Newcomer Pemvidutide

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Anyone tried this yet? It has shown the best results in phase 3 clinical trials for liver fat reduction and a massive reduction of blood cholesterol/lipids. Also a reduction of considerable amount of body weight and a preservation of lean body mass.
 
Anyone tried this yet? It has shown the best results in phase 3 clinical trials for liver fat reduction and a massive reduction of blood cholesterol/lipids. Also a reduction of considerable amount of body weight and a preservation of lean body mass.

It's just getting the approval for phase 3 now. Those were phase 2 trials.
 
If they can find anyone to pay for phase 3. AltImmune has no money.
That reminds me, have you or anyone else ever seen their stock prices?

This is the weirdest company to me. Wtf was going on with this company when they first began trading?

Screenshot_20241111_234824_Samsung Internet.jpg
 
hmmm... so its similar to mazdutide.
also reading about it,

"Altimmune Targets Obesity Market With Weight-Loss Drug That Preserves Lean Muscle Mass"​

 
hmmm... so its similar to mazdutide.
also reading about it,

"Altimmune Targets Obesity Market With Weight-Loss Drug That Preserves Lean Muscle Mass"​

Mazdutide and Survoditude have much less glucagon receptor agonism.. still treat diabetes. Pemvidutide does not treat diabetes. Way higher glucagon agonism, "BUT", less muscle loss.
 
That reminds me, have you or anyone else ever seen their stock prices?

This is the weirdest company to me. Wtf was going on with this company when they first began trading?

View attachment 3586
This is how share price of companies that do stock reverse splits looks like, this is pretty normal for failing companies. If you want to look at the logical extreme of this, go look at the MULN graph.
 
Yeah, unfortunately I think ALT missed the boat with Pemvidutide. Who knows though, maybe they find a partner.. Oral GLP-1's will wipe out these injectables. Probably should buy Viking stock.
 
Mazdutide and Survoditude have much less glucagon receptor agonism.. still treat diabetes. Pemvidutide does not treat diabetes. Way higher glucagon agonism, "BUT", less muscle loss.
Mazdutide yes weaker on glucagon
Survodutide no stronger on glucagon in comparison with maz.
To date the strongest we have is reta with regards to glucagon agonism.

Have a look at this photo and see.

I wonder where pemvidutide falls into this chart?
 

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Mazdutide yes weaker on glucagon
Survodutide no stronger on glucagon in comparison with maz.
To date the strongest we have is reta with regards to glucagon agonism.

Have a look at this photo and see.

I wonder where pemvidutide falls into this chart?

Everyone keeps sharing this chart without labels which I find hilarious. Is this receptor binding or receptor response?
 
Everyone keeps sharing this chart without labels which I find hilarious. Is this receptor binding or receptor response?
It's been about two decades since I did chemistry and molecular biology. Be gentle.

Ki is the is the affinity of a molecule to its' receptor, usually measured in Nanomoles, the lower the number, the less concentration of molecules required to fully bind to the receptor.

Or something like that.
 
You need a degree in pharmacology to understand this. Let me try and explain;

What I posted were Ki values.

Ki represents the concentration at which the inhibitor ligand occupies 50% of the receptor sites when no competing ligand is present.

The smaller the Ki number, the greater the binding affinity and the smaller the amount of ligand is needed to inhibit its binding partners activity.

Notice how little Sema is needed for the Glp1 receptors to be saturated? Also make note of how doses of sema are 1mg to a max of 2.4mg per week.

Now in comparison notice tirz and how much of a higher dose you need to equal the GLP1 effect of Sema? Also keep in mind the molecules at hand are not one and the same. Chemically different structures and different makeups entirely.

Tirz and reta are more similar in chemical structure to one another than sema or tirz or reta and sema.

Now what you use this for is up to you.

Sema is not better than tirz
Tirz is not better than reta
Reta is not better than sema

It just comes down to your basic need? What is it you want. Let me give you an example. For hunger suppression and food noise reduction, nothing beats sema in this regard (from these 3 drugs we are comparing).

If you are looking for weight loss then you should target a drug with a higher affinity towards GIP, Reta is your friend here with approx 8x the binding affinity compared to tirz’s GIP strength. Sema has no GIP activity as it is a single agonist Glp1 drug.

As reta activates your glucagon pathways it can increase your heart rate as well, so if your body cannot handle this and you still want weight loss then go with tirz.

Tirz has no glucagon activation so in theory it should not affect your heart rate.

Reta has one added advantage in that it lowers blood cholesterol and blood lipids as well. Activation of Glucagon pathways actually inhibits PCSK9 and that directly lowers blood lipids profile.

Now if it is blood lipids/triglycerides/cholesterol that is your main concern and this is what you want to reduce then a drug with higher affinity towards Glucagon is needed.

A new drug currently being tested which is called Pemvidutide (a dual receptor agonist of Glp1/Glucagon) has a stronger affinity towards glucagon compared to reta.

So the point I am trying to make here is you have different strokes for different folks. Ask yourself what is it you are trying to address and then do your research to find your answers.

I hope this helps.

My fingers are so sore right now … I feel as though I typed an essay on my phone lol …
 
You need a degree in pharmacology to understand this. Let me try and explain;

What I posted were Ki values.

Ki represents the concentration at which the inhibitor ligand occupies 50% of the receptor sites when no competing ligand is present.

The smaller the Ki number, the greater the binding affinity and the smaller the amount of ligand is needed to inhibit its binding partners activity.

I definitely don't have a degree in pharmacology and I agree that it would be generally useful in conversations like this which are quite complex.

The reason I mentioned the lack of labels is because in addition to binding affinity (strength of attraction between a drug and the receptor it targets) drug efficacy (strength of the reaction a drug causes after binding to a receptor) is also important.

It is possible to have a drug with great affinity but poor efficacy, or great efficacy but poor affinity, and that particular chart tells tells us nothing about the efficacy of those specific drugs.
 
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