Celebration Thread TrueBinding Galectin-3

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SusanJ
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Re: Celebration Thread TrueBinding Galectin-3

Post by SusanJ »

J11 wrote:This is where GWAS would be of considerable benefit. All you would need to do is look at the genome and see what genetic variants protect or enhance AD risk. In the above table we see a number of SNPs in the gal-3 protein which is actually in the LGALS3 gene. So for instance rs4652 was found to enhance AD risk by 11%. This gives you a starting point to rationally investigate LGALS3 further.
Thanks for adding to the pile of investigations underway. I personally don't spend much time looking at them and appreciate your posts about what's going on.

GWAS makes so much sense to find places to investigate, and for elucidating potential treatment paths based on our genetics. Hope they have continued success.
J11
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Re: Celebration Thread TrueBinding Galectin-3

Post by J11 »

Thank you for your comment SusanJ!

Yes, it is difficult to know what to follow in AD research as there is such an ocean of research. The strategy that I used recently was to go to clinical trials gov search for Alzheimer Disease and then use the autofilter from there. I wound up with a list of about 400 treatments in development; TrueBinding was on the list. From the perspective of patients and caregivers you want to know of the treatments that are on the nearish term time horizon of 2-3 years.

Gal-3 does look impressive. It side steps the problem of directly attacking beta amyloid and thus seems free of ARIA. Interestingly, patients even at the severe stage appear to have benefited.

What really caught my eye was how the human genome seems to have unlocked. Mega AD GWAS offer the opportunity to take a hit like LGLS4 do a knock out with CRISPR and immediately see whether there is phenotypic benefit in AD cognitive impairment. This is very exciting! Biotech companies must be scrambling to find the targets that are now visibly in the open. Right now will surely be seen in the days ahead as the golden age of medical discovery.

The GWAS discovery approach presents a highly scalable workflow. You take hundreds of hits and work through the entire list. A very comprehensive knowledge base about treatment options for AD could then be developed. Without such a well defined method I would be at a great loss to know where to even start to find an effective AD therapy. Yet, with such background it would seem almost self-evident how to proceed. Once a hit such as LGLS3 were found then it would be off to the chem lab to find some way to disable it. At this time mabs seem to be this goto; though perhaps small molecules might also be effective.
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Re: Celebration Thread TrueBinding Galectin-3

Post by broiler_x »

I've been following this quite closely for the last 12 months or so. The data is very impressive! IF it is true, then this would be a huge breakthrough. Big 'IF', though. Full disclosure: I'm consulting with another biotech that is also pursuing this axis of biology for AD. There are a lot of questions, even just about TrueBinding itself, and how they are funded. They are incredibly secretive. But they could just be trying to fly under the radar and not get the big companies interested in this as competitors. The good news is that their trials are being run by legit U.S. CRO's and hospitals.

They have recently reported vague positive results with the open label extension of the trial mentioned above (without showing any data): https://alzheimersnewstoday.com/news/si ... ths-tb006/

And they are going to be having a Type B meeting with the FDA to try and get an accelerated approval pathway:
https://www.biospace.com/article/releas ... treatment/

They wouldn't try for that Type B meeting unless they really felt their data was strong and valid.

This is very interesting stuff indeed.
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Re: Celebration Thread TrueBinding Galectin-3

Post by J11 »

broiler_x, this is exciting! They first narrowed in on amyloid ... and amyloid checks out. Now they can move around the amyloid universe of biology and find targets that are adjacent to but not exactly amyloid. This can improve safety and possibly efficacy. I wonder how much such biology is still left to be explored?

Yes, TrueBinding was under my awareness until recently. Typically, at the big meetings you just pay attention to where the party is happening and everything else just fades into the background. The amyloid mabs have been center stage for a while. They have helped to provide unequivocal evidence that amyloid is a problem. Many others might then find new ways of reducing amyloid.

I sometimes wonder why these emerging biotechs are not able to more rapidly buildup. I suppose even with great data
one needs to the financing to be there. So those with strong research and weak wallets, will always be a few steps behind on financing.

This is a super exciting time in AD research. It feels like clinical AD treatment is launching now. Medicine can be a lot of watching paint dry for decades and decades and then something launches and it is extremely fun! The clinical development that is happening now is a century scale event.
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