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Sep 2

Men’s Health Expert Tracy Gapin, MD Unveils Male 2.0 with a Revolutionary Protocol to Conquer the Men’s Health Epidemic – PRNewswire

SARASOTA, Fla., Sept. 1, 2020 /PRNewswire/ --Transcendent Publishing today announced the release of Male 2.0: Cracking the Code to Limitless Health and Vitality by author Tracy Gapin, MD, FACS. Since its August release, the book has already reached Amazon bestseller status. Dr. Gapin, a men's health and performance expert and member of the American Urological Association, provides a meaningful impact for men's health with this leading-edge approach.

Over the past thirty years, there has been a relentless population-based decline in mens' testosterone levels by over thirty percent. We've also seen a dramatic increase in the incidence of obesity. Over seventy percent of men are either overweight or obese, which is directly tied to energy, productivity, and overall health and performance. This has led to a men's health epidemic for the 159 million men in the United States.

The Male Method described throughout Male 2.0 was developed to help men lose weight, regain energy, optimize their hormones, and regain peak performance. "We need to go beyond testosterone. We need to take an individualized, systems-based approach to optimize men's health, performance and longevity," says Tracy Gapin, MD, FACS. "Driven by the power of epigenetics, genetics, peptides, and wearable technologies, we have gained incredible insight into some of the most misunderstood aspects of men's health and longevity."

JJ Virgin, New York Times Bestselling author of The Virgin Diet & Sugar Impact Diet said, "As a thought leader in men's health, Dr. Gapin has provided the modern-day blueprint to help men optimize their health and regain their vitality. Every man should read this book."

Clete Walker, CEO of Vituro Health, a prostate health company, said, "Male 2.0 is a revolution for men's health. After my father was diagnosed with prostate cancer, I made it my mission to seek out potential new modalities, and this data-driven approach is the future."

Male 2.0: Cracking the Code to Limitless Health and Vitalityis available on Amazon and during the month of September the print version is available for free at The Gapin Institute. http://www.GapinInstitute.com

About Tracy Gapin, MD FACS:Dr. Gapin is board-certified Urologist, world renowned Men's Health & Performance Expert, Author, and Professional Speaker. Using state-of-the-art biometric monitoring, nutrition and lifestyle intervention, Dr. Gapin coaches Fortune 500 executives and evolutionary leaders of business, sports medicine, and high performance. He specializes in cutting-edge precision medicine with an emphasis on epigenetics, providing men with a personalized path to optimizing health & performance. http://www.GapinInstitute.comEmail: [emailprotected]

About Transcendent Publishing:Since 2012, Transcendent Publishing has specialized in offering a variety of publishing and design services for today's indie author. http://www.transcendentpublishing.com

CONTACT:Leann Spofford[emailprotected]Tel: (941) 524-4592

SOURCE Gapin Institute

Home – MMG

Link:
Men's Health Expert Tracy Gapin, MD Unveils Male 2.0 with a Revolutionary Protocol to Conquer the Men's Health Epidemic - PRNewswire


Sep 2

Dr Matthew Budoff on the Benefits of Cardiac CT Use – AJMC.com Managed Markets Network

Advances in imaging have made assessment of atherosclerosis non-invasive, while the EVAPORATE trial demonstrates how cardiac CT can assist in looking at a host of different therapies, said Matthew Budoff, MD, professor of medicine at the David Geffen School of Medicine at UCLA and investigator at The Lundquist Institute.

Transcript:

The American Journal of Managed Care (AJMC):In EVAPORATE the only secondary endpoint which did not achieve a significant difference between control and intervention groups was dense calcium. What might account for this?

Dr. Budoff: Calcification is probably the last of the stages of atherosclerosis, so it's the least modifiable. So we saw low attenuation plaque, the vulnerable, or necrotic, core changed a lot, fibrofatty plaque, the softer plaque, changed moderately and fibrous plaque change less and then calcified plaque change the least. So I think that actually makes sense from a biological mechanism, that the most earliest plaques and the most vulnerable plaques changed the most, and the more stable plaques, like those with a lot of fibrous tissue or those with dense calcium, changed less. The P-value for calcification in multivariate analysis was .0531. So, you know, from a purist standpoint, it didn't change significantly. But some people would say .053 is pretty close to .05 and is close to statistical significance. But either way, I think it makes sense biologically that the more stable plaque changes less than the earlier softer plaques.

AJMC: As reduction of triglycerides on its own is not producing the dramatic drop in CV events, what are your thoughts on expanding the scope of patients receiving icosapent ethyl (Vascepa)?

Dr. Budoff: While I agree that triglyceride lowering isn't the primary benefit, I think those with high triglycerides are still a potential target. We have a number of populations where the target population is based on an abnormality of something, but we don't always treat that specific thing. For many years, diabetes, for example, the presence of diabetes meant your high cardiovascular risk and the treatment wasn't control the Hemoglobin A1c, the treatment was add other therapies. I think we still should be using icosapent ethyl largely in patients who have elevated triglycerides because that's where the benefit was shown to be the greatest. We have data now from triglycerides of 135 and up, and this group is still high risk. I want to emphasize that patients with elevated triglycerides, maybe because of metabolic syndrome and diabetes, and other factors, patients with elevated triglycerides are high risk, and they appear to benefit from icosapent ethyl. Whether it works in patients with normal triglycerides, I think that does deserve further study. We could not address that in EVAPORATE, because we did the EVAPORATE trial the same as the REDUCE IT study, and both of them used entry criteria for triglycerides of 135 and up.

AJMC: Do you have any final thoughts you would like to share?

Dr. Budoff: Well, I just wanted to point out that the use of cardiac CT now has become highly reproducible. The reduction in radiation dose does allow us to do these type of trials, where we can do serial studies and assess does drug A do better than drug B, or does drug A do better than placebo over time .We've had some early studies looking at statins with this serial CT angiography and we've published on the testosterone, that testosterone increases atherosclerosis plaque in our placebo controlled randomized trial. Now we've been able to show that icosapent ethyl reduces plaque. So I do think that it's a nice model. It's not invasive, it's easy, but I do think it's an important way to assess some of the benefits without having to do intravascular ultrasound, and take patients to the catheterization lab twice, with all of the associated risks.

I think the advances in imaging have made our assessment of atherosclerosis now non-invasive. And I think that's an important part of the message of EVAPORATE, that this is a potential tool to look at a host of different therapies that we now have. We're now doing a trial with GLP-1 receptor agonists with semaglutide to see if that slows plaque progression, because that's also shown outcome benefit without a clear mechanism of action.

See more here:
Dr Matthew Budoff on the Benefits of Cardiac CT Use - AJMC.com Managed Markets Network


Sep 2

This nonsense between the Yankees and Rays must stop. Immediately. – Tampa Bay Times

Kevin Cash is likely facing a suspension, and Im okay with that.

Im okay with his overt threat to the Yankees because a manager must defend his players, and Im okay if Major League Baseball says that type of threat cannot be tolerated because this situation is rapidly growing dangerous.

Aroldis Chapman will almost certainly be suspended, and Im okay with that, too.

Its one thing to pitch up-and-in for effectiveness, its another thing to throw at a hitters torso to send a message, and its an entirely different world to throw a 101-mph fastball at someones head. Chapman must sit for a minimum of a week.

But Yankees manager Aaron Boone will likely skate free, and thats regrettable.

This bad blood between Tampa Bay and New York was arguably hastened by the Rays two years ago, but the Yankees have since acted like testosterone-fueled frat boys. And thats on Boone. As well as third base coach Phil Nevin, who has a history of being less-than-level-headed.

First, lets review what happened Tuesday night. Yankees starter Masahiro Tanaka, who has impeccable control, threw a pitch near Joey Wendles legs with two outs and nobody on in the first inning. On his next pitch, he drilled Wendle in the side with a 95-mph fastball, the hardest pitch he threw all night.

Was this retaliation for the Rays throwing up-and-in on D.J. LeMahieu the night before? Probably. Was it handled the right way by Tanaka? If you believe in old-school baseball justice then, yes, that was a proper response. And Cash seemed to say as much. So did Rays pitchers who did not try to hit any Yankees.

Then in the ninth inning, Chapman threw a 95-mph pitch high-and-tight on Wendle. He followed with a 99-mph pitch up-and-in on Austin Meadows. With two outs and nobody on, he uncorked a 101-mph pitch directly at the head of Mike Brosseau. The Rays infielder barely eluded the baseball as Chapman walked off the mound toward the plate.

The umpires huddled, decided to warn both benches, then automatically ejected Cash when he came out of the dugout to protest. Chapman eventually struck out Brosseau to end the game, then posed like a playground bully on the mound.

Brousseau was heading to the dugout when he clearly heard shouting from the Yankees side centerfielder Kevin Kiermaier specifically singled out Nevin for chirping and turned to say something himself. The benches emptied, but the confrontation ended quickly.

Then Cash unloaded in his postgame news conference.

Its absolutely ridiculous, he said. It was mishandled by the Yankees. Certainly, the pitcher on the mound. It was mishandled by the umpires. They hit Joey Wendle intentionally in the first inning. It was clear as day. Chapman comes in, he throws three different balls up and in. I get it they dont like being thrown up-and-in. But enoughs enough. Were talking about a 100-mph fastball over a young mans head.

Its poor judgment. Poor coaching. Its just poor teaching, what theyre doing, and what theyre allowing to do. The chirping from the dugout.

Had he stopped there, Cash would have been on solid ground. What followed was inflammatory, but also seemed purposeful. As if Cash knew he was risking suspension by drawing a line in the sand to force MLBs hand.

And the last thing Ill say on it is Ive got a whole damn stable full of guys that throw 98 mph. Period.

You could argue Cashs intent was understandable in a mutually-assured-destruction kind of way, but its hard to imagine MLB allowing a manager to threaten a beanball war, even if it was only a preemptive strike.

The umpires, who are supposed to be notified about previous altercations between teams, should have seen the situation for what it was, and immediately ejected Chapman and Boone. Their failure to act led to Cashs comments, and now will force MLB to step in today before somebody gets seriously hurt.

So how did we get here? The story is long and somewhat silly.

In September of 2018, the Rays hit Yankees with pitches in the first, second and third games of a series. The Yankees hit Rays in the second, third and fourth games of the series. After C.C. Sabathia hit Jake Bauers in that fourth game the third of four Rays he hit with a pitch that season Tampa Bays Andrew Kittredge threw near the head of Austin Romine.

It was a dangerous pitch and never should have been thrown. Kittredge was justifiably fined and suspended three games by the league. Sabathia, however, did not wait for official justice, and hit Jesus Sucre in the thigh later in the game. He was ejected, then pointed at the Rays dugout and shouted Thats for you, b---h, as he was leaving the field.

It could have ended there. It should have ended there.

Except the Yankees have continued to complain. And they seem to think every inside pitch is an affront to their glory.

The teams also exchanged taunts at Tropicana Field last month that stemmed from Nevins constant chirping. Every time a Rays pitcher got in trouble and was visited on the mound, Nevin could be heard shouting something to the effect of, Get him out of there.

When Yankees pitcher James Paxton gave up back-to-back home runs to tie the score in the seventh, it appeared Mike Zunino offered his own version of Get him out of there from the Rays dugout. The Yankees were not pleased.

Yet, from the time Sabathia walked off the mound in 2018, this has had the appearance of a one-sided feud.

Once again, there is a huge difference between pitching inside and headhunting. And there has been no indication that the Rays have tried to hit or hurt anyone in two years.

In fact, the Yankees have hit Rays batters 19 times since 2018. The Rays have hit 14 Yankees.

At this point, MLB needs to be involved. Someones career, even their life, could be jeopardized if this is allowed to escalate. And, frankly, Id be surprised if there was any intentional hit-by-pitches in Wednesdays game, considering the heightened attention.

And, just to be clear, the Rays are no choirboys in this episode, beginning with Kittredges pitch two years ago. But Tampa Bay took its punishment from Sabathia and MLB and seemed to move on.

As evidenced by Chapman last night, the Yankees have not.

John Romano can be reached at jromano@tampabay.com. Follow @romano_tbtimes.

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This nonsense between the Yankees and Rays must stop. Immediately. - Tampa Bay Times


Sep 2

World Rugby defends proposals to ban trans women from womens rugby – The Irish Times

World Rugbys proposals to ban trans women from playing womens rugby have been criticised by dozens of academics, who have written to the sports governing body to insist there is no evidence that trans women pose a safety risk to others playing the sport.

The letter, which has been co-signed by 84 leading academics from a range of fields including sport, public health and sociology, also questions the science behind the proposed ban and warns it will discriminate against vulnerable people.

We are opposed to World Rugbys proposed ban of an entire population group from playing womens rugby: non-binary people assumed male at birth and transgender women, it says. There is no peer-reviewed, scientific evidence to justify a ban which would only be harmful to trans and gender diverse people.

The letter, which has been seen by the Guardian newspaper, also reminds World Rugby that this is not a fringe population affected and that recent research by the American centers for disease control and prevention found 3.4 per cent of American school students (year 9-12) identify as trans or gender diverse, or they were not sure about their gender identity.

The letter adds: to develop appropriate guidelines requires ongoing work with transgender athletes and community representatives, and engagement with rigorous, peer-reviewed evidence. These guidelines fail on both accounts.

However, World Rugby has issued a robust defence of the research on which its recommendations are based, as well as its application of that research, which has concluded there is a minimum of 20 per cent to 30 per cent increase in injury risk factors when typical male-bodied and female-bodied players are involved in tackles even when trans women suppress their testosterone in line with International Olympic Committee rules.

From the outset, we have sought to balance inclusion, safety and fairness within the context of a physical sport based on strength, power, speed and contact, World Rugby said in a statement. However, the scientific medical evidence position regarding the impact of testosterone suppression for trans women athletes is compelling, the injury risk at the elite level is real, and should be tackled.

While welcoming all contributions, it is simply false to state that the research is not peer-reviewed and insufficient to warrant the approach as evidenced by the numerous published studies, which consider biological advantages of males over females and the slight reduction of advantages when testosterone is suppressed.

World Rugby has operated a fully inclusive and extensive transgender guideline consultation process with relevant bodies as evidenced by the ground-breaking workshop in London. Every element was considered and input from trans advocacy groups was sought, and valued for all the reasons raised by the academics.

When the Guardian first broke the story that World Rugby was considering implementing a ban on trans women playing womens rugby, the news was immediately welcomed by some womens groups. Since then, however, a fightback from those opposed to the changes has begun.

This week the US womens player Naima Reddick joined the fray by warning the proposed ban attempts to solve a problem that isnt there.

In the decades I have spent playing, Ive learned that what truly makes someone an elite athlete isnt size, speed or strength, but mental toughness, agility and resilience, she said. Ive taken on cisgender male athletes in training and female athletes much bigger than me without hesitation because I am confident in my skill set. - Guardian

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World Rugby defends proposals to ban trans women from womens rugby - The Irish Times


Sep 2

H.C. Wainwright Reiterated Lipocine Inc. [LPCN]. What else is Wall St. saying? – The DBT News

Lipocine Inc. [NASDAQ: LPCN] stock went on a downward path that fall over -5.41% on Tuesday, amounting to a one-week price decrease of less than -2.78%. The company report on August 28, 2020 that Lipocine Provides Regulatory Update for TLANDO.

Lipocine Inc. (NASDAQ: LPCN), a clinical-stage biopharmaceutical company focused on metabolic and endocrine disorders, today announced that the U.S. Food and Drug Administration (FDA) has informed the Company that it needs additional time to complete its review of TLANDOs New Drug Application (NDA) and is committed to taking action as expeditiously as possible. The anticipated Prescription Drug User Food Act (PDUFA) goal date was August 28, 2020 for TLANDO. Although the FDA did not provide a timeline on a new action date, the FDA informed the Company that the review is expected to be completed in the coming weeks. The FDA has not asked for any additional data and the Company has provided the FDA with all information requested to date.

TLANDO is the Companys oral testosterone product candidate for testosterone replacement therapy (TRT) in adult males for conditions associated with a deficiency of endogenous testosterone, also known as hypogonadism.

Over the last 12 months, LPCN stock dropped by -55.70%. The average equity rating for LPCN stock is currently 2.50, trading closer to a bullish pattern in the stock market.

The market cap for the stock reached $91.98 million, with 65.69 million shares outstanding and 63.81 million shares in the current float. Compared to the average trading volume of 3.98M shares, LPCN stock reached a trading volume of 3277408 in the most recent trading day, which is why market watchdogs consider the stock to be active.

H.C. Wainwright have made an estimate for Lipocine Inc. shares, keeping their opinion on the stock as Buy, with their previous recommendation back on January 12, 2018. While these analysts kept the previous recommendation, Canaccord Genuity raised their target price from $11 to $2. The new note on the price target was released on January 11, 2018, representing the official price target for Lipocine Inc. stock. Previously, the target price had yet another raise to $10, while H.C. Wainwright analysts kept a Buy rating on LPCN stock.

The Average True Range (ATR) for Lipocine Inc. is set at 0.20, with the Price to Sales ratio for LPCN stock in the period of the last 12 months amounting to 459.90. The Price to Book ratio for the last quarter was 5.38, with the Price to Cash per share for the same quarter was set at 0.28.

Lipocine Inc. [LPCN] fell into the red zone at the end of the last week, falling into a negative trend and dropping by -2.78. With this latest performance, LPCN shares dropped by -18.13% in over the last four-week period, additionally plugging by 142.21% over the last 6 months not to mention a drop of -55.70% in the past year of trading.

Overbought and oversold stocks can be easily traced with the Relative Strength Index (RSI), where an RSI result of over 70 would be overbought, and any rate below 30 would indicate oversold conditions. An RSI rate of 50 would represent a neutral market momentum. The current RSI for LPCN stock in for the last two-week period is set at 38.05, with the RSI for the last a single of trading hit 33.01, and the three-weeks RSI is set at 43.43 for Lipocine Inc. [LPCN]. The present Moving Average for the last 50 days of trading for this stock 1.5779, while it was recorded at 1.5920 for the last single week of trading, and 0.8038 for the last 200 days.

Operating Margin for any stock indicates how profitable investing would be, and Lipocine Inc. [LPCN] shares currently have an operating margin of -7818.83. Lipocine Inc.s Net Margin is presently recorded at -7883.72.

Return on Total Capital for LPCN is now -77.88, given the latest momentum, and Return on Invested Capital for the company is -98.31. Return on Equity for this stock declined to -165.47, with Return on Assets sitting at -64.22. When it comes to the capital structure of this company, Lipocine Inc. [LPCN] has a Total Debt to Total Equity ratio set at 113.68. Additionally, LPCN Total Debt to Total Capital is recorded at 53.20, with Total Debt to Total Assets ending up at 36.36. Long-Term Debt to Equity for the company is recorded at 60.66, with the Long-Term Debt to Total Capital now at 28.39.

Reflecting on the efficiency of the workforce at the company, Lipocine Inc. [LPCN] managed to generate an average of -$1,083,945 per employee. Receivables Turnover for the company is 6.00 with a Total Asset Turnover recorded at a value of 0.01.Lipocine Inc.s liquidity data is similarly interesting compelling, with a Quick Ratio of 5.50 and a Current Ratio set at 5.50.

With the latest financial reports released by the company, Lipocine Inc. posted -0.12/share EPS, while the average EPS was predicted by analysts to be reported at -0.16/share. When compared, the two values demonstrate that the company surpassed the estimates by a Surprise Factor of 25.00%. The progress of the company may be observed through the prism of EPS growth rate, while Wall Street analysts are focusing on predicting the 5-year EPS growth rate for LPCN.

There are presently around $6 million, or 6.60% of LPCN stock, in the hands of institutional investors. The top three institutional holders of LPCN stocks are: VANGUARD GROUP INC with ownership of 1,104,304, which is approximately 3.554% of the companys market cap and around 1.10% of the total institutional ownership; AMERIPRISE FINANCIAL INC, holding 788,500 shares of the stock with an approximate value of $1.1 million in LPCN stocks shares; and BLACKROCK INC., currently with $1.01 million in LPCN stock with ownership of nearly -10.223% of the companys market capitalization.

Positions in Lipocine Inc. stocks held by institutional investors increased at the end of August and at the time of the August reporting period, where 20 institutional holders increased their position in Lipocine Inc. [NASDAQ:LPCN] by around 836,911 shares. Additionally, 9 investors decreased positions by around 171,052 shares, while 12 investors held positions by with 3,319,043 shares. The mentioned changes placed institutional holdings at 4,327,006 shares, according to the latest SEC report filing. LPCN stock had 11 new institutional investments in for a total of 550,302 shares, while 6 institutional investors sold positions of 84,899 shares during the same period.

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H.C. Wainwright Reiterated Lipocine Inc. [LPCN]. What else is Wall St. saying? - The DBT News


Aug 31

Testosterone Replacement Therapy Market 2020 : Analysis by Geographical Regions, Type and Application Till 2025 – The Daily Chronicle

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Testosterone Replacement Therapy Market 2020 : Analysis by Geographical Regions, Type and Application Till 2025 - The Daily Chronicle


Aug 31

Efstathiou Compares the Efficacy and Safety of AR Inhibitors in Nonmetastatic CRPC – Targeted Oncology

During a virtual Case Base Peer Perspectives event, Eleni Efstathiou, MD, PhD, associate professor, Department of Genitourinary Medical Oncology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX discussed treatment options for a 57-year-old African American man with nonmetastaic castration resistant prostate cancer (CRPC)

CASE:

October 2016

November 2016

February 2017

October 2019 - Restaging

Targeted OncologyTM: What are your impressions of this case?

Efstathiou: It looks [as though] after he nadired, he quickly recurred with a detectable PSA and a doubling time of 8.6 months. This is a case thats pointing toward the nonmetastatic castration-resistant prostate cancer [CRPC] status. And in the case, we dont have it, but testosterone would be checked, and it is within the castrate levels.

According to the case, this was followed with conventional imaging. This gentleman is now 60 years old in October 2019.

According to the case, the patient refused [radiotherapy]. Having said that, if you look at the data from the phase 3 trials that were done, you would see that 24% of patients who were included, at least in 1, had not been offered any treatment at the beginning, at their diagnosis, even of their primary [tumor]. So its quite impressive that still, to this day, a lot of patients do not get radiation even on the primary [tumor] when it is needed, and it calls for more education. We dont know if these cases were from the European side, the Asia side, or the United States side. Its not exactly granular, but it was disappointing for me to see.

Would you get advanced testing done for this patient?

Ive been sending patients who can [go for PSMA PET] to University of California, Los Angeles, recently, because I believe that Axumin and PSMA, looking at the data, are equally sensitive. However, it appears that PSMA is more specific. Ive had a lot of false positives on PETs. Im not pointing fingers, but its from different places that I got them, so Im not relying on the results. But, for this case, if the Axumin is still lining up in the prostate, then you have a clear move forward. But, to this day, for nonmetastatic CRPC or for PSA-recurring CRPC only, we do not have an indication to do the PET scan. That is in line with these studies being done with conventional imaging, and that can be a concern with approvals.

Now, this man was given conventional imaging, and this is more the standard across the board.

Do you actively pursue germline testing in high-risk disease or metastatic disease?

I was recently on an ad board, and I was speaking to people from Duke University, Mayo Clinic, and the like. Nobody has any systemic approach yet, and its not even routine in most cases. Its up to the physicians, and it can be more taxing that way, I find, because its 1 more thing added and sometimes can be missed. So I hope that in the future it will become as straightforward as doing the PSA, doing the testosterone, and [other processes such as that].

What are your thoughts on the results of this poll? What would you have voted for?

Most seem to have gone for any of the novel hormonal agents. Somebody put down chemotherapy. Somebody else also voted for nilutamide, flutamide, or bicalutamide.

I would go for other.

Seventy-seven percent voted for enzalutamide [Xtandi], apalutamide [Erleada], darolutamide [Nubeqa], or abiraterone [Zytiga].

How would you compare these agents?

Ive been starting to use [darolutamide] recently. Its approval was more recent.

I dont see a big difference between enzalutamide and apalutamide, not only in the fatigue, per se, but also the central nervous system [CNS] effect, which has to do with some extra depression, some extra insomnia, some extra effects that are not trivial. The difference is small [between these 2]. But the claim from the preclinical data was that apalutamide would have less of a CNS impact. Of course, when you test it in humans is when you see the real deal, and more so in the real-world experience.

With enzalutamide, my experience had always been that at least I can draw a line that I can say if a patient is over 70 years old, he may not perform that well. But, more recently, Ive even seen young men not being able to tolerate it.

And, in the case of this patient, I would say that we should all agree that both enzalutamide and apalutamide would be totally contraindicated because of the seizure disorder. So darolutamide is the only path forward.

What about abiraterone?

These [other] 3 drugs have an indication for nonmetastatic CRPC. Would you expect the insurance to go for abiraterone? I would find it hard [to believe the insurance would accept it,] because its not within the indication.

What are the takeaways from this poll?

Essentially, the bottom line is, you dont see any difference in the efficacy between the 3 agents, but you see an advantage in the safety profile.

Im starting to use darolutamide more, and I was reluctant at first. But now that most data are out, I would say I would agree; theres nothing holding me back in that aspect.

CASE (continued)

After shared decision-making, darolutamide was initiated.

What are your thoughts on the choice of darolutamide?

[The PSA doubling time] was a major concern in the beginning and now, as of this ASCO [American Society of Clinical Oncology Annual Meeting], we have overall survival [OS] data that exceed a year in the CRPC space, which has not been shown before.

I dont know how patients tolerate it yet. I gradually started to give it to the first patient, the second, but Ive got about 10 patients who are on it now, so Im getting there. Its a big deal, because I always say that if we havent had the hands-on experience in research or a clinical trial, it hits the market and then youre [deciding], I dont know this drug, Im going to stay with my comfort level. I can use enzalutamide and abiraterone blindfolded, but it looks [as though] darolutamide is going to be pretty easy. I want to see their data.

My only thing is I want to see more data coming from them with regards to bone density, and I think theyre getting ready to give those datathe effects of that antiandrogen. Were also looking forward to getting their hormone-nave data, which is also going to come forth. Theres a trial where investigators are combining it with chemotherapy. So its pretty new; its the new agent, but Im feeling more and more comfortable with it.

What are the data supporting the use of the 3 newest agentsapalutamide, enzalutamide, and darolutamidein this setting?

My impression of the NCCN [National Comprehensive Cancer Network] guidelines is that theyre there to help us get through the insurance, because most of us are familiar with the datasets. And here [with] a PSA doubling time of less than 2 months in a man who has, by conventional imaging criteria, negative disease, you can use either apalutamide, darolutamide, [or] enzalutamideall category 1 [recommendations].1 But theyre also leaving open the option for other secondary hormonal therapy, allowing for older agents, which I think is not fair in view of all primary and secondary end points being met.

All 3 trialsSPARTAN [NCT01946204], PROSPER [NCT02003924], and ARAMIS [NCT02200614]were identical, with a primary end point looking at metastasis-free survival [MFS] of the agent plus ADT versus placebo, and secondary end points including progression-free survival [PFS], local progression, quality of life, and OS. That was [not a] secondary end point for a lot of the physicians. They still held [off] on it until they heard the final OS data. My prior chair would say, If Im going to treat a patient with an agent for 3 extra years, I need to make sure Im not compromising his quality of life or making his other morbidities worse. But there was a point in the SPARTAN trial [of apalutamide and ADT versus ADT and placebo in patients with nonmetastatic CRPC] that was important for me. It was the only [trial] that looked at the PFS2, which essentially compared starting earlier versus starting later and showed that starting earlier is better.

I think, in the interest of science, we should not stick with, This is what the SPARTAN trial says, this is what the PROSPER trial says, this is what ARAMIS trial says. We have 11 phase 3 trials across the board, across the cancer with novel androgen signaling inhibitors that are all positive. There has been no negative trial, which is phenomenal. The data is superimposable. You cant see a big difference in the efficacy. For efficacy assessment, I dont see a difference between the agents, and I use the datasets across the board. I think they are supportive of each other rather than antagonizing each other.

The [SPARTAN] results are old news now. There was a phenomenal difference in MFS that exceeds the 2-year mark [median MFS, 40.5 months with apalutamide versus 16.2 months without; HR, 0.28; 95% CI, 0.23-0.35; P<.001].2

The new finding that was reported at the [2020] ASCO meeting [was OS], and it was a poster discussion for all 3 [trials]. I like that they made them poster discussions rather than making them big oral discussions. They left oral discussions for more innovative things, [such as] the trials that we do with finding prescriptive markers. A lot of people complained that this was a big deal and should have been more showcased, but I think the fact that they were lumped together and discussed as a success for novel androgen signaling inhibitors is enough, and now we all would agree that their use in this space is valid. The main concern is finding these patients. The OS [had] about a median difference of a little over a year, which is not trivial, for the apalutamide [73.9 versus 59.9 months with ADT/placebo; HR, 0.78; 95% CI, 0.64-0.96; P=.0161].3

I was not involved in the SPARTAN or the ARAMIS trials, but I am an investigator on the PROSPER trial [of enzalutamide and ADT versus ADT and placebo in patients with nonmetastatic CRPC], and I was [included] in this New England Journal of Medicine paper that came out where we showed an OS benefit.4 [The design of the PROSPER trial was] exactly like SPARTAN.

Similar data [were] originally presented. OS difference looking at a year again [67.0 months with enzalutamide vs 56.3 months without; HR, 0.73; 95% CI, 0.61-0.89; P<.001]. The analysis that we saw on SPARTAN is the final analysis with the longest follow-up, but this is not far behind, [with] 48 months of median follow-up.

The ARAMIS trial [of darolutamide and ADT versus ADT and placebo in patients with high-risk nonmetastatic CRPC,] was the one that took us by surprise, because a lot of us were not familiar with this agent. I was seeing it in the background when it was developed, and I could hear Karim Fizazi, MD, PhD, whos a good friend, speaking about it. And I [said], We already have 3, what is this extra fourth going to come through with? And it turns out that they were right in pursuing it. Because they did exactly the same trial as the previous [trials of the other androgen signaling inhibitors], but with an agent that had all the prerequisites to be potentially safer, and they delivered.

The MFS with a short median follow-up [of 17.9 months], looking at about 2 years of difference of MFS [40.4 months with darolutamide versus 18.4 months with placebo], a hazard ratio of 0.41 [95% CI, 0.34-0.50; P<.0001]. Just as a reminder, for the other 2, it was about 0.3. Some people have commented on this, but I would not be able to compare.5

Now, their secondary end points were [more] defiant. At the first presentation, the OS was already starting to look good [with a hazard ratio of 0.71 (95% CI, 0.50-0.99; P<.045)]. It had not [yet] met their threshold, but it was close, and there was a short follow-up compared [with] the other trials.

The time to progression data [show a median time to pain progression of 40.3 months with darolutamide vs 25.4 months without (HR, 0.65; 95% CI, 0.53-0.79; P<.0001)]the other 2 trials also had similar data, which, as I see it, are supportive of each other rather than the inverse. This, for our patients, is a big deal.

Their PFS data [showing a median PFS of 36.8 versus 14.8 months (HR, 0.38; 95% CI, 0.32-0.45; P<.0001)] confirm what I said: superimposable MFS to PFSreinforcing the fact that the addition of a drug [such as] darolutamide, that seems to be safer, adds to these patients more time without need for further interventions and amounts to about 2 years.

The OS at a median follow-up of 29.1 months [was not reached in either arm]; its rather early compared [with] the rest but an obvious improvement here. The hazard ratio was around 0.69 and a P value of 0.003.6 So positive OS data for all 3 trials.

How do the safety profiles of these 3 agents compare?

[In terms of] adverse event reporting [from the PROSPER trial], the main concern, according to them, seems to be grade 3 and above hypertension and some fatigue. I would not pay a lot of attention to what is over grade 3 because when I use a drug for 2 to 3 years, for me even grade 1 and 2 matters. It makes absolute sense to use the least-compromising agent.4

Now, the [ARAMIS safety profile] the winner. They had little adverse events that are treatment related [with darolutamide] [TABLE].5 Its impressive if you look at it versus placebo. And if you want to look at a difference thats at least 2%, I see almost nothing. Its impressive.

When we were working on apalutamide, I got excited because I saw for the first time that 15% of patients were getting a weight decrease. If you look at the data from SPARTAN, it shows up. If you see [the data with] darolutamide, its 3.6%. We started doing some measurements, and its [because of] loss of muscle, and it adds on to the CNS effects. So the falls are not just a result of the CNS effect; its also a lot of muscle weakness, as well.

Overall, how do these 3 trials and drugs compare?

Of course, we shouldnt be [comparing these 3 trials] officially. But there is really no difference between the 3 trials when it comes to the primary and secondary end points. The only difference between the 3 trials with regard to their contact was that, in the apalutamide trial, patients came every month; in the other 2, it was every 4 months. But for MFS and OS, theres no difference between them. They had close hazard ratios.

So we have all [these] agents approved at this pointabiraterone acetate, enzalutamide, apalutamide, and darolutamide. Abiraterone is approved for the hormone-nave metastatic setting, and its also approved for metastatic CRPC; enzalutamide for hormone-nave and nonmetastatic and metastatic CRPC; apalutamide for nonmetastatic CRPC and hormone-nave; and darolutamide for nonmetastatic CRPC. I would argue that for me, these 4 agents have equivalence in their efficacy, and its more a matter of safety.

How does the use of novel imaging affect the duration of treatment and quality of life of these patients?

With the advent of enhanced androgen signaling in the hormone-nave space, I feel that were adding these drugs for an indefinite amount of time. Were going to try to do that with finite-duration hormones, so that we may get the opportunity to prolong the quality of life of the patients. But, as its standing right now, if you do a PET early on in the disease, you may end up treating those men indefinitely.

We know well that if you dont take care to look out for cardiovascular morbidity, bone health, and the like, especially in the older men, you can get a tradeoff thats not to the benefit of the patient. Its a big discussion. But I sometimes say that 1 option is to be more diligent about making sure that the patients are followed at least by their primary care physicians and their cardiologist more carefully.

What are some of the drugs that should be avoided during use with these agents?

Thankfully most of us use electronic prescribing, so we see the drug-drug interactions show up. I dont think we can ever remember all of that by heart.

References:

1. NCCN Clinical Practice Guidelines in Oncology: Prostate cancer. Version 2.2020. May 21, 2020. Accessed August 17, 2020. https://bit.ly/32pmz7H

2. Smith MR, Saad F, Chowdhury S, et al. Apalutamide (APA) and overall survival (OS) in patients (pts) with nonmetastatic castration-resistant prostate cancer (nmCRPC): updated results from the phase III SPARTAN study. Ann Oncol. 2019;30(suppl 5):v325. doi:10.1093/annonc/mdz248

3. Small EJ, Saad F, Chowdhury S, et al. Final survival results from SPARTAN, a phase III study of apalutamide (APA) versus placebo (PBO) in patients (pts) with nonmetastatic castration-resistant prostate cancer (nmCRPC). J Clin Oncol. 2020;30(suppl 15):5516. doi:10.1200/JCO.2020.38.15_suppl.5516

4. Sternberg CN, Fizazi K, Saad F, et al; PROSPER Investigators. Enzalutamide and survival in nonmetastatic, castration-resistant prostate cancer. N Engl J Med. 2020;382:2197-2206. doi:10.1056/NEJMoa2003892

5. Fizazi K, Shore ND, Tammela TL, et al; ARAMIS Investigators. Darolutamide in nonmetastatic, castration-resistant prostate cancer. N Engl J Med. 2019;380:1235-1246. doi:10.1056/NEJMoa1815671

6. Fizazi K, Shore ND, Tammela T, et al. Overall survival (OS) results of phase III ARAMIS study of darolutamide (DARO) added to androgen deprivation therapy (ADT) for nonmetastatic castration-resistant prostate cancer (nmCRPC). J Clin Oncol. 2020;38(suppl 15):5514. doi:10.1200/JCO.2020.38.15_suppl.5514

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Efstathiou Compares the Efficacy and Safety of AR Inhibitors in Nonmetastatic CRPC - Targeted Oncology


Aug 31

LETTER TO THE EDITOR: Safety first | Weaponry | scnow.com – SCNow

A friend related to me that his home recently had been broken into and that he went to the door with gun in hand to face the robber. How he is in his 80s with many health issues, has never taken classes in gun management nor has he fired a weapon in 20 years.

I laughed and asked him why such a smart guy could make such a thoughtless decision.

Sometimes discretion is the better part of valor. While growing up, I watched foolish men on the screen take on Matt Dillon and John Wayne, and they received a tombstone for their efforts. They were driven to destruction by too much testosterone and an overabundance of ego. They believed as do many young people, including myself that they were indestructible.

All of us have been distressed by the loss of life on the streets of America. Those horrific acts define race, creed or status in life. We grieve for those on both sides of the law and wonder how and when the destruction will stop.

Wildlife specialists warn us all that when faced with a carnivore such as a bear, lion or tiger, never run but simply back away cautiously. That clear message applies to the streets of America and if followed would have prevented most of the deaths that have occurred during confrontations.

Do not run. Do not fight! Save your life. By not resisting, jail could be the result. Dont feel bad, because some of the greatest people in the world have ended up behind bars. We have seen time and again that isolation and the quietness of incarceration gives time for thought and freedom from drug addiction. This could be the magic ingredients to a better life.

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LETTER TO THE EDITOR: Safety first | Weaponry | scnow.com - SCNow


Aug 31

Due to its ‘X’ chromosome, the immunity of women is being overshadowed by the corona – Pledge Times

We have informed you many times through our news that the infection of Coronavirus is proving to be more fatal for men than women. At the initial stage, the reason for this difference was revealed only by the male hormone testosteron. But now some more new information has been revealed about this. These include chromosomes, ACE-2 proteins and certain activities related to daily life.

Role of ACE-2 receptors Scientists from different teams doing research on the infection of corona virus and its effects on the human body have found many different reasons, which coronas infection in mens body is much faster than the body of women. Causes of spreading.

One of the main reasons is ACE-2 receptors. Actually, these receptors are a special type of protein. After taking control, the corona virus spreads rapidly in the body. Scientists say that these receptors are more in the body of men than women.

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In addition, ACE-2 receptors are found in greater amounts in people who have heart disease or diabetes. This is a big reason that coronas are suffering from heart disease and sugar patients are coming in large numbers. This research is published in the month of April in Frontiers in Public Health.

Chromosome update-Most people know that XX chromosomes are found in the body of women and XY chromosomes are found in the body of men. These chromosomes determine our gender. Studies on corona have recently revealed that they also affect chromosome immunity.

Health experts say that XX chromosomes are very fast in preventing corona infection from spreading in the body. These help in making the body immune system active and effective.

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Causes of corona infection in men

Role of hormones Men who lack testosterone hormone in their body, they get corona infection very fast. This happens because the same hormone does not allow the corona virus to enter the body, due to infection, swelling in lungs and other parts of the body.

If there is a deficiency of this hormone in the body, then our body is not able to give antiinflammatory response and corona infection starts spreading rapidly in the body. This hormone must be at least 70 percent in their body to protect men from corona.

-Testosteron is a male hormone and controls mens sex life. But this hormone is also found in women. Testosterone also works brilliantly even when women are 60 percent in body and reduces the effects of corona virus in them.

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Due to excess corona infection in men

other activities Health experts say that even if we talk about the total population, even today, activities like smoking, consuming alcohol and following a lazy lifestyle are rarely seen in women. Whereas in contrast, men live their lives with such large number of activities. This has a dangerous effect on their immunity, which is seen more in the Corona era at this time.

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Due to its 'X' chromosome, the immunity of women is being overshadowed by the corona - Pledge Times


Aug 31

Fortress Reports Positive Data And Other News: The Good, Bad And Ugly Of Biopharma – Seeking Alpha

Fortress Biotech reports positive data from CUTX-101

Fortress Biotech Inc. (FBIO) reported positive topline clinical efficacy data for CUTX-101. The trial is being conducted by its partner company Cyprium Therapeutics. The data showed the drug candidate brought about statistically significant improvement in overall survival for Menkes disease. CUTX-101 has been given Orphan Drug, Fast Track and Rare Pediatric Disease Designations by the FDA.

The primary efficacy endpoint for the trial is overall survival measured from birth. The primary efficacy analysis compared overall survival in Menkes disease patients who were administered daily dose of CUTX-101 beginning within four weeks of age to a historical control cohort of patients who were not given copper therapy. Primary efficacy analysis included 31 Menkes disease patients who received ET with CUTX-101 and 18 HC Menkes disease patients. The trial met the primary endpoint of overall survival.

The drug candidate brought about nearly 80 percent reduction in the risk of death whereas median survival for the ET cohort was 14.8 years or 177.1 months compared to 1.3 years 15.9 months for the untreated HC cohort. S. Yam, CEO of Cyprium said, These positive topline clinical efficacy data highlight the potential of CUTX-101 as an effective therapy for Menkes disease patients. With no currently approved U.S. Food and Drug Administration (FDA) treatments, Menkes disease is a serious condition with a significant unmet medical need.

The ET cohort participants carried a severe pathogenic mutation of the ATP7A gene and were born within the past 20 years. The treatment with CUTX-101 was initiated within four weeks of age, adjusted for prematurity. The participants survived at least four weeks after birth and were asymptomatic for significant neurological signs and symptoms during the first four weeks.

HC cohort participants carried a severe pathogenic mutation of the ATP7A gene and were also born within the past 20 years. These participants have not received CUTX-101 therapy and have survived at least four weeks after birth. The patients were asymptomatic for significant neurological signs and symptoms during the first four weeks.

CUTX-101 is a subcutaneous injectable formulation of Copper Histidinate. It has been manufactured to offer improved tolerability due to physiological pH and to circumvent the oral absorption of copper, which is diminished in patients suffering from Menkes disease. The drug candidate is being clinically developed for treating Menkes disease. It aims to treat the ailment by reloading Copper Histidinate, repairing copper homeostasis, and retaining serum copper levels in the normal age appropriate range. The enrollment for a Phase 3 trial of CUTX-101 has been completed. Currently, a Cypriot-sponsored expanded access protocol for Menkes disease patients is being carried out.

Cyprium Therapeutics is mainly engaged in developing therapies for treating Menkes disease and related copper metabolism disorders. It has been founded by Fortress Biotech Inc., which is mainly invested in acquiring, developing and commercializing high-potential marketed pharmaceutical products. It also deals in development-stage pharmaceutical product candidates. Fortress Biotech has five marketed prescription pharmaceutical products in its portfolio. It has robust development pipeline with over 25 programs spanning a wide range of market segments including oncology and gene therapy.

Lipocine Inc. (LPCN) provided regulatory update for its lead drug candidate Tlando. The company has been informed by the FDA that it required additional time to complete its review of the New Drug Application. The anticipated Prescription Drug User Food Act goal date was set at August 28, 2020. The FDA has not provided any alternate timeline or a new action date. The regulator has not demanded any additional data.

TLANDO is an oral testosterone replacement therapy product candidate. It comprises Testosterone Undecanoate, which helps in restoring normal testosterone levels in males for conditions associated with a deficiency or absence of endogenous testosterone. Lipocine has faced several roadblocks for Tlando. The company had received its third Complete Response Letter in November 2019. It had previously received CRLs in June 2016 and May 2018 as well.

The company had recently reported its second quarter results. Lipocine suffered a net loss of $6.4 million or $0.13 per diluted shares for the second quarter. The company had reported $3.4 million in net loss for the corresponding quarter of the previous year. Its research and development expenses for the quarter increased from $2 million to $2.3 million on year over year basis. Its General and Administrative expenses also jumped from $1.4 million to $2 million for the second quarter.

Lipocine Inc. has a robust developmental pipeline with various candidates such as TLANDO, LPCN 1144, TLANDO XR, LPCN 1148 and LPCN 1107. LPCN 1144 is a product of bioidentical testosterone. The drug candidate recently completed a proof-of-concept clinical study showing its potential effectiveness in treating non-cirrhotic NASH. TLANDO XR is a novel oral prodrug of testosterone and LPCN 1148 is an oral prodrug of bioidentical testosterone aimed to treat cirrhosis.

Enanta Pharmaceuticals Inc. (ENTA) reported updates for its non-alcoholic steatohepatitis (NASH) and hepatitis B virus (HBV) development programs. The company is currently working on EDP-305 and EDP-297 for treating NASH. Its EDP-514 is being developed for treating HBV.

Phase 2a ARGON-1 study of EDP-305, its lead Farnesoid Xreceptor (FXR) agonist, showed that the drug candidate met its primary endpoint with statistically significant reduction in alanine transaminase of 28 U/L in comparison to 15 U/L in the placebo cohort at week 12. EDP-305 at the 2.5mg dose also showed statistically significant reduction in liver fat content as measured by MRI-PDFF. The drug candidate also showed robust target engagement as evidenced by decrease in C4 and the increase in FGF-19.

EDP-297 substantially decreased fibrosis progression and enhanced liver function as measured by key biomarkers in a rat model. Rats were randomized to be administered either vehicle control (0.5% methylcellulose), 0.1 mg/kg EDP-297, or 0.3 mg/kg EDP-297 by once-daily oral gavage at the first signs of fibrosis. The data showed that the drug candidate may have a potent anti-fibrotic effect in NASH patients, including those with late-stage F3/4 fibrosis.

The data from first in human, Phase 1 study of EDP-514 showed that it was rapidly absorbed. Its exposure magnified with escalating single and multiple dosing of 600 mg and 400 mg, respectively. The drug candidate was found to be generally safe and well tolerated over a broad spectrum of single and multiple doses for up to 14 days. The trial did not report any discontinuations due to adverse events. EDP-514 demonstrated pharmacokinetics suitable for once daily oral dosing. The geometric mean plasma concentration at 24 hours was found to be significantly higher after multiple dosing with and without a standard meal. The drug candidate is currently being evaluate in two Phase 1b clinical studies.

Thanks for reading. At the Total Pharma Tracker, we do more than follow biotech news. Using our IOMachine, our team of analysts work to be ahead of the curve.

That means that when the catalyst comes that will make or break a stock, weve positioned ourselves for success. And we share that positioning and all the analysis behind it with our members.

Disclosure: I/we have no positions in any stocks mentioned, and no plans to initiate any positions within the next 72 hours. I wrote this article myself, and it expresses my own opinions. I am not receiving compensation for it (other than from Seeking Alpha). I have no business relationship with any company whose stock is mentioned in this article.

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Fortress Reports Positive Data And Other News: The Good, Bad And Ugly Of Biopharma - Seeking Alpha



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