There is one talking point that almost every bioscam on the verge of collapse eventually reaches for, known at BuyersStrike! HQ as “but teh science be so gud.” We have reached that moment in the saga of everyone’s favorite reverse-merger pink sheet Coronacrapper, Cytodyn (CYDY), when criminal stock promoters, various shills, and the retail shareholder base of complete morons suddenly become “experts” in “teh science”.

So, while we wait for the next delusional ranting from The NaDDir*, and while we wait for the company to fess up that their quest for a Nasdaq listing is clearly doomed, in this series we’ll explore “teh science” behind leronlimab (hereafter known as loserlimab), and explain how it is basically completely useless.

Useless against HIV.

Useless against Cancer

And yes, even utterly useless against Covid-19.

First, we’ll look at the history of loserlimab and what it does, and doesn’t do, with regards to HIV. 

Far from being a new drug, loserlimab can trace its roots back to the late 1990s. Scientists discovered that people carrying a particular genetic mutation, known as “Delta 32” were immune to infection by one strain of HIV (known as “CCR5-Tropic” HIV). People carrying this mutation did not express the CCR5 receptor on the outside of their cells. This gave the CCR5-tropic HIV particles nowhere to latch onto in order to enter the cell. 

After this discovery scientists rushed to create treatments that would mimic this genetic mutation. In 2007 the first of them, Selzentry (also known generically as maraviroc) was approved for sale in the USA. Selzentry blocks the CCR5 receptor on the outside of cells, stopping CCR5-Tropic HIV from entering and doing their nasty business.

Selzentry is a daily pill that is taken in combination with other daily medications. Why in combination? Because as explained above blocking CCR5 only stops one form of HIV. CCR5 blocking monotherapy is a mono-mentally (sic) stupid idea in practice because it would fail to protect from the other form of HIV, known as CXCR4-Tropic. Any company, any tout, any deluded investor who believes that monotherapy to block only CCR5 would be a real breakthrough, and have any commercial potential, is either a con artist, or a mark. 

Although it happens to be the only one to successfully make it onto the market, maraviroc was not the only therapy developed back in the late 90s. There were many other attempts. One scientist who was working on such therapies was William Olson. Along with Paul Maddon and others at Progenics Pharmaceuticals (PGNX) he developed a series of murine (mouse) antibodies to block CCR5. One of them was originally known as PA14. 

Progenics then hired another firm, Protein Design Labs, to “humanize” the antibody. This process makes antibodies developed in other species, like mice, more tolerable (technically less “immunogenic”) in human patients. The resulting humanized antibody was christened PRO-140. 

PRO-140 had some interesting attributes. For one, it did not completely block CCR5 receptors. It only bound to a very small part of the CCR5 receptor, just the part necessary for one particular strain of HIV to enter the cell. PRO-140 also does not interfere with normal CCR5 receptor functions. According to Olson:

“Moreover, unlike other candidate CCR5 inhibitors, PRO 140 does not block CCR5’s natural activity“

And, because this is a very important point that bears repeating, in another paper by Olson and Maddon, from 2001: 

Because PRO 140 does not induce signaling or downregulation of CCR5, its antiviral effect is probably exerted through a mechanism involving receptor blockade.

Eventually, after playing around with both IV and subcutaneous administration, and seeing the approval of more convenient oral Selzentry (remember that CCR5 blocking therapy MUST be given in combination with other medications in order to treat and block both forms of HIV), Progenics gave up on PRO-140. After putting it on the shelf, a small desperate reverse merger abomination known as Cytodyn came calling, bought it for a small sum, and renamed it leronlimab.

Hopefully, dear reader, you can now see that loserlimab is actually fairly useless against HIV, because it does not protect against both strains. At best one could say that it might protect against only one (the jury is still out, as the drug has not been approved anywhere, for this purpose). 

But, but, but, cry the Cytodummies, what about the plan to “cure” AIDS patients getting bone marrow transplants by adding loserlimab, announced two weeks ago?

Yeah, that won’t work either. Why not? Because it will not protect from the other form of HIV. And this has been known for years. 

As for cancer, Covid, and the rest? Stay tuned…

THE CONTENT CONTAINED IN THIS BLOG REPRESENTS ONLY THE OPINIONS OF THE AUTHOR. THE AUTHOR MAY HOLD EITHER LONG OR SHORT POSITIONS IN SECURITIES OF VARIOUS COMPANIES DISCUSSED IN THE BLOG. THIS COMMENTARY IN NO WAY CONSTITUTES INVESTMENT ADVICE, AND SHOULD NEVER BE RELIED ON IN MAKING AN INVESTMENT DECISION, EVER. THIS BLOG IS NOT A SOLICITATION OF BUSINESS: ALL INQUIRIES WILL BE IGNORED. THE CONTENT HEREIN IS INTENDED SOLELY FOR THE ENTERTAINMENT OF THE READER, AND THE AUTHOR.

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