depression), a type of major depressive disorder with onseteither during pregnancy or within four weeks of delivery, refers to depressionpersisting up to 12 months after childbirth. PPD can be clinically segmented bythe severity of symptoms and presence of a comorbidity, including epilepsy.Approximately 1 in 9 mothers suffers from PPD in the United States alone; thisequates to approximately 500,000 women being affected by PPD annually.

Approximately, 1 in 9 mothers suffer from PPD in the United States alone, whichequates to approximately 500,000 women affected by PPD annually. We believethere is considerable unmet need within women with PPD due to lack of convenientand fast-acting oral therapies. Selective Serotonin Reuptake Inhibitors (SSRIs)have been the traditional first-line choice for women with severe PPD requiringweeks for onset of efficacy; therefore, a need for a faster onset of actionremains a significant unmet need in treating PPD, especially in women withepilepsy risk wherein psychiatric comorbidity is common and PPD rates are higherthan the general population.

Injectable brexanolone (ZulressoTM, Sage Therapeutics) became the firstFDA-approved treatment for postpartum depression. However, numerous factorslimit the utilization of injectable brexanolone such as method ofadministration, cost, and safety concerns. Administration of injectablebrexanolone requires a 60-hour continuous infusion in a supervised medicalsetting, a demanding ask for a mother with a newborn. Besides associated privacyconcerns and social stigma, hospitalization may also require separation of themother and child for a few days, which may be difficult to the already strainedmother-infant bond and may present breast feeding challenges. Moreover, thepharmacotherapy costs coupled with hospitalization/childcare costs limits itsaccessibility and affordability to women most in need of the therapy. Finally,due to concerns about the safety of injectable ZulressoTM including excessivesedation or loss of consciousness, Zulresso has a Black Box Warning in its labeland is only available through a restricted distribution program (REMS), andsites need significant time to become treatment ready.

We believe the need for a convenient, at-home treatment with faster onset ofaction which could offer privacy and affordability, independent ofsocio-economic status, for women with PPD is a significant unmet need. LPCN 1154targets this unmet need with affordable NAS.

LPCN 2101: NAS for epilepsy

We are currently evaluating an additional NAS candidate, LPCN 2101, for womenwith epilepsy ("WWE"). We have completed a pre-clinical study for LPCN 2101. Weplan to file an IND with the U.S. FDA for LPCN 2101 to conduct aproof-of-concept study for the evaluation of safety, tolerability, and efficacyin adult female subjects of childbearing age diagnosed with epilepsy.

Disease Overview - Epilepsy

Epilepsy is defined by the 1) occurrence of at least two unprovoked seizuresmore than 24 hours apart, 2) occurrence of one unprovoked seizure and aprobability of further seizures occurring over the next 10 years, and/or 3)diagnosis of an epilepsy syndrome. Patients with epilepsy are more likely to becomorbid with other conditions, including depression and anxiety.

Patients with epilepsy have increased risk of mortality due to direct effects ofseizures (e.g., status epilepticus, car accidents) and indirect effects ofseizures (e.g., suicide, cardiovascular effects.)

Epilepsy is a disorder of the brain that causes seizures, affecting thephysical, mental, and social well-being of persons, and is associated with a 2to 3 times greater mortality rate compared with the general population. About60-65% of epilepsy is idiopathic and about 30% of patients are refractory (i.e.,epilepsy not well managed with currently available antiepileptic drugs("AEDs")). Epilepsy is the most common neurological disorder during pregnancy.

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LIPOCINE INC. MANAGEMENT'S DISCUSSION AND ANALYSIS OF FINANCIAL CONDITION AND RESULTS OF OPERATIONS (form 10-Q) - Marketscreener.com

Red light therapy, mentioned by Fox News host Tucker Carlson as a way to increase testosterone levels in men, is not medically approved for that purpose.

Fox News host Tucker Carlson recently interviewed personal trainer Andrew McGovern, who advocates for the use of red light therapy to increase testosterone levels in men as part of his Tucker Carlson Originals series.

During the interview, Carlson refers to red light therapy as testicle tanning, a phraseshared widely on social media platforms like Twitter. This comes as Carlson is promoting his documentary The End of Men, which states that decreasing testosterone levels in men is a problem in the U.S.

A urologist said later in a viral tweet that there is absolutely no data on testicle tanning, adding that it doesnt stimulate the production of testosterone.

THE QUESTION

Is red light therapy a medically approved treatment for increasing testosterone levels?

THE SOURCES

THE ANSWER

No, red light therapy isnt a medically approved treatment for increasing testosterone levels.

WHAT WE FOUND

Red light therapy is often promoted as a treatment for common skin woes, such as stretch marks, scars, acne and others, along with improving hair growth and reducing inflammation. Cleveland Clinic says red light therapy, which is also known as low-level laser light therapy and low-power laser therapy among other names, is an emerging therapy but holds a lot of promise.

During red light therapy, you expose your skin to a lamp, device or laser with a red light. Its thought to work by acting on the power plant in your bodys cells called mitochondria. With more energy, cells can work more efficiently to do things like repairing a persons skin.

But red light therapy isnt approved as a medical treatment for increasing testosterone levels and many experts dont recommend it.

The U.S. Food and Drug Administration (FDA) has approved oral testosterone capsules like Jatenzo as a treatment for men with low testosterone levels due to certain medical conditions.

According to mens health website prostate.net, the FDA hasnt approved any light therapy devices to increase testosterone production. There are red light therapy devices available online that dont need FDA clearance, but they arent meant for raising testosterone.

One medical professional who spoke to VERIFY said red light therapy could do more harm to testosterone levels than good.

The risks of it come with temperature changes as you elevate the temperature of the scrotum. If there is a temperature increase, sperm production will diminish, testosterone production will diminish, so there's that potential, said Amin Herati, M.D., director of male infertility and mens health at Johns Hopkins School of Medicine.

Additionally, there is absolutely no controlled study that proves red light therapy increases testosterone, Adam Friedman, M.D., professor and chair of dermatology at The George Washington School of Medicine and Health Sciences, said. The science is just simply not there.

There are some studies that show low-level light therapy or low intensity red light could increase testosterone levels. But they were conducted on animals like rats and birds not humans.

A 2013 study on 30 six-week-old rats found that low-level light therapy might be an alternative treatment modality to the conventional types of testosterone replacement therapy.

Some proponents of red light therapy also point to a 2016 study conducted by researchers at the University of Siena in Italy that focuses on a lack of interest in sex being remedied by exposure to bright light. But those researchers studied a relatively small group of only 38 men.

One group received regular treatment with a specially adapted light box, while the control group received treatment with a light box that gave out significantly less light, researchers said. After two weeks of treatment or placebo, researchers found that those who received treatment through higher levels of light had increased testosterone levels and reported greater levels of sexual satisfaction.

One reason could be that light therapy inhibits the pineal gland in the center of the brain, which may allow the production of testosterone, researchers said.

Though the study found some indication the treatment might increase testosterone, the researchers still said they could not yet recommend light therapy as a clinical treatment. It may be a viable solution to a lack of interest in sex if its shown to work in a larger study, they added.

Many published studies looking into red light therapy for a variety of uses apart from testosterone production have only included a small number of people, were absent a placebo group, or were limited to animals as well, Cleveland Clinic says.

Testicle tanning is a misnomer for red light therapy

The way Carlson referred to red light therapy as testicle tanning is also a misnomer.

Red light therapy uses low wavelength red light, Cleveland Clinic explains, unlike cancer-causing UV rays from the sun or tanning booths. Thats why medical professionals say it appears to be safe for treating certain skin conditions.

Theres no such thing as a safe tan, since its actually the way skin responds to being injured or harmed by ultraviolet radiation in an effort to limit further damage, Friedman said. Exposure to UV rays can also lead to painful sunburns and increase the risk of developing skin cancer.

Its unlikely that a tanning bed or direct exposure to sunlight will increase testosterone production in the testicles, either, according to Herati.

For the light to be able to reach the testicles, it has to penetrate through multiple layers of tissue has to go through the skin, the layer muscle under the skin, a couple other layers of fascia before it reaches the lining of the testicle and it has to penetrate within the testicle, he said. So the likelihood that the UV would be able to penetrate would be unlikely in that situation, or to have an effect.

Some natural ways that men can boost their testosterone include a healthy diet, an exercise routine that incorporates cardio and strength training, and getting enough sleep, experts say.

The VERIFY team works to separate fact from fiction so that you can understand what is true and false. Please consider subscribing to our daily newsletter, text alerts and our YouTube channel. You can also follow us on Snapchat, Twitter, Instagram, Facebook and TikTok. Learn More

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No, red light therapy isnt a medically approved treatment for increasing testosterone - ABC10.com KXTV

Are there three words in the English language that can strike quite as much trepidation into the hearts of the sane and rational person as Tucker Carlson original? Yes, the documentary strand that brought you such titles as Hungary vs Soros: The Fight for Civilization and Patriot Purge, a BS-laden fantasy about the January 6 riots that contained so many bonkers claims about false-flag operations that it forced a tranche of Fox News veterans to quit the network, has returned.

The latest addition to the Carlson oeuvre is called The End of Men and its Magic Mike-style trailer just dropped.

It begins with a familiar Make America Great Again-style montage, centering on a John F Kennedy speech in which he extols the virtues of strength and exercise and berates Americas soft, chubby fat-looking children. Quickly, Kennedys reasonable-for-the-time approach to childhood obesity is equated with a precipitous decline in sperm counts and testosterone over the last 50 years.

And then what could only be described as a series of money shots. As the booming timpanis of a Richard Strauss piece from 2001: A Space Odyssey swell we see huge buff topless men, cutting wood, milking cows, firing guns, barbecuing, fighting, drinking egg yolks and most strikingly, tanning their genitals. This supposed sequence of real red-blooded males is perhaps the campest thing Fox News has aired since Glenn Beck doused a handsome model in gasoline.

Carlsons deeply homoerotic version of real men looks more xVideos than ex-mining town but the testosterone-based view of masculinity hes pushing has been a common theme for Fox News over the past decade, and a profitable one.

The testicle tanning, or red-light therapy, shown in the video is explained further in an interview Carlson does with a self-proclaimed bromeotherapy expert. He claims that by dousing your balls in red LEDs, you can create higher levels of testosterone.

The potential for UV or red light to increase testosterone levels has been quite well documented but there are no peer-reviewed double-blind studies that are able to prove these claims. Testosterone levels also change dramatically throughout the day, and also see dramatic increases from exercise, new sexual partners and changes to diet.

Its no surprise to see Fox News suggest that the answer to all of mankinds problems are testosterone related. The channel is heavily invested in the idea that a decrease in testosterone is making men more liberal and less masculine, and many of its remaining advertisers sell pills that promise to increase mens testosterones levels.

I spent some time reporting this story three years ago, that testosterone was becoming heavily politicised, particularly by Trump-supporting radio hosts who equated liberalism to having low T (one rightwing radio doctor even offered a free testosterone test to any listener thinking about voting for Hillary Clinton). The US is awash with ads for testosterone supplements that make a similar claim, many of them airing on Fox News. Trump himself used to insinuate that his opponents were tired and had low T.

Many men are injecting themselves with testosterone with political motivations but in reality the idea that testosterone is the male hormone and oestrogen is the female one is wrong. Both men and women have both hormones, at highly varied levels, and most men have far more testosterone than they need (indeed, testosterone, which is critical to heart function, is often converted into oestrogen, which means that people who routinely inject testosterone often end up growing breasts). Low testosterone can make some men feel tired and impotent and they need replacement therapy, but others get by on low levels of blood testosterone just fine.

Carlson is right that sperm counts and overall testosterone have been decreasing over the last 50 years due to lifestyle changes including rising obesity. But the idea that this in some way is a problem of manliness, and that if only we tanned our balls men would become happier, is patently untrue.

The show is also a reflection of how far Carlson has shifted into the world of pseudo-scientific and bezerk solutions in the past few years. Just four years ago he was still talking about falling testosterone levels but as part of a wider soul-searching about men in America, doing pieces about why men were more likely to kill themselves, commit mass shootings, be incarcerated, be medicated as children and are performing worse by some educational measures. In the video above, Carlson takes a rightwing anti-feminist position but at least makes some reasonable points about the problems facing American men.

Since then Carlson has fallen off a deep end of trolling and insanity and would rather entertain wild medical interventions than political change. Perhaps hed be happier doing some red light therapy instead of his nightly red face therapy.

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Tucker Carlsons answer to masculinitys supposed crisis? Testicle tanning - The Guardian

PALM BEACH, Fla., April 14, 2022 /PRNewswire/ -- FinancialNewsMedia.com News Commentary - CAR-T therapy is a sort of treatment in which a patient's T cells which is a type of immune system cell, are genetically modified to attack cancer cells in the lab. T cells are extracted from the blood of a patient. The gene for a specific receptor that binds to a specific protein on the patient's cancer cells is then transferred to T cells in the lab. A chimeric antigen receptor is a unique type of receptor (CAR). CAR-T units are generated in large numbers in the lab and then infused into the patient. CAR-T therapy is used to treat specific types of blood malignancies, and it is also being researched for other cancers. CAR T therapy is also known as Chimeric antigen receptor T-cell therapy. T cells are used in CAR T therapy since they are generally responsible for destroying malignant cells and virus-infected cells. Cancer cells are known to hide from the immune system, but scientists have been able to improve T cells' ability to locate and kill cancer cells using CAR T therapy. A report from Polaris Market Research projected that the global CAR-T cell therapy market was valued at USD 1,965.8 million in 2021, expected to grow at a CAGR of 31.16 % during the forecast period (2029). The report said: "CAR T therapy market is expected to grow due to the growing prevalence of cancer cases across the globe. This treatment has captured the attention of researchers and the public because of the remarkable responses they have produced in patients. The Food and Drug Administration (FDA) approved two CAR T treatments in 2017, one for children with acute lymphoblastic leukaemia (ALL) and the other for adults with advanced lymphomas." Active biotech and pharma companies in the markets this week include Oncolytics Biotech Inc. (NASDAQ: ONCY) (TSX: ONC), Sierra Oncology, Inc (NASDAQ: SRRA), Antares Pharma, Inc. (NASDAQ: ATRS), Clovis Oncology, Inc. (NASDAQ: CLVS), Turning Point Therapeutics, Inc. (NASDAQ: TPTX).

"Continuous growth has been witnessed in biotechnology and life science sectors for the treatment of cancer using chimeric antigen receptors. Increased patient assistance programs (PAPs), increased government activities for cancer awareness, rising cancer prevalence worldwide, and strong R&D initiatives from key companies are all driving CAR-T cell therapy market expansion. With the growing need for cell-based therapy, producers have started investing in the manufacturing of this therapy. North America is expected to dominate the global CAR-T cell therapy market due to the increasing cancer cases and growing emergence of the biotechnological sector. North America is witnessing an increasing number of cancer cases which is increasing the market demand for cancer therapies in the region The presence of key players in the region are focusing on expanding their global presence, is fueling the CAR-T cell therapy market."

Oncolytics Biotech Inc. (NASDAQ: ONCY) (TSX: ONC) BREAKING NEWS: Oncolytics Biotech Announces Publication of Preclinical Data Demonstrating the Synergistic Anti-Cancer Activity of Pelareorep Combined with CAR T Cell Therapy in Solid Tumors in Science Translational Medicine- Oncolytics Biotech today announced the publication of preclinical data demonstrating the synergistic anti-cancer activity of pelareorep combined with chimeric antigen receptor (CAR) T cell therapy in solid tumors. The paper, entitled "Oncolytic virus-mediated expansion of dual-specific CAR T cells improves efficacy against solid tumors in mice," was published in Science Translational Medicine in collaboration with researchers at several prestigious institutions, including the Mayo Clinic and Duke University. A link to the paper can be found by clicking here.

"Having these results published in such a high-impact journal provides important external validation of their significance," said Thomas Heineman, M.D., Ph.D., Chief Medical Officer of Oncolytics Biotech Inc. "While CAR T cells have generated long-term cures in hematologic malignancies1, the immunosuppressive tumor microenvironments (TMEs) of solid organ cancers have thus far limited their efficacy in these indications. Pelareorep has repeatedly been shown to reverse immunosuppressive TMEs, and in the present publication pelareorep is shown to enable the effectiveness of CAR T cells in multiple murine solid tumor models. This is a powerful finding that, if translated to the clinic, could significantly improve the prognosis of patients with a variety of highly prevalent cancers by providing a novel and potentially durable treatment option. By demonstrating the ability to improve T cell perseverance, reduce antigen escape, and overcome challenging solid tumor TMEs, the inclusion of pelareorep addresses the three most challenging roadblocks to effective CAR T therapy."

Andrew de Guttadauro, President of Oncolytics Biotech U.S. and Global Head of Business Development, added, "Despite revolutionizing the treatment of certain cancers and surpassing a billion dollars in sales last year, CAR T therapies currently only serve a small subset of patients suffering from hematologic malignancies. With these latest results, we now have strong preclinical evidence that pelareorep can fully unlock the value of CAR T therapies by expanding their commercial potential to the significantly larger market of cancer patients who are battling solid tumors."

Preclinical studies published in the paper evaluated the persistence and efficacy of pelareorep-loaded CAR T cells ("CAR/Pela therapy") in multiple murine solid tumor models. The effects of combining CAR/Pela therapy with a subsequent intravenous dose of pelareorep ("pelareorep boost") were also investigated. Key data and conclusions from the paper include:

Dr. Matt Coffey, President and Chief Executive Officer of Oncolytics Biotech Inc. and co-author of the paper commented, "These exciting results are an excellent example of how we are leveraging collaborations with key opinion leaders and premier research institutions to broaden pelareorep's potential therapeutic impact. This allows us to remain primarily focused on our lead breast cancer program, which has shown how pelareorep's ability to promote tumor T cell infiltration leads to synergy with checkpoint inhibitors in the clinic. These newly published preclinical findings show pelareorep's synergistic benefits extend even beyond checkpoint inhibitors and highlight an opportunity to increase our addressable patient population. As we pursue this opportunity moving forward, we intend to utilize relationships with academic or industry partners so that we can continue to execute on our clinical and corporate objectives with efficiency." CONTINUED Read this full press release and more news for ONCY at: https://www.financialnewsmedia.com/news-oncy/

Other recent developments in the biotech industry of note include:

GlaxoSmithKline plc (NYSE: GSK) and Sierra Oncology, Inc (NASDAQ: SRRA)recently announced that the companies have entered into an agreement under which GSK will acquire Sierra Oncology, a California-based, late-stage biopharmaceutical company focused on targeted therapies for the treatment of rare forms of cancer, for $55 per share of common stock in cash representing an approximate total equity value of $1.9 billion (1.5 billion).

Myelofibrosis is a fatal cancer of the bone marrow impacting the normal production of blood cells. Anaemia represents a high unmet medical need in patients with myelofibrosis. At diagnosis, approximately 40% of patients are already anaemic, and it is estimated that nearly all patients will eventually develop anaemia.Patients treated with the most commonly used JAK inhibitor will often require transfusions, and more than 30% will discontinue treatment due to anaemia.Anaemia and transfusion dependence are strongly correlated with poor prognosis and decreased overall survival. Momelotinib has a differentiated mode of action with inhibitory activity along key signalling pathways.

Antares Pharma, Inc. (NASDAQ: ATRS) recently announced that the U.S. Food and Drug Administration granted final approval for TLANDO (testosterone undecanoate), an oral treatment for testosterone replacement therapy ("TRT") indicated for conditions associated with a deficiency or absence of endogenous testosterone, or hypogonadism in adult males.

Robert F. Apple, President and Chief Executive Officer of Antares Pharma, commented, "The FDA approval of TLANDO brings to market an oral formulation of testosterone that we believe will prove beneficial to physicians and their patients. We have recently expanded our commercial organization to 108 sales representatives and expect to leverage our relationships with urologists and endocrinologists to drive adoption of TLANDO. This approval also reinforces the opportunity for Antares to continue to drive share gains in the TRT market with both TLANDO and XYOSTED and support our future growth with an expanded commercial portfolio.

Clovis Oncology, Inc. (NASDAQ: CLVS), recently announced that two abstracts featuring non-clinical data from studies evaluating FAP-2286 and Rubraca and a Trial-in-Progress poster detailing the Phase 1 portion of the LuMIERE study will be presented at the upcoming American Association for Cancer Research (AACR) Annual Meeting 2022, being held April 8-13, 2022, in New Orleans.

In a new non-clinical data analysis, FAP-2286 demonstrated potent affinity for human fibroblast activation protein (FAP) by biochemical and cell-based assays. Additionally, lutetium-177 (177Lu)-FAP-2286 showed longer tumor retention, resulting in greater tumor inhibition as compared to lutetium-177 (177Lu)-FAPI-46, a FAP-targeted radiotracer developed for therapeutic applications at the University of Heidelberg, Germany.

Turning Point Therapeutics, Inc. (NASDAQ: TPTX), a clinical-stage precision oncology company developing next-generation therapies that target genetic drivers of cancer, recently announced positive topline results from the registrational TRIDENT-1 study across all fourROS1-positive advanced non-small cell lung cancer (NSCLC) cohorts, as reported by Blinded Independent Central Review (BICR).

"We are very encouraged by the topline results from the pooled Phase 1 and Phase 2 portions of TRIDENT-1 by BICR shared today and continue to believe repotrectinib is a potentially best-in-class drug candidate for patients withROS1-positive advanced NSCLC," said Athena Countouriotis, M.D., President and Chief Executive Officer. "The confirmed ORR data and 95% confidence intervals across all four cohorts remain strong, and the initial estimated Kaplan-Meier landmark analyses based on limited median follow-up of approximately 10 months for both duration of response and progression free survival in the TKI-nave population are trending in the direction we had hoped for given this is the highest area of unmet medical need. We believe a differentiated profile is built upon a strong ORR and durability of response that could improve upon the current standard of care."

DISCLAIMER: FN Media Group LLC (FNM), which owns and operates FinancialNewsMedia.com and MarketNewsUpdates.com, is a third party publisher and news dissemination service provider, which disseminates electronic information through multiple online media channels. FNM is NOT affiliated in any manner with any company mentioned herein. FNM and its affiliated companies are a news dissemination solutions provider and are NOT a registered broker/dealer/analyst/adviser, holds no investment licenses and may NOT sell, offer to sell or offer to buy any security. FNM's market updates, news alerts and corporate profiles are NOT a solicitation or recommendation to buy, sell or hold securities. The material in this release is intended to be strictly informational and is NEVER to be construed or interpreted as research material. All readers are strongly urged to perform research and due diligence on their own and consult a licensed financial professional before considering any level of investing in stocks. All material included herein is republished content and details which were previously disseminated by the companies mentioned in this release. FNM is not liable for any investment decisions by its readers or subscribers. Investors are cautioned that they may lose all or a portion of their investment when investing in stocks. For current services performed FNM expects to be compensated forty nine hundred dollars for news coverage of the current press releases issued by Oncolytics Biotech Inc. by a non-affiliated third party. FNM HOLDS NO SHARES OF ANY COMPANY NAMED IN THIS RELEASE.

This release contains "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E the Securities Exchange Act of 1934, as amended and such forward-looking statements are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. "Forward-looking statements" describe future expectations, plans, results, or strategies and are generally preceded by words such as "may", "future", "plan" or "planned", "will" or "should", "expected," "anticipates", "draft", "eventually" or "projected". You are cautioned that such statements are subject to a multitude of risks and uncertainties that could cause future circumstances, events, or results to differ materially from those projected in the forward-looking statements, including the risks that actual results may differ materially from those projected in the forward-looking statements as a result of various factors, and other risks identified in a company's annual report on Form 10-K or 10-KSB and other filings made by such company with the Securities and Exchange Commission. You should consider these factors in evaluating the forward-looking statements included herein, and not place undue reliance on such statements. The forward-looking statements in this release are made as of the date hereof and FNM undertakes no obligation to update such statements.

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Advancements of CAR-T Cell Therapies Importance Grows While Cancer Cases Increasing - PR Newswire

The Eagles swim against the University of North Carolina (UNC)-Wilmington in the WoodPEC in 2014. (Courtesy of Jason Oh)

Following the end of University of Pennsylvania swimmer and transgender woman athlete Lia Thomas collegiate career in March, the subsequent wave of nationwide anti-trans athlete legislation has jeopardized the future of inclusion in sports. But while the world becomes increasingly embroiled in legislative battles designed to maximize exclusion, the nuances of the controversiality of fairness and inclusion have been swept to the wayside.

Thomas broke barriers as the first trans female athlete to win a title at the NCAA Swimming and Diving championships. Despite following NCAA policy and undergoing over two years of hormone replacement therapy (HRT), she endured hate from not only her teammates, but also politicians and avid swim fans arguing about her eligibility. The uproar of concern about compromising the integrity and fairness of womens sports could be labeled as transphobic and for some, it certainly comes from a place of bigotry. But perhaps the arguments also stem from our curiosity surrounding the creation of the policy and how we reconcile existing laws with a future in which binary classifications no longer apply.

After consulting with athletes, sports organizations and medical experts in 2015, the International Olympic Committee (IOC) determined that while transgender men can take part in competitions without any restrictions, testosterone levels of transwomen must be below 10 nanomoles/liter for at least one year prior to competing. Later in 2021, however, the guidelines were adjusted to consider hyperandrogenism, a medical condition commonly affecting more women than men, which may result in higher testosterone levels irrespective of HRT. Instead of an overarching criteria for all athletes, IOC now shifts to an evidence-based, sport-specific framework where the data must strongly suggest a consistent, unfair, disproportionate competitive advantage. While the change is a step forward in the right direction, defining a disproportionate advantage remains vague and is not conducive to conversation.

Current political debates emphasize the most widely accepted definition of inclusion and equity: that all people, regardless of gender identity or expression, be afforded the same chances and opportunities. Transgender folks deserve the same basic respect as those who conform to now outdated gender binary classifications. At the same time, failing to consider the biological differences such as lean body mass, pelvic width and lung capacity neglects the full story.

Physicality is undeniably a more pertinent factor in sports than in other aspects of life. The innately different build of cisgender men offers them a significant and often insurmountable competitive advantage over women. For instance, men have a longer and larger bone structure which supports more powerful muscles and a wider frame. Their high muscle mass to body-weight ratio also gives men a noticeable advantage in speed-based competitions. In sports such as swimming, where athletes race against the clock and one another, female records will always be slower than male ones.

Different body compositions are advantageous in different sports, and forcing the same sweeping ban on all athletes would not be equitable or fair. Body composition can be measured by a number of factors, namely body fat and the ratio of strength-to-mass. While lower body fat and higher levels of lean body mass might benefit weightlifters, boxers and footballers, this body type doesnt necessarily work for everyone. Many distance runners and track athletes would be faster with lower body fat as it reduces air drag. Higher strength-to-mass ratios like martial artists and gymnasts have may hold their bodies up with more ease and better counteract the effects of gravity. But for swimmers, its not as clear cut. Body fat may be more buoyant, but too much concentrated in one area will lead to drag. Too much lean body mass may also result in sinking. Optimal body composition is not universal, so we shouldnt treat everyone the same way either.

In Florida, Texas and other traditionally right-leaning states, legislators have recently passed laws forcing public school students to only compete on sports teams based on the sex they were assigned at birth. The policies continue, despite a persisting lack of research and evidence indicating that innate biological differences give trans athletes a significant advantage. I would be remiss not to consider the nuance behind the substantial physical advantages of trans female athletes. HRT may increase body fat and decrease lean muscle mass. But with a lack of research, it is unclear how long it takes for this to occur, and to what extent it will affect the bodies of trans athletes and subsequently, their swimming technique.

Its foolish to dismiss such stark time differences during formal competitions. For the duration of the 2021-2022 season and at the 2022 Ivy League Womens Swimming and Diving Championships, Thomas competed on the womens team; at the championships, she won the 200 freestyle with a time of 1:43.12. The top finisher on the mens side, Dean Farris from Harvard University (Mass.), finished in 1:32.67. In many parts of life, nine seconds isnt much: being nine seconds late to class or taking nine seconds to remove a pie from the oven is inconsequential. But in swimming, especially on an elite level such as the NCAA, being nine seconds slower could cause an athlete to fall behind by nearly an entire pool length.

Striving to bridge the gap between the divisiveness of transgender policies in sports is an admirable goal, but it grows complicated when we continuously try to consolidate contradictory research claims on sex and gender. For instance, HRT, which transgender women sometimes use to lower their testosterone levels, can be an essential part of the transition process for transgender people. It not only has beneficial physical effects, such as blocking testosterone or increasing estrogen, but also has psychological effects like mitigating gender dysphoria. On the other hand, a 2018 study also claimed that medicine would be unable to completely suppress testosterone levels in about 25% of the transgender women who participated in the study. Another quarter of trans women were able to lower testosterone levels, whereas another quarter could not reach typical female levels but remained below typical male testosterone values.

Scientific research, raging pundits and international sports committees on both sides of the debate have all put forth opinions and claims that often contradict with another. The effects of HRT and studies on hormones are still relatively new. Coming to a consensus on fair policies requires more than just political squabbling. No one can seem to propose a solution that is both equitable and inclusive, and I still have several unanswered questions: how long should an individual have to undergo HRT to be considered athletically equivalent to a cisgender women? How should fairness be defined in sports is it about unequivocal inclusion or about ensuring equal competitive opportunity? Do trans female athletes have a significant competitive advantage over cisgender women and, if so, to what extent? Hopefully, with more research and involving transgender people in these discussions, we will be able to answer these questions and reconstruct fairness in sports.

I must admit that the news of Thomas record-breaking swims perplexed me, likely for the same reasons it has angered elite athletes: how could it ever be fair? At the same time, I cant help but be in awe and admiration of the time and effort Thomas must have spent training in order to win so definitively in the face of so much vitriol.

Truly, asking Thomas to give up swimming or banning her from the sport would be a devastating blow. For any elite athlete, the dedication, passion and love they have for a sport is ingrained in their identity. Taking those opportunities away because of someones gender expression or identity fails to coincide with the spirit of sportsmanship we try to teach. Continuous accusations of injustice to womens sports come from desperation, to be part of a fight for or against Thomas and all other trans athletes. The true root of the issue lies with clumsy, contradictory and uninformed legislative and administrative voices unwilling to do any research that might unravel their biases.

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Lia Thomas started a conversation about transgender rights. It's time we dive into it. - The Emory Wheel

CLEVELAND, Ohio Stand-up comedian and actor Gilbert Gottfried, who died this week at 67, lived for years with the rare genetic muscle disorder myotonic dystrophy type 2, a common form of muscular dystrophy.

The cause of death was recurrent ventricular tachycardia, a heart condition, his longtime friend and publicist Glenn Schwartz announced.

Gottfried, known for his distinctive voice, was a cast member on Saturday Night Live, and the wisecracking parrot Iago in the animated Disney film Aladdin, among other roles.

Here are five things to know about myotonic dystrophy, with information provided by Med Page Today, the Myotonic Dystrophy Foundation and the Cleveland Clinic.

1. What is myotonic dystrophy?

Myotonic dystrophy is a rare, inherited disease that affects the muscles and other body systems. It is usually diagnosed in adulthood, often when a person is in their 20s or 30s. In this disorder, muscles throughout the body are unable to relax after they contract.

The condition is classified into two types: myotonic dystrophy type 1 (DM1), sometimes called Steinert disease, and myotonic dystrophy type 2 (DM2).

DM2 is generally considered less severe than DM1 -- though symptoms may vary among patients.

2. What causes it?

Myotonic dystrophy is usually caused by a gene mutation. It can be passed on by a family member, but may occur without a family history of the illness. People living with myotonic dystrophy have a 50% chance of passing on the mutated gene to their children.

3. What are the symptoms?

Symptoms include problems with muscles, heart, breathing, digestive system, hormonal, speech, swallowing, diabetic, immune system, vision, daytime sleepiness and cognition. Different people can have different symptoms.

The DM2 that Gottfried had is characterized by muscle weakness, wasting and pain. Muscles in the neck, fingers, elbows and hips are typically affected.

While the diseases rate of progression can vary, symptoms generally progress slowly.

4. How is it treated?

There are no treatments or cure available. Patients manage symptoms in a variety of ways, such as wearing ankle-foot braces, using a wheelchair, having cataracts removed or undergoing testosterone replacement therapy.

An implantable cardiac defibrillator devices that monitor the heart rate and send an electric pulse or shock to the heart to restore a normal heartbeat may be used to treat heart arrhythmias.

5. How many people have myotonic dystrophy?

It affects an estimated 1-in-2,100 people, or more than 3.6 million people globally. The muscular dystrophies as a whole are estimated to affect 250,000 Americans.

For more information:

Myotonic Dystrophy Foundation

Muscular Dystrophy Association

National Organization for Rare Disorders

Excerpt from:
Gilbert Gottfrieds myotonic dystrophy: 5 things to know about the rare genetic disorder - cleveland.com

Parents of four teens suing Alabama over its ban on treatment for transgender minors say the new law will drastically change their kids lives, taking them from happy teenagers back to their lives of depression and confusion they faced before starting treatment and leaving them a shell of themselves.

At least two federal lawsuits have been filed since Alabama Gov. Kay Ivey signed a law last week making it a crime for transgender minors to receive gender-affirming medical treatment. The new law goes into effect May 8.

The standard of care for gender dysphoriathe clinical diagnosis for when a persons gender identity doesnt match their birth sextypically includes treatments like puberty-blocking medication, hormone-replacement therapy, and surgical treatment. Doctors and experts say no gender-affirming surgeries are performed on transgender minors in the state of Alabama.

One lawsuit was filed in the Northern District of Alabama by the families of two transgender teens and two Childrens of Alabama and University of Alabama at Birmingham doctors. The other suit was filed in the Middle District of Alabama by two different families of trans teens.

Teens in the first federal suit, filed in Birmingham, are identified under the pseudonyms Mary Roe and John Doe. The second lawsuit, filed in Montgomery, lists the plaintiffs as teenagers identified by their initials, H.W. and C.W.

These are not random kids. These are kids in your communities who will suffer tremendously, said Asaf Orr, an attorney with the National Center for Lesbian Rights, which is one of the groups representing the parents and their children.

A spokesperson for the governors office said, We are prepared to defend our Alabama values and this legislation. The Alabama Attorney Generals Office did not respond to requests for comment.

Heres what we know about the teenagers who are fighting Alabamas new law based on the lawsuits:

Mary Roe

Mary, 13, is a transgender girl in Jefferson County. She started showing symptoms of gender dysphoria from a young age and began to tell her family that she was a girl starting around age 6. After seeking therapy and advice from medical professionals, Mary started to dress like a girl and her mental health greatly improved.

Following issues at school the next year with her new gender identity, Marys parents enrolled her in a new school, where Mary was allowed to dress like a girl and go by her new name. Since Marys transfer to the new school, she has returned to being the happy, active child she was during the summer prior to first grade, the lawsuit suit states.

In early 2021, Marys pediatrician evaluated her for puberty blockers. She began taking the medicine in April 2021 and has been taking it since.

It is essential for Marys mental health that she continues to receive puberty-blocking medications every three months and is able to obtain any future medical treatments that her healthcare providers determine are medically necessary to treat her gender dysphoria, her lawsuit states. For Mary to be forced to go through male puberty would be devastating; it would predictably result in her experiencing isolation, depression, anxiety, and distress. Marys parents are also concerned that without access to the puberty-blocking medication she needs, Mary would resort to self-harm as a means of coping with her psychological distress or even attempt suicide.

If the law goes into effect on May 8, Mary will have to stop her medication.

Without access to puberty-blocking medication, Marys body will produce testosterone, and she will begin to develop secondary sex characteristics associated with males. The changes to Marys bodysome of which would be permanent or would require surgery to reversewould make visible to others that she is a transgender girl and would cause her to experience again the distress she experiences from having a body seen by others as inconsistent with her female identity.

John Doe

John, a 17-year-old in Shelby County, also began showing symptoms of gender dysphoria at a young age. While his parents thought the behavior was a phase, they were accepting. He began to see a therapist when he was about 8. While it helped at first, the suit said Johns mental health declined when he started puberty.

He quickly developed large breasts, which was very distressing for John. He would often cry in the shower because of the shape of his chest, wear multiple sports bras at a time, and slouch his shoulders to make the appearance of his chest less prominent, the lawsuit said. Getting his period was equally distressing for John. Johns dysphoria was so severe that he stayed home from school for at least one day each month.

When John was in high school, he told his parents he was transgender. With the help of his parents, John connected with mental health and medical providers at UAB. He started medication to stop his period and, about a year later, he started testosterone treatments.

Starting testosterone has been amazing for John, his lawsuit states. He finally is feeling more like himself, building greater confidence, and is happier overall. Over the past year and a half, Johns voice has dropped, and he has developed facial hair. Those features have allowed him to feel more comfortable in his body and eased his anxieties about not being treated as a male by others.

John will also be forced to stop his medications if the law goes into effect, leading to what the legal team calls devastating physical and psychological consequences.

The stories of Roe and Does experiences are the norm for transgender minors, Orr said, and the new law means parents cant be in charge of their childs medical decisions.

That should be frightening to people who identify as political conservatives, he said.

H.W.

A transgender 15-year-old, H.W., came out to her parents as trans at 10. She began her social transition soon after and legally changed her name and altered her clothing and appearance. Those changes were very helpful to H. W., but she remained terrified about what would happen when she started puberty, as she could not imagine having a body like a teenage boy, the lawsuit states.

At the recommendation of her multiple doctors and after evaluations, H.W. started puberty-suppressing medicine at 12. The treatment has prevented H. W. from having to undergo a puberty that would cause changes in her body- some irreversible- that would severely exacerbate her gender dysphoria. By allowing H. W. to pause puberty and not experience the physical changes that terrified her, puberty-suppressing medication has significantly improved H.W. s health, according to the lawsuit.

She is also set to begin hormone therapy in the fall.

Growing up in a body that did not match who she was made H.W. miserable, lawyers said in the suit. Accessing medical care has been transformative for H.W. She became less shy and more confident and began thriving in school.

Without H.W. s puberty-suppressing medication, she would be forced to undergo a typical male puberty, which would cause her to develop a deep voice, a typically masculine jawline, an Adams apple, hair growth on her body, and a broadening of her shoulders. The changes are potentially irreversible, the suit said, and would cause H.W. to not feel like herself anymore, and cause her to likely be bullied.

H.W.s family would have to leave Alabama if the law goes into effect, the suit said, leaving her parents without work and splitting her apart from her siblings.

C.W.

C.W., 13, is a transgender girl who first told her parents about her severe stress and anxiety at 9, and soon after came out as trans. After sharing her new pronouns and name with those around her, the lawsuit said, C.W.s outlook, demeanor, and overall well-being immediately improved.

When she was in fourth grade in 2018 and asked people at school to call her by her new name, there were incidents of bullying and harassment, which lasted several years. In 2019, her parents legally changed her name and submitted the legal name change to the school.

At 11, C.W. consulted with a team of doctors and was diagnosed with gender dysphoria. Later that year, she started puberty suppressing medication. According to the lawsuit, the medicine has made an incredible difference in C.W.s life. She, too, would suffer possibly irreversible changes to her body if she stopped the medications.

C.W. s parents are concerned that without her medical treatment, C.W. s confident self would fade away, the suit said, adding her family would consider moving out of Alabama and leaving behind their families, support networks and jobs.

Claims

Both lawsuits say the teens are being denied medical treatments and taking the decision out of the hands of doctors and parents.

The (law) abandons science and seeks to stop safe, effective, and medically necessary treatments for children with gender dysphoria in Alabama without any rational basis, the Doe and Roe lawsuit states. The law also ignores established medical science.

Doctors and parents of transgender minors are forced to choose between withholding medically necessary treatment from their minor transgender patients or children, on the one hand, or facing criminal prosecution, on the other, that lawsuit adds.

Orr and lawsuits also point out the treatments themselves are not bannedif another minor needed puberty blockers or hormone therapy for issues that were not related to gender dysphoria or being transgender, they could receive them. Orr said thats a clear discrimination based on sex.

RELATED: Alabama schools chief: Teachers could have to navigate tricky conversations after new law - al.com

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Who are the teens at the center of the legal fight over Alabamas law banning transgender treatment? - AL.com

VENICE, Italy From the time he was a child, Edoardo Beniamin could envision paddling a gondola through the waterways of Venice, his native city. He saw himself, dressed in a striped jersey and ribboned straw hat, following his father and an uncle into a profession that has served as the enduring symbol of La Serenissima for a thousand years.

To be a gondolier was always my dream, Mr. Beniamin, 22, said one bright winter day in a Venice rendered vacant by a wave of Covid-19 sweeping across Europe.

Seated at an outdoor cafe near the San Zaccaria waterbus station on the Grand Canal, Mr. Beniamin explained why his childhood imaginings had felt to him unrealistic. In the gondola business, it matters a lot if you are the son of someone, he said. But I really didnt think it could be possible, since girls could not do it.

A slight man with a thatch of coppery hair and facial scruff, Mr. Beniamin was assigned female at birth. For the first 16 years of his life, he said turning up the collar of his shearling jacket against the chill he had not felt a need to call that into question.

When I was very very young lets say, 6 or 7 I wanted to be a man but it was more for fun, he said. I preferred boys clothes, for example, and I used to say these things I want to dress like a man that were not serious. I thought I was a girl and so I forgot all about it.

Five years ago, while still in high school and dating his girlfriend Claudia Nardelli, now 22 and his fiance he experienced what some in the trans community term an egg moment, an emergence. He began questioning whether the crippling migraine headaches and related health complaints that plagued him, most notably after gym class and that led his mother to take him from one doctor to another had origins that were not neurological.

Lets say everything started from my health, he said. I was suffering and feeling bad with myself, but I didnt know it was dysphoria: I didnt even know the word existed. It was Claudia who opened my mind. She said, Maybe something else is going on. And then, you know, gradually this thing happened that I found out I was a guy.

In a sense Mr. Beniamins experience resembles that of many trans people, who for reasons that may be societal, cultural, legal or psychological or all of those things combined are often forced to confront a constellation of challenges when reconciling the divergence between the gender assigned them and who they truly are. In his case there was an additional hurdle. Mr. Beniamin had always assumed that entering his fathers profession was impossible.

It is not that there are no female gondoliers, although thats how it was for 10 centuries. In 2010, Giorgia Boscolo became the first woman officially recognized by the Associazione Gondolieri di Venezia, or Venice Gondoliers Association. Now, of the 433 licensed gondoliers at work in Venice, five are women, according to Andrea Balbi, the president of the gondoliers association.

There is, in addition, Alex Hai, a German-Algerian transgender man who runs a private gondola service under the auspices of a hotel. Mr. Hai took the licensing test before transitioning to male in 2016, but did not pass it, Mr. Balbi said.

That test is open to all, Mr. Balbi insisted. Our job is for everyone male, female, transgender, maybe some other kind of gender we dont even know about, he said. Yet breaking into this signature profession is not so simple.

Nicolo Casarin, 37, was well established as a boat captain on the citys waterbus system when he finally passed the gondoliers test on his fourth try. I started when I was 19, and I got my license at 34, Mr. Casarin said. Its super-hard to get in, almost impossible if there is not someone in your family in the business.

The test, administered annually, entails much more than knowing how to master the art of balancing and rowing an asymmetrical 36-foot vessel through Venices 177 canals.

There are many hours of art history, histories of the city, navigation, routes, foreign languages to learn in addition to Italian and Venetian dialect, Mr. Casarin said. There is, too, boat maintenance and study of the tides and fickle winds along the Adriatic Sea.

Those things came easily enough to Mr. Beniamin, a byproduct of his upbringing around watercraft, a city kids easy familiarity with Venices six distinct districts, as well as a series of part-time high school gigs working as a tour guide. Although his comparatively small frame could be seen as an impediment to him as an oarsman, the toughest barrier he confronts as he begins training to enter the family business as the first openly transmasculine and licensed Venetian gondolier is also, in some ways, the least expected.

Since 2019, when he began hormone replacement therapy, Edoardo Beniamins outward appearance has increasingly conformed to conventional masculine ideals. Since December of last year, when he succeeded in petitioning the Italian bureaucracy to amend his birth certificate and other official documents to reflect his gender, he has been legally male.

What happened next, Mr. Beniamin said, is that, once I figured out I was a male, I also realized I had always had a certain idea of what masculinity is. I thought that to be a man is to be a certain way. Now what I think about is different. What I ask myself all the time is, What is a man?

In certain ways Venice is an ideal backdrop for his question. Insular, cryptic, ineffable in its appeal and yet riddled with clich, the labyrinthine city is intricately mapped and yet, as any visitor knows, confounding to navigate. Masculinity can also be like that.

Before I encountered Edoardo Beniamin, at the office of his speech therapist, Eleonora Magnelli, in Florence in January, I had given little thought to what bearing the sounds produced when air passes over my vocal cords had on my identity. I took for granted that I sounded like a cisgender man or, anyway, myself.

When Mr. Beniamin first contacted Ms. Magnelli, via Instagram, seeking information about a program to help transgender singers, his voice was, as she said, very metallic, and it bothered him. At the time there was little in the clinical literature about voice and gender stereotype. Many in her field assumed that taking testosterone and lowering vocal tones was sufficient to address the concerns of a transgender man.

But pitch is not the only parameter, Ms. Magnelli said. And the training we do differs from other kinds of speech therapy, because clinicians must always remember that clients are not affected by any pathology. We are just helping them in affirming their identity.

For Mr. Beniamin, the process of affirming himself through vocalization was as critical as some of the medical procedures underway to alter his physical appearance. You need to talk a lot if you want to be a gondolier, he said.

In fact, a gondoliers palaver and (less often these days) crooning is a large part of what tourists expect when they pay $85 for a half-hour of being rowed along a preset route in a velvet-upholstered craft. Changing my voice changed my life, Mr. Beniamin said.

It is not just that strangers no longer call him madam. (I dont just want a deeper voice at the end of this journey, he said.) Neither is it that Rambo, the Chihuahua he shares with fiance, now obeys his commands after years of ostentatiously ignoring him.

Obviously, its more than that, Mr. Beniamin said. What brings me euphoria is feeling people see me as I see me.

On an unseasonably warm January day in Florence, I accompanied Mr. Beniamin on a visit to Dr. Giulia Lo Russo, an aesthetic surgeon with a subspecialty in performing chest masculinization, or so-called top, surgery on transgender men. A video Dr. Lo Russo brought up on an iPad illustrated how broad the range of results can be. The point is not just to remove the breasts and reduce a female torso, Dr. Lo Russo said. You have to make a male torso.

Asked to explain the difference, Dr. Lo Russo spoke instead about her therapist. My psychologist asked me why I do these surgeries, she said. Why me? Im not L.G.B.T.Q. But I am deeply anti-conformist. I have had three children with three different men.

While we chatted, Mr. Beniamin casually prepared for his examination by stripping off a pullover sweater and T-shirt and unwinding the kinesiology tape he uses to bind his chest.

The state doesnt make it easy for people to get this surgery, Dr. Lo Russo continued. You have to wait one year for documents and, because of that, its hard to get on my schedule. I only do one top surgery a month, though with Edoardo, I put him on the roster a year in advance because it was clear to me that this was the right thing.

In the end, she added, as she held up a smartphone to snap before photos of her patient, people must be true to themselves.

For Sara Mion, 51, Mr. Beniamins mother, Edoardo is now her son the apprentice gondolier, a guy with a future wife and plans to start a family after marriage. If for a long while she was reluctant to accept her sons transition, she no longer has any such hesitation. As a mother, I decided, Do I lose her or do I try to understand him? she said.

Ms. Mion is a renal care nurse at a hospital in Venice and so it is somehow more poignant that the moment she accepted Edoardo as her son occurred when she administered one of his early testosterone injections. I told him then, I gave birth to you twice the first time in the hospital and now again with this, she said.

Ms. Mion and I were sitting in the sun near one of Venices many (opinions vary, but the overall consensus is there are about 450) footbridges. Gondoliers gossiped nearby in clusters, awaiting the tourists that uniquely in recent Venetian history were nowhere to be found.

Ms. Mion and Mr. Beniamins father, Paolo, divorced when their two children were young. Their relationship since then has remained cordial, if distant or as detached as any Venetian can hope to be in a city whose native population is small enough to see itself as endangered.

Paolo Beniamins gondola bobs in a prime berth along the Grand Canal, just outside the water gates of the luxurious Hotel Danieli. Ms. Mion said she finds it reassuring to know that, when the time comes for Edoardo to join in the family business, he can rely on his father as a cicerone.

Things were not always like that, as Edoardo Beniamin explained one day on a gondola piloted by Mr. Casarin. My dad tried to push the reality away for a long time, he said as Mr. Casarin propelled us through a series of especially narrow canals, or rii. He didnt want to use the pronouns, Mr. Beniamin said, referring to his preferred he and him. But then, the last time we talked, my dad said to call him when it was time for my top surgery and he would drive me to the hospital.

Venice that day was eerily tranquil, as at various times since the start of the pandemic, and this must also have been true during the great plague that permanently altered its history as a great world power. The lagoons bottle-green surface remained relatively placid as wavelets hit the gondolas glossy hull with lulling slaps.

Suddenly, a chevron of Italian Air Force jets blasted across the horizon toward the city, arcing through the sky above the St. Marks Square and the Doges Palace and leaving behind a trail of tricolor plumes. The mysterious aerial acrobatics continued for the next 20 minutes as jets zoomed in and out of view, the din from their turbines making it difficult to be heard.

Then, as abruptly as they had appeared, the aircraft tipped upward and vanished into the ether. That was when Mr. Beniamin noted how it seemed as if downdraft from the flyover had disturbed the waters surface, jostling the iron prows of vessels at mooring.

Gondolas are basically flat at the bottom, he said. Its an interesting thing to know about them, that it takes very little disturbance to rock the boat.

Originally posted here:
In Venice, a Young Boatman Steers a Course of His Own - The New York Times

The Kansas Senate passed a bill last month that would prevent transgender women from competing in girls sports in public schools from the elementary level to the state collegiate level. Kansas is the eighteenth state to propose a ban on transgender athletes competing in girls sports.

Labeled pro-girl and pro-women, proponents of the Kansas bill and similar bills claim that these actions protect female athletes.

However, I think this is one of the most covert misogynistic pieces of legislation ever written.

The bill, also called the Fairness in Womens Sports Act, requires teams to designate themselves as males, females or mixed, solely based on biological sex. The bill then explicitly states that sports designated for females, women or girls shall not be open to members of the male sex. If a person or organization sues on grounds of athletic opportunity deprivation and prevails on that claim, it is entitled to a broad remedy of monetary damages, including for any psychological, emotional and physical harm suffered, reasonable attorney fees and costs and any other appropriate relief.

Labeling transgender women and girls as members of the male sex is transphobic. Transgender folks are already at risk for discrimination because there are no laws in the state of Kansas that protect LGBTQ+ people from discrimination in housing, employment and public accommodations.

This bill would allow for schools to freely refuse to recognize students gender identity, who already experience higher rates of suicide, bullying and feelings of isolation at school.

School should be a safe place for all students. Recognizing students' differences especially those whose identities put them at riskis a key part of supporting students.

This legislation implies that there is no physical way that any woman born female could beat anyone born male in any sport under any circumstances. It continues the decades-long trend of underestimating female athletes by implying that they are fundamentally weaker.

The bill makes no express mention of people born female competing in male sports teams, only choosing to target those born male competing in women's and girls sports teams. Additionally, there has been almost no discourse around people born female competing in boys sports. Most of the bills passed focus solely on people born male competing in girls sports.

States such as Oklahoma, whose bill is titled the Save Womens Sports Act, Arkansas, Mississippi, Florida and other states only target transgender peoples participation in girls sports only with little to no mention of transgender participation in boys sports.

This is further indication that the ideas behind the bills are sexist and discredit female athletes. Legislators seem to have little to no concern for transgender males competing in boys sports further implying that legislators believe female athletes are inferior to male athletes.

Legislatures do not see people born female as threats to athletes born male because of traditionally sexist attitudes that state that women are weaker than men from the moment they are born.

This legislation also portrays people born male as predisposed athletic machines who would beat any woman simply because they have one X and one Y chromosome.

Saying this is offensive and simply untrue.

In reality, men and women have different strengths, such as women excelling more than men in endurance sports and men excelling in strength-related sports.

Further, Dr. Josha D. Safer, an endocrinologist at Mount Sinai Beth Israel with over 20 years of experience and the president of the U.S. Professional Association for Transgender Health, said it best: A persons genetic make-up and internal and external reproductive anatomy are not useful indicators of athletic performance and have not been used in elite competition for decades.

People born male are not automatically better at sports in the same way that people born female are not automatically better at cooking. Pushing these ideas just serves to reinforce offensive stereotypes.

Though the presence of testosterone can boost athletic performance, the differences in testosterone levels in males and females do not show up until after puberty.

Therefore, banning elementary-aged transgender women from competing in sports is unproductive and does not protect women (who, by the way, dont need your protection). It only serves to further alienate and bully children who are already among one of the highest-risk groups in the country.

Transgender youths are predisposed to experience higher levels of physical violence, sexual violence, discrimination and mental health struggles than their cisgender counterparts.

Other proponents of the bill have argued that transgender female athletes have a biological advantage after puberty due to the presence of testosterone in transgender women and that their athletic presence ensures that the playing field for cisgender women would not be equal.

However, 94% of transgender women have less than two nanomoles of testosterone per liter when on hormone replacement therapy, congruent with 95% of cisgender women having less than two nanomoles of testosterone per liter. So, where is the competitive advantage?

If legislatures really cared about female sportsmanship, I would encourage them to follow and engage with professional womens sports. Or I would encourage them to allocate more funding to women and girls in sports, to raise awareness for sexual assault and harassment in sports or invest in campaigns to encourage women and girls, cisgender and transgender, to get involved in sports. However, no legislatures have taken such action.

Their worry for womens sports is merely a facade for underlying sexism and transphobia.

These bills do not help women. Instead, they grossly alienate transgender children and belittle the work that female athletes put in nearly every day.

Allow transgender girls to have a childhood beyond discrimination and stop underestimating female athletes.

Read more here:
Female athletes are as capable as male athletes | Opinion | kansan.com - The University Daily Kansan