13 replies to this topic

[sub7]

Unless I missed it, this has not been discussed

 

https://newsramp.com...690aed4eec003a8

 

Any idea at all what the drug might be? No mention of what it is, what MOA it has and what the mode of administration is...

[simon007]

I found this

https://www.pharmain...maceuticals-inc

and

https://www.sec.gov/...696/forms-1.htm

 

See https://www.google.c...r-1 ingredients

Edited by simon007, 04 September 2024 - 12:57 PM.

[sub7]

Thanks a ton

In the first link you provided, he first talks how Telomir-1 extends telomeres and then says this too

 

Telomir-1 reversibly binds to essential metals preventing the ionization of those metals due to the Fenton reaction and therefore limiting their biological effects. Age-related diseases such as osteoarthritis, senile dementia, macular degeneration, hemochromatosis, and muscle wasting are just some of the potential applications. Although metal reactivity is required for eukaryotic organisms to reach healthy maturity, continued elevated and unregulated metal-induced enzymatic activity contributes to oxidation and inflammation. It has long been recognized that enzymatic reactions also play a key role in the formation of cancerous mutations and the development of diseases like hemochromatosis. By limiting available metals, thus inhibiting metal-induced enzymatic activity, Telomir-1 may prove to be an effective platform for treating a variety of diseases.

 

So  does this drug do 2 totally unrelated things -as in extend telomeres and bind to metals???

[sub7]

 

See https://www.google.c...r-1 ingredients

 

So do we know what the ingredient is?

BTW it says orally dosed...

[QuestforLife]

Thanks a ton

In the first link you provided, he first talks how Telomir-1 extends telomeres and then says this too

 

Telomir-1 reversibly binds to essential metals preventing the ionization of those metals due to the Fenton reaction and therefore limiting their biological effects. Age-related diseases such as osteoarthritis, senile dementia, macular degeneration, hemochromatosis, and muscle wasting are just some of the potential applications. Although metal reactivity is required for eukaryotic organisms to reach healthy maturity, continued elevated and unregulated metal-induced enzymatic activity contributes to oxidation and inflammation. It has long been recognized that enzymatic reactions also play a key role in the formation of cancerous mutations and the development of diseases like hemochromatosis. By limiting available metals, thus inhibiting metal-induced enzymatic activity, Telomir-1 may prove to be an effective platform for treating a variety of diseases.

 

So  does this drug do 2 totally unrelated things -as in extend telomeres and bind to metals???

 

Annoyingly, the article make certain claims about telomere lengthening and telomerase activity increases, but it is rather vague and no plots are given. If it increases telomerase activity, then what is this bench marked against, given they are examining telomerase negative cells?

 

Given the claimed mechanism of action, it appears whatever benefit this substance may have on cells, it is not via telomerase activation. The whole thing smells of BS (this is the first substance that increases telomerase, etc, etc.).

But it is worth keeping a watching brief on in case I am wrong...

[eighthman]

The CEO reportedly died with no mention of cause.  There are two reports about miraculous changes in old dogs, one with terminal cancer.

 

Any chance somebody could get us some? 

[QuestforLife]

I just don't get this company - google is absolutely full of new stories about it, but there is not one piece of data for us to find out more details, for example, what is the evidence for their claims that it turns on telomerase (in stem cells)? 

 

I am not revising my view that this is BS, but I will maintain a watching brief...

[ortcloud]

 what is the evidence for their claims that it turns on telomerase (in stem cells)? 

 

 

 

It is strange. It seems to work by chelating iron out and that restores the telomerase.

 

I found these blurbs in their literature

 

"Similar to doxycycline, TELOMIR-1 is also a metal ion chelating drug, which underlies its ability to inhibit TACE by competing for the zinc"

 

"TACE, or TNFα Converting Enzyme, is a metalloproteinase that plays a crucial role in the release of TNFα, a key inflammatory cytokine.

Dysregulated TACE activity is linked to various inflammatory disorders and cancer progression

 

"Telomir-Zn will exchange the free Iron levels in the cells with beneficial Zinc and will chelate the free iron and take it outside the cell."

 

 "..An increasing number of researches have demonstrated that environmental heavy metals can influence the telomere length of Peripheral Blood Mononuclear Cells (PBMCs)"

 

So is this the secret of the antiaging effect of IV chelation works by removing oxidative metal ions and restoring telomerase?

 

 

https://ml.globenews...9e5d/Slide1.JPG

[QuestforLife]

So it decreases cell proliferation. Quite possibly there are progenitor cells mixed into the culture and they are renewing telomere length in the main culture, whilst the reduced division is reducing telomere shortening. The result of this would be increased telomere length.

I still don't believe any telomerase activation is occurring.

I admit I'd like to see more data though. Sequestering iron probably would be beneficial provided it was done carefully.

[sub7]

 Sequestering iron probably would be beneficial provided it was done carefully.

 

is there any method of doing this currently (and is such method available to and accessible by regular guys?)

[QuestforLife]

There are various chelators that remove metals. But iron is pretty important, so it wouldn't be the right thing to do for everyone. The simplest way of reducing iron load is giving blood. 

[sub7]

yeah I was going to say giving blood is perhaps the most practical approach

 

can you dumb down what it is that we need to do in order to achieve the telomere lengthening effect of the drug discussed here? 

Iron exists in many forms and performs numerous functions. It is bound to ferritin in blood. I believe even inside the cell it doesn't tend to be in free form and is often bound to ferritin and/or used as part of enzymes and cofactors as opposed to sitting there in the pure Fe form.
So what is it we need to do? Just reduce the total amount of moles of iron all over the body regardless of what form it takes and where it resides? Probably not? From where and what form thereof should we most aim to reduce?

[QuestforLife]

I don't know what the mechanism is this pharmaceutical purports to use (to lengthen telomeres). I have stated that I doubt it is via telomerase activation. To the extent it works (if it does), it must be acting via another mechanism such as decreasing oxidative stress, and this will have a downstream benefit on blood cells like those of the immune system. 

 

So just the usual anti oxidants, healthy lifestyle, etc. 

 

If they release more actual data about this pharmaceutical we could maybe say more. 

 

[sub7]

thanks a lot Sir