Searching for others who share an autoimmune diagnosis

[Racin4t]

A newbie is exactly what I would call myself. There is soo much more for me to learn, so I lurked for a long time until now..

My diagnosis is MOGAD - Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease. Because the disease is so rare it went undiagnosed for an extremely long time, which has left me pretty much paralyzed from the waist down with a great many complications. Day and night I have been scrolling through these threads, looking for anyone who might be experiencing something similar and might want more information. Specificlly for MOGAD itself I have of course found little, but there is plenty on reducing inflammation in general, which can stop some flare ups. Gaining back some level of function below my level of injury is the goal. If you, or someone you know, has had any success in researching, I would like to hear more about their journey.

ARA-290

NVG-291 I know clinical trials are going on with this one now specifically for SCI.

BPC-157

TB-500

KPV

 

[Throttle883]

Racin4t said:

A newbie is exactly what I would call myself. There is soo much more for me to learn, so I lurked for a long time until now..

My diagnosis is MOGAD - Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease. Because the disease is so rare it went undiagnosed for an extremely long time, which has left me pretty much paralyzed from the waist down with a great many complications. Day and night I have been scrolling through these threads, looking for anyone who might be experiencing something similar and might want more information. Specificlly for MOGAD itself I have of course found little, but there is plenty on reducing inflammation in general, which can stop some flare ups. Gaining back some level of function below my level of injury is the goal. If you, or someone you know, has had any success in researching, I would like to hear more about their journey.

ARA-290

NVG-291 I know clinical trials are going on with this one now specifically for SCI.

BPC-157

TB-500

KPV

Giving you advice on this is not something I can do... yet an auto immune disease is something I live with too. "Undifferentiated Connective Tissue Disease" is the name it goes by. My first bout with Covid, back in 2021, is when it began flaring, and it has stayed with me since.

That pair you are already using (BPC-157-TB-500)

An enormous amount of relief has come my way from those! Auto immune conditions are common among the people here, I know. With any luck somebody will chime in and point you somewhere useful.

May you get the answers you are after!!!!!!

 

[Calm Logic]

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:

Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

 

[Racin4t]

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

This! That particular risk is why TA1 holds very little appeal for me. I have read a little about it, mind you. It is not ruled out entirely - I simply need to study TA1 a great deal more before starting my own research.

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

A little reading on TA 1 was enough to put me off it pretty quickly, this risk being the reason. Perhaps the upside ends up justifying the danger, but far more digging is needed on my part before any research process with TA1 gets under way.

 

[eidos]

During one of my usual literature searches, a piece on myelin regeneration turned up. Whether it is the very same piece I read, I could not say, but this may be useful to you: https://www.nature.com/articles/s41598-024-53615-x

 

[JP.MOTM]

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

Racin4t said:

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

This! That particular risk is why TA1 holds very little appeal for me. I have read a little about it, mind you. It is not ruled out entirely - I simply need to study TA1 a great deal more before starting my own research.

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

A little reading on TA 1 was enough to put me off it pretty quickly, this risk being the reason. Perhaps the upside ends up justifying the danger, but far more digging is needed on my part before any research process with TA1 gets under way.

There is nothing unreasonable about either worry, and I had that same question myself: would this simply make autoimmune problems worse? To my mind it is a fascinating subject and one I have gone into quite deeply. Plenty of the writing amounts to speculation about mechanisms, or straightforward observations, yet the picture becomes more comforting the further into it you go (though it is not a completely settled matter).

Parts of the immune system do get "boosted" by TA1 in the published work. Vaccine antibody responses and Th1 immunity can both be strengthened, which makes the worry about autoimmunity-linked antibodies entirely legitimate. A fair question. What the evidence indicates, though, is that this does not happen - and there is considerably more evidence here than I had assumed.

A simple immune "booster" is not what TA1 looks like. It behaves far more like a regulator. Context decides which parts of immunity get turned up or down, and interestingly both can happen simultaneously. On the mechanism side, the selfsame TLR9 signal that drives antiviral and anti-tumour immunity is also capable of switching on tolerance pathways through IDO, IL-10 and regulatory T-cells. Plainly put, the accelerator is not the only pedal it presses. It also looks like it helps reset the immune system, quietening attacks that ought not to occur.

Nowhere is that clearer than in the multiple sclerosis work. MS involves B-cells, yet "B-cells" are not one uniform population. Some of them help hold autoimmune inflammation on; others are regulatory and act to calm the immune response. Those calming regulatory B-cells look too few in relapsing-remitting MS. When TA1 was added to immune cells from such patients, the underactive regulatory population expanded and calming signals such as IL-10 and IL-35 rose, while "bad" inflammatory signals including IFN-gamma and IL-17 fell. TA1 also reduced the capacity of B-cells to turn into IgM- or IgG-secreting cells, which points away from antibody production rather than towards it. What TA1 was doing was restoring balance, bringing the "bad" response down and the "good" response up at once.

An autoimmune-like model of gut inflammation displays the same broad pattern. Colitis triggered by cancer immunotherapy in mice was held off by TA1, which switched on an IDO-dependent tolerance pathway and protected the gut. Taken with the mechanism, the MS findings and the colitis model, everything therefore points at regulation and recalibration rather than an autoimmune boost.

Calling it "proven safe in every autoimmune condition" would be overstating things, since no such study exists. Nobody has run a clinical trial among people with established autoimmune disease that follows real-world flares over time. Still, the data available is genuinely solid and, in my opinion, more persuasive than the particular items discussed so far.

Nor is TA1 some brand-new compound assessed only on the studies just mentioned. Under the name Zadaxin/thymalfasin it has held approvals in many countries for years, applied to hepatitis B, immune deficiency and improved vaccine response. Routine use in places such as China, notably in intensive-care and oncology settings, goes back years as well.

Two distinct kinds of safety data follow from that. The first is the formal trial data, covering over 11,000 people in more than 30 trials. The second is the much larger real-world clinical experience, in which over 600,000 patients have reportedly been treated since approval. Being less controlled than a trial, that second group cannot establish the absence of rare or subtle risks. It remains informative all the same, since a common tendency for TA1 to produce obvious autoimmune flares ought to have surfaced after that much routine use. It has not. Nor was I able to find any data in which an autoimmune response appeared while TA1 was being used. So again: not a perfect all-clear, but definitely reassuring.

Sources I drew on:

Romani L, et al. Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through Toll-like receptor signalling. Blood. 2004.

Giacomini E, et al. Dual effect of thymosin alpha1 on human monocyte-derived dendritic cells stimulated with viral and bacterial toll-like receptor agonists. Expert Opin Biol Ther. 2015.

Romani L, et al. Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance. Blood. 2006.

Giacomini E, et al. Thymosin-alpha1 expands deficient IL-10-producing regulatory B cell subsets in relapsing-remitting multiple sclerosis patients. Multiple Sclerosis. 2018.

Renga G, et al. Thymosin alpha1 protects from CTLA-4 intestinal immunopathology. Life Science Alliance. 2020.

Dinetz E, et al. Comprehensive review of the safety and efficacy of thymosin alpha 1 in human clinical trials. Altern Ther Health Med. 2024.

 

[Gorby2025]

@Racin4t - welcome, and good luck on your journey. Auto-immune disorders are something I know about first hand, since I have one as well (Ankylosing Spondylitis), and there was a spell when getting out of bed was impossible, sitting or lying down was impossible, and nothing could be done without excruciating pain. On top of that I was dealing with a very high level of inflammation. Because of the possible risks I avoided biologics (Humira and equivalents) as much as I could, but finally caved in since the pain and the effect on my life had simply become too much. It changed my life - they worked like magic. The idea of being on biologics for the rest of my life bothered me all the same, so I carried on researching. That is how I stumbled onto peptides. Some of my results are documented in my intro thread here. The TL;DR is that I credit a stack of Reta, TA-1, BPC/TB/KPV and ARA-290 peptides with getting me off biologics without my symptoms or pain returning. I have been biologics-free for 7 months so far, I feel great, I get bloodwork every few months and my tests and inflammation markers are not only in the normal range but the best I have had in many years.

Does that mean the same will work for you? Nobody can tell unfortunately... but in my humble opinion it is definitely worth reading about, learning from and trying. Good luck to you, and I hope you feel better.

 

[bbvvin]

Gorby2025 said:

@Racin4t - welcome, and good luck on your journey. Auto-immune disorders are something I know about first hand, since I have one as well (Ankylosing Spondylitis), and there was a spell when getting out of bed was impossible, sitting or lying down was impossible, and nothing could be done without excruciating pain. On top of that I was dealing with a very high level of inflammation. Because of the possible risks I avoided biologics (Humira and equivalents) as much as I could, but finally caved in since the pain and the effect on my life had simply become too much. It changed my life - they worked like magic. The idea of being on biologics for the rest of my life bothered me all the same, so I carried on researching. That is how I stumbled onto peptides. Some of my results are documented in my intro thread here. The TL;DR is that I credit a stack of Reta, TA-1, BPC/TB/KPV and ARA-290 peptides with getting me off biologics without my symptoms or pain returning. I have been biologics-free for 7 months so far, I feel great, I get bloodwork every few months and my tests and inflammation markers are not only in the normal range but the best I have had in many years.

Does that mean the same will work for you? Nobody can tell unfortunately... but in my humble opinion it is definitely worth reading about, learning from and trying. Good luck to you, and I hope you feel better.

Was getting off the biologics down mostly to the weight you lost on Reta, or to the other peptides?

 

[Gorby2025]

bbvvin said:

Gorby2025 said:

@Racin4t - welcome, and good luck on your journey. Auto-immune disorders are something I know about first hand, since I have one as well (Ankylosing Spondylitis), and there was a spell when getting out of bed was impossible, sitting or lying down was impossible, and nothing could be done without excruciating pain. On top of that I was dealing with a very high level of inflammation. Because of the possible risks I avoided biologics (Humira and equivalents) as much as I could, but finally caved in since the pain and the effect on my life had simply become too much. It changed my life - they worked like magic. The idea of being on biologics for the rest of my life bothered me all the same, so I carried on researching. That is how I stumbled onto peptides. Some of my results are documented in my intro thread here. The TL;DR is that I credit a stack of Reta, TA-1, BPC/TB/KPV and ARA-290 peptides with getting me off biologics without my symptoms or pain returning. I have been biologics-free for 7 months so far, I feel great, I get bloodwork every few months and my tests and inflammation markers are not only in the normal range but the best I have had in many years.

Does that mean the same will work for you? Nobody can tell unfortunately... but in my humble opinion it is definitely worth reading about, learning from and trying. Good luck to you, and I hope you feel better.

Was getting off the biologics down mostly to the weight you lost on Reta, or to the other peptides?

The combination is what does it, in my view.

 

[zooombasaurus [I1]]

Helloooo... I have Hypermobile Ehlers danlos Syndrome (hEDS), an inherited condition affecting connective tissue. Given the tissue is weak here throughout the body, the pain it produces is global and widespread. Dysautonomia (Autonomic Nervous Systen dysfunction) and Mast Cell Activation syndrome are linked to it as well. Some further comorbidities come with it, but the main diagnoses are the ones above. I am in my 40's, and getting a proper diagnosis took my entire life - it only happened a couple of years back. Anyway, wanting to manage pain and treat my chronic fatigue is why my peptide journey started, plus helping with ageing, since trying to mask everything with beauty and be a bit vain still matters to me I guess. Microdosing Tizepatide was my first step, because about 10 lbs was the struggle. Obviously that worked. Beyond that, KLOW is the peptide that has helped my pain the most. KPV, GHK-CU, TB 500 and BC 157 all go into KLOW, so out of the gate this blend offers plenty for those of us hurting everywhere (the constant pain sits in my lower back, both shoulders and cervical spine, and it is literally gone - but stop taking it and back it comes). Separately - and this only just happened - I really thought something for energy had finally come my way, and boy was I wrong. Glutathione it was. Yesterday I actually skipped it, but the three days before that I had used it, and my energy was good. Then by yesterday evening, energy turned into an MCAS flare plus a histamine reaction, which became a Dysautonomia flare too - a widespread system allergic response, and not a good one. No more Glutathione for me! Which means N-acetylcysteine (NAC) is out as well, since it gets converted into glutathione. Just wanted to share the experience, in case it proves useful in some way!

 

[cujet]

Retatrutide belongs on the list too. The genuine article, rather than the counterfeit gear that circulates so widely on the gray market. Various autoimmune diseases have been talked about in YouTube videos as being pushed close to remission by Reta, and in some instances all the way into it.

My own tally is 4 diseases: Sec Adrl Insf (severe), Myasthenia Gravis (where the nerves and muscles do not communicate), Hashimoto's thyroid failure, and Mixed Connective Tissue Disease (MCTD, along the lines of Lupus).

Real Reta let me drop prednisone altogether for roughly 6 months. Remarkable on its own. Then a bunk vial came my way and the need for pred was straight back.

 

[DunningKruger]

Racin4t said:

A newbie is exactly what I would call myself. There is soo much more for me to learn, so I lurked for a long time until now..

My diagnosis is MOGAD - Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease. Because the disease is so rare it went undiagnosed for an extremely long time, which has left me pretty much paralyzed from the waist down with a great many complications. Day and night I have been scrolling through these threads, looking for anyone who might be experiencing something similar and might want more information. Specificlly for MOGAD itself I have of course found little, but there is plenty on reducing inflammation in general, which can stop some flare ups. Gaining back some level of function below my level of injury is the goal. If you, or someone you know, has had any success in researching, I would like to hear more about their journey.

ARA-290

NVG-291 I know clinical trials are going on with this one now specifically for SCI.

BPC-157

TB-500

KPV

That list for autoimmunity is a really good one. Considerable thought has gone into which peptides you picked, and the first two in particular suit your situation.

Different case here, but what I am running at present is ARA-290, TA-1 and KLOW. Nerve pain relief from ARA-290 at low doses has been better than I expected, and the whole combination does a good job of holding inflammatory/autoimmune flares down. Further ahead I want to try Thymulin and VIP, doing so only after this run finishes so that my results are not confounded.

- - - - - -

Two papers on NVG-291/PTPσ strike me as especially relevant to the questions you are exploring:

Luo et al., 2018 — Nature Communications

https://www.nature.com/articles/s41467-018-06505-6

For me this is the important one. Where PTPσ was blocked, remyelination and functional recovery in an autoimmune CNS demyelination model followed, and that is what makes NVG-291 so interesting in the context of MOGAD.

Niknam et al., 2019 — Experimental Neurology

https://pubmed.ncbi.nlm.nih.gov/31276750/

Here the focus was a demyelinated optic pathway, with more remyelinated axons and better visual electrophysiology once PTPσ was inhibited - a finding that matters given how often optic neuritis features in MOGAD.

MOGAD-specific they are not, and neither counts as human evidence, but together they make a fairly solid mechanistic case for treating NVG-291 as a neural repair/remyelination strategy.

- - - - - -

Some ARA-290 papers that strike me as especially relevant to the questions you are exploring:

Chen et al., 2014 — Journal of Neuroimmunology

https://pubmed.ncbi.nlm.nih.gov/24518674/

Probably the most relevant of them. T-cell activity was modulated and CNS inflammation reduced, and ARA-290 improved experimental autoimmune encephalomyelitis (EAE) as a result, so a direct autoimmune demyelination connection exists at the very least.

Liu et al., 2014 — Neural Regeneration Research

https://pmc.ncbi.nlm.nih.gov/articles/PMC3946253/

Peripheral rather than CNS in this study, but nerve regeneration and remyelination improved on ARA-290 while inflammatory damage to nerves fell, which is why a repair standpoint seems worth taking.

Dahan et al., 2013 — Molecular Medicine

https://pmc.ncbi.nlm.nih.gov/articles/PMC3883966/

The human study. In inflammatory small-fibre neuropathy, corneal nerve fibre density rose on ARA-290, which is genuine human evidence pointing at nerve-fibre repair rather than pain reduction alone.

All the best with your peptide journey.

 

[amosmylove]

zooombasaurus said:

Helloooo... I have Hypermobile Ehlers danlos Syndrome (hEDS), an inherited condition affecting connective tissue. Given the tissue is weak here throughout the body, the pain it produces is global and widespread. Dysautonomia (Autonomic Nervous Systen dysfunction) and Mast Cell Activation syndrome are linked to it as well. Some further comorbidities come with it, but the main diagnoses are the ones above. I am in my 40's, and getting a proper diagnosis took my entire life - it only happened a couple of years back. Anyway, wanting to manage pain and treat my chronic fatigue is why my peptide journey started, plus helping with ageing, since trying to mask everything with beauty and be a bit vain still matters to me I guess. Microdosing Tizepatide was my first step, because about 10 lbs was the struggle. Obviously that worked. Beyond that, KLOW is the peptide that has helped my pain the most. KPV, GHK-CU, TB 500 and BC 157 all go into KLOW, so out of the gate this blend offers plenty for those of us hurting everywhere (the constant pain sits in my lower back, both shoulders and cervical spine, and it is literally gone - but stop taking it and back it comes). Separately - and this only just happened - I really thought something for energy had finally come my way, and boy was I wrong. Glutathione it was. Yesterday I actually skipped it, but the three days before that I had used it, and my energy was good. Then by yesterday evening, energy turned into an MCAS flare plus a histamine reaction, which became a Dysautonomia flare too - a widespread system allergic response, and not a good one. No more Glutathione for me! Which means N-acetylcysteine (NAC) is out as well, since it gets converted into glutathione. Just wanted to share the experience, in case it proves useful in some way!

hEDS is my diagnosis as well. The klow stack is what I use, though I do it seperately. Insane relief/healing is what tb500/Bpc157 has given me. What is interesting is that I can tell the cartilage has become firmer. After noticing the nose and ears are less squishy/flexible, I have been keeping an eye on it. Pushing the tip of my nose would always just flatten and squish it, for lack of a better description. It used to get me made fun of, and family would poke my nose, though not meanly. Tougher ears are the other change, and they do not bend the way they once did. Almost like my husband's, they feel now. Strange, but after a whole life of being extra bendy and squishy wherever cartilage is, the difference is really noticeable! bpc/tb/ghkcu came into the picture in February, so 6 months. More than I could ever have hoped, the improvements have been.

 

[zooombasaurus [I1]]

amosmylove said:

zooombasaurus said:

Helloooo... I have Hypermobile Ehlers danlos Syndrome (hEDS), an inherited condition affecting connective tissue. Given the tissue is weak here throughout the body, the pain it produces is global and widespread. Dysautonomia (Autonomic Nervous Systen dysfunction) and Mast Cell Activation syndrome are linked to it as well. Some further comorbidities come with it, but the main diagnoses are the ones above. I am in my 40's, and getting a proper diagnosis took my entire life - it only happened a couple of years back. Anyway, wanting to manage pain and treat my chronic fatigue is why my peptide journey started, plus helping with ageing, since trying to mask everything with beauty and be a bit vain still matters to me I guess. Microdosing Tizepatide was my first step, because about 10 lbs was the struggle. Obviously that worked. Beyond that, KLOW is the peptide that has helped my pain the most. KPV, GHK-CU, TB 500 and BC 157 all go into KLOW, so out of the gate this blend offers plenty for those of us hurting everywhere (the constant pain sits in my lower back, both shoulders and cervical spine, and it is literally gone - but stop taking it and back it comes). Separately - and this only just happened - I really thought something for energy had finally come my way, and boy was I wrong. Glutathione it was. Yesterday I actually skipped it, but the three days before that I had used it, and my energy was good. Then by yesterday evening, energy turned into an MCAS flare plus a histamine reaction, which became a Dysautonomia flare too - a widespread system allergic response, and not a good one. No more Glutathione for me! Which means N-acetylcysteine (NAC) is out as well, since it gets converted into glutathione. Just wanted to share the experience, in case it proves useful in some way!

hEDS is my diagnosis as well. The klow stack is what I use, though I do it seperately. Insane relief/healing is what tb500/Bpc157 has given me. What is interesting is that I can tell the cartilage has become firmer. After noticing the nose and ears are less squishy/flexible, I have been keeping an eye on it. Pushing the tip of my nose would always just flatten and squish it, for lack of a better description. It used to get me made fun of, and family would poke my nose, though not meanly. Tougher ears are the other change, and they do not bend the way they once did. Almost like my husband's, they feel now. Strange, but after a whole life of being extra bendy and squishy wherever cartilage is, the difference is really noticeable! bpc/tb/ghkcu came into the picture in February, so 6 months. More than I could ever have hoped, the improvements have been.

It is actually wild. Whether other people really benefit as much from it, or whether we just notice more because we have so many injuries so to speak, I question. A toe on my right foot was actually fractured by me earlier this year and I kid you not, 3 months passed before there was no pain. Another toe on my right foot got literally fractured by me last week. Black it turned immediately, even more so than the first time. Sooooo upset was I, bc getting my foot pain-free had taken so long. And already it literally feels like it is better. Whether it is fractured this time I question, but pressing on it still finds it extremely swollen and tender. Idk. Trying Cartalax is something I was actually interested in for this reason, thinking more healing of cartilage was going to be necessary. But just as good as I was thinking Cartalax might be needed, KLOW actually works for us, I think. Awesome! Do you take any breaks from it?

 

[Researcher6076]

DunningKruger said:

Racin4t said:

A newbie is exactly what I would call myself. There is soo much more for me to learn, so I lurked for a long time until now..

My diagnosis is MOGAD - Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease. Because the disease is so rare it went undiagnosed for an extremely long time, which has left me pretty much paralyzed from the waist down with a great many complications. Day and night I have been scrolling through these threads, looking for anyone who might be experiencing something similar and might want more information. Specificlly for MOGAD itself I have of course found little, but there is plenty on reducing inflammation in general, which can stop some flare ups. Gaining back some level of function below my level of injury is the goal. If you, or someone you know, has had any success in researching, I would like to hear more about their journey.

ARA-290

NVG-291 I know clinical trials are going on with this one now specifically for SCI.

BPC-157

TB-500

KPV

That list for autoimmunity is a really good one. Considerable thought has gone into which peptides you picked, and the first two in particular suit your situation.

Different case here, but what I am running at present is ARA-290, TA-1 and KLOW. Nerve pain relief from ARA-290 at low doses has been better than I expected, and the whole combination does a good job of holding inflammatory/autoimmune flares down. Further ahead I want to try Thymulin and VIP, doing so only after this run finishes so that my results are not confounded.

- - - - - -

Two papers on NVG-291/PTPσ strike me as especially relevant to the questions you are exploring:

Luo et al., 2018 — Nature Communications

https://www.nature.com/articles/s41467-018-06505-6

For me this is the important one. Where PTPσ was blocked, remyelination and functional recovery in an autoimmune CNS demyelination model followed, and that is what makes NVG-291 so interesting in the context of MOGAD.

Niknam et al., 2019 — Experimental Neurology

https://pubmed.ncbi.nlm.nih.gov/31276750/

Here the focus was a demyelinated optic pathway, with more remyelinated axons and better visual electrophysiology once PTPσ was inhibited - a finding that matters given how often optic neuritis features in MOGAD.

MOGAD-specific they are not, and neither counts as human evidence, but together they make a fairly solid mechanistic case for treating NVG-291 as a neural repair/remyelination strategy.

- - - - - -

Some ARA-290 papers that strike me as especially relevant to the questions you are exploring:

Chen et al., 2014 — Journal of Neuroimmunology

https://pubmed.ncbi.nlm.nih.gov/24518674/

Probably the most relevant of them. T-cell activity was modulated and CNS inflammation reduced, and ARA-290 improved experimental autoimmune encephalomyelitis (EAE) as a result, so a direct autoimmune demyelination connection exists at the very least.

Liu et al., 2014 — Neural Regeneration Research

https://pmc.ncbi.nlm.nih.gov/articles/PMC3946253/

Peripheral rather than CNS in this study, but nerve regeneration and remyelination improved on ARA-290 while inflammatory damage to nerves fell, which is why a repair standpoint seems worth taking.

Dahan et al., 2013 — Molecular Medicine

https://pmc.ncbi.nlm.nih.gov/articles/PMC3883966/

The human study. In inflammatory small-fibre neuropathy, corneal nerve fibre density rose on ARA-290, which is genuine human evidence pointing at nerve-fibre repair rather than pain reduction alone.

All the best with your peptide journey.

Could you walk me through how you dose ARA-290? I would like to hear what protocol you follow.

 

[DunningKruger]

Researcher6076 said:

DunningKruger said:

Racin4t said:

A newbie is exactly what I would call myself. There is soo much more for me to learn, so I lurked for a long time until now..

My diagnosis is MOGAD - Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease. Because the disease is so rare it went undiagnosed for an extremely long time, which has left me pretty much paralyzed from the waist down with a great many complications. Day and night I have been scrolling through these threads, looking for anyone who might be experiencing something similar and might want more information. Specificlly for MOGAD itself I have of course found little, but there is plenty on reducing inflammation in general, which can stop some flare ups. Gaining back some level of function below my level of injury is the goal. If you, or someone you know, has had any success in researching, I would like to hear more about their journey.

ARA-290

NVG-291 I know clinical trials are going on with this one now specifically for SCI.

BPC-157

TB-500

KPV

That list for autoimmunity is a really good one. Considerable thought has gone into which peptides you picked, and the first two in particular suit your situation.

Different case here, but what I am running at present is ARA-290, TA-1 and KLOW. Nerve pain relief from ARA-290 at low doses has been better than I expected, and the whole combination does a good job of holding inflammatory/autoimmune flares down. Further ahead I want to try Thymulin and VIP, doing so only after this run finishes so that my results are not confounded.

- - - - - -

Two papers on NVG-291/PTPσ strike me as especially relevant to the questions you are exploring:

Luo et al., 2018 — Nature Communications

https://www.nature.com/articles/s41467-018-06505-6

For me this is the important one. Where PTPσ was blocked, remyelination and functional recovery in an autoimmune CNS demyelination model followed, and that is what makes NVG-291 so interesting in the context of MOGAD.

Niknam et al., 2019 — Experimental Neurology

https://pubmed.ncbi.nlm.nih.gov/31276750/

Here the focus was a demyelinated optic pathway, with more remyelinated axons and better visual electrophysiology once PTPσ was inhibited - a finding that matters given how often optic neuritis features in MOGAD.

MOGAD-specific they are not, and neither counts as human evidence, but together they make a fairly solid mechanistic case for treating NVG-291 as a neural repair/remyelination strategy.

- - - - - -

Some ARA-290 papers that strike me as especially relevant to the questions you are exploring:

Chen et al., 2014 — Journal of Neuroimmunology

https://pubmed.ncbi.nlm.nih.gov/24518674/

Probably the most relevant of them. T-cell activity was modulated and CNS inflammation reduced, and ARA-290 improved experimental autoimmune encephalomyelitis (EAE) as a result, so a direct autoimmune demyelination connection exists at the very least.

Liu et al., 2014 — Neural Regeneration Research

https://pmc.ncbi.nlm.nih.gov/articles/PMC3946253/

Peripheral rather than CNS in this study, but nerve regeneration and remyelination improved on ARA-290 while inflammatory damage to nerves fell, which is why a repair standpoint seems worth taking.

Dahan et al., 2013 — Molecular Medicine

https://pmc.ncbi.nlm.nih.gov/articles/PMC3883966/

The human study. In inflammatory small-fibre neuropathy, corneal nerve fibre density rose on ARA-290, which is genuine human evidence pointing at nerve-fibre repair rather than pain reduction alone.

All the best with your peptide journey.

Could you walk me through how you dose ARA-290? I would like to hear what protocol you follow.

There is no protocol as such. Anything from 500mcg to 1mg daily, chosen by how much pain I have when I wake up. That is well under the doses used in studies and the protocols most people follow, yet for my double crush it does the job.

 

[bamagirl26]

amosmylove said:

zooombasaurus said:

Helloooo... I have Hypermobile Ehlers danlos Syndrome (hEDS), an inherited condition affecting connective tissue. Given the tissue is weak here throughout the body, the pain it produces is global and widespread. Dysautonomia (Autonomic Nervous Systen dysfunction) and Mast Cell Activation syndrome are linked to it as well. Some further comorbidities come with it, but the main diagnoses are the ones above. I am in my 40's, and getting a proper diagnosis took my entire life - it only happened a couple of years back. Anyway, wanting to manage pain and treat my chronic fatigue is why my peptide journey started, plus helping with ageing, since trying to mask everything with beauty and be a bit vain still matters to me I guess. Microdosing Tizepatide was my first step, because about 10 lbs was the struggle. Obviously that worked. Beyond that, KLOW is the peptide that has helped my pain the most. KPV, GHK-CU, TB 500 and BC 157 all go into KLOW, so out of the gate this blend offers plenty for those of us hurting everywhere (the constant pain sits in my lower back, both shoulders and cervical spine, and it is literally gone - but stop taking it and back it comes). Separately - and this only just happened - I really thought something for energy had finally come my way, and boy was I wrong. Glutathione it was. Yesterday I actually skipped it, but the three days before that I had used it, and my energy was good. Then by yesterday evening, energy turned into an MCAS flare plus a histamine reaction, which became a Dysautonomia flare too - a widespread system allergic response, and not a good one. No more Glutathione for me! Which means N-acetylcysteine (NAC) is out as well, since it gets converted into glutathione. Just wanted to share the experience, in case it proves useful in some way!

hEDS is my diagnosis as well. The klow stack is what I use, though I do it seperately. Insane relief/healing is what tb500/Bpc157 has given me. What is interesting is that I can tell the cartilage has become firmer. After noticing the nose and ears are less squishy/flexible, I have been keeping an eye on it. Pushing the tip of my nose would always just flatten and squish it, for lack of a better description. It used to get me made fun of, and family would poke my nose, though not meanly. Tougher ears are the other change, and they do not bend the way they once did. Almost like my husband's, they feel now. Strange, but after a whole life of being extra bendy and squishy wherever cartilage is, the difference is really noticeable! bpc/tb/ghkcu came into the picture in February, so 6 months. More than I could ever have hoped, the improvements have been.

Once I pluck up the courage to order a pen and deal with all the rest of it, I would really like to discuss this with you further. Hypermobile for sure here - I tick the markers for EDS without having the diagnosis. Stronger joints are definitely something I want, so this sounds like a combo that could work well in my case. For the sake of testing, making my own rather than buying a ready-made blend is probably what I will do.

 

[kazza94x]

Racin4t said:

A newbie is exactly what I would call myself. There is soo much more for me to learn, so I lurked for a long time until now..

My diagnosis is MOGAD - Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease. Because the disease is so rare it went undiagnosed for an extremely long time, which has left me pretty much paralyzed from the waist down with a great many complications. Day and night I have been scrolling through these threads, looking for anyone who might be experiencing something similar and might want more information. Specificlly for MOGAD itself I have of course found little, but there is plenty on reducing inflammation in general, which can stop some flare ups. Gaining back some level of function below my level of injury is the goal. If you, or someone you know, has had any success in researching, I would like to hear more about their journey.

ARA-290

NVG-291 I know clinical trials are going on with this one now specifically for SCI.

BPC-157

TB-500

KPV

Hey there !! Sorry to read about the paralysis below the waist. Auto-immune disorders rank among the most heavily researched areas in the whole of human medicine.

Living in the US as you do, I would look at MOGAD research first, before going anywhere near grey-market peptides. I say that only because whether your immune system is compromised is something I do not know. If you were going to try any of them, though - BPC157/TB500 appears to give the best results in people with chronic pain and tissue damage.

Australia is where I am, but the last half hour has gone on some heavy reading, and a few links have turned up that may be worth your while, given your condition:


https://wearesrna.org/resources/2026-open-q-and-a-on-mogad


According to SRNA there are 31 U.S. sites that are enrolling this year, or soon will be. Worth double checking - from Australia my view of it may be limited.

7T MOGAD: Application of 7T MRI in MOG-Associated Disorders | Cleveland Clinic

my.clevelandclinic.org

Adults with MOGAD are being actively recruited for a study that uses 7-Tesla MRI, looking at changes related to MOGAD and at predictors of outcomes.

Same goes for this one, so please double check.

With spinal-cord involvement as severe as yours, it would also be worth asking a MOGAD neuroimmunologist about any neurorehabilitation or neuroregeneration studies taking people in your area.

Hope this is of use - everything above is drawn, in paraphrase, from those links.

 

[Atlas27]

JP.MOTM said:

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

Racin4t said:

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

This! That particular risk is why TA1 holds very little appeal for me. I have read a little about it, mind you. It is not ruled out entirely - I simply need to study TA1 a great deal more before starting my own research.

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

A little reading on TA 1 was enough to put me off it pretty quickly, this risk being the reason. Perhaps the upside ends up justifying the danger, but far more digging is needed on my part before any research process with TA1 gets under way.

There is nothing unreasonable about either worry, and I had that same question myself: would this simply make autoimmune problems worse? To my mind it is a fascinating subject and one I have gone into quite deeply. Plenty of the writing amounts to speculation about mechanisms, or straightforward observations, yet the picture becomes more comforting the further into it you go (though it is not a completely settled matter).

Parts of the immune system do get "boosted" by TA1 in the published work. Vaccine antibody responses and Th1 immunity can both be strengthened, which makes the worry about autoimmunity-linked antibodies entirely legitimate. A fair question. What the evidence indicates, though, is that this does not happen - and there is considerably more evidence here than I had assumed.

A simple immune "booster" is not what TA1 looks like. It behaves far more like a regulator. Context decides which parts of immunity get turned up or down, and interestingly both can happen simultaneously. On the mechanism side, the selfsame TLR9 signal that drives antiviral and anti-tumour immunity is also capable of switching on tolerance pathways through IDO, IL-10 and regulatory T-cells. Plainly put, the accelerator is not the only pedal it presses. It also looks like it helps reset the immune system, quietening attacks that ought not to occur.

Nowhere is that clearer than in the multiple sclerosis work. MS involves B-cells, yet "B-cells" are not one uniform population. Some of them help hold autoimmune inflammation on; others are regulatory and act to calm the immune response. Those calming regulatory B-cells look too few in relapsing-remitting MS. When TA1 was added to immune cells from such patients, the underactive regulatory population expanded and calming signals such as IL-10 and IL-35 rose, while "bad" inflammatory signals including IFN-gamma and IL-17 fell. TA1 also reduced the capacity of B-cells to turn into IgM- or IgG-secreting cells, which points away from antibody production rather than towards it. What TA1 was doing was restoring balance, bringing the "bad" response down and the "good" response up at once.

An autoimmune-like model of gut inflammation displays the same broad pattern. Colitis triggered by cancer immunotherapy in mice was held off by TA1, which switched on an IDO-dependent tolerance pathway and protected the gut. Taken with the mechanism, the MS findings and the colitis model, everything therefore points at regulation and recalibration rather than an autoimmune boost.

Calling it "proven safe in every autoimmune condition" would be overstating things, since no such study exists. Nobody has run a clinical trial among people with established autoimmune disease that follows real-world flares over time. Still, the data available is genuinely solid and, in my opinion, more persuasive than the particular items discussed so far.

Nor is TA1 some brand-new compound assessed only on the studies just mentioned. Under the name Zadaxin/thymalfasin it has held approvals in many countries for years, applied to hepatitis B, immune deficiency and improved vaccine response. Routine use in places such as China, notably in intensive-care and oncology settings, goes back years as well.

Two distinct kinds of safety data follow from that. The first is the formal trial data, covering over 11,000 people in more than 30 trials. The second is the much larger real-world clinical experience, in which over 600,000 patients have reportedly been treated since approval. Being less controlled than a trial, that second group cannot establish the absence of rare or subtle risks. It remains informative all the same, since a common tendency for TA1 to produce obvious autoimmune flares ought to have surfaced after that much routine use. It has not. Nor was I able to find any data in which an autoimmune response appeared while TA1 was being used. So again: not a perfect all-clear, but definitely reassuring.

Sources I drew on:

Romani L, et al. Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through Toll-like receptor signalling. Blood. 2004.

Giacomini E, et al. Dual effect of thymosin alpha1 on human monocyte-derived dendritic cells stimulated with viral and bacterial toll-like receptor agonists. Expert Opin Biol Ther. 2015.

Romani L, et al. Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance. Blood. 2006.

Giacomini E, et al. Thymosin-alpha1 expands deficient IL-10-producing regulatory B cell subsets in relapsing-remitting multiple sclerosis patients. Multiple Sclerosis. 2018.

Renga G, et al. Thymosin alpha1 protects from CTLA-4 intestinal immunopathology. Life Science Alliance. 2020.

Dinetz E, et al. Comprehensive review of the safety and efficacy of thymosin alpha 1 in human clinical trials. Altern Ther Health Med. 2024.

TA-1 has me genuinely intrigued, and I want to run it on myself this Fall. The thinking is that you dose through Oct/Nov so that illness is dodged from Dec through Apr. A doctor mentioned wanting to try that experiment, so I decided to begin with myself. The snag is that none of the suppliers carrying it have shown me a COA

 

[Katiushka]

JP.MOTM said:

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

Racin4t said:

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

This! That particular risk is why TA1 holds very little appeal for me. I have read a little about it, mind you. It is not ruled out entirely - I simply need to study TA1 a great deal more before starting my own research.

Calm Logic said:

For autoimmune conditions such as RA, the first candidate that springs to mind for experimental use is TA1, though it may be too experimental:



View attachment 8708



Thymosin Alpha 1: View Uses, Side Effects and Medicines - MrMed



Belonging to the synthetic thymic peptides, Thymosin Alpha 1 is an anticancer medicine. In chronic hepatitis B and C it is given as an adjuvant therapy.

Image unavailable


www.mrmed.in

This medicine may stimulate the immune system, which could exacerbate autoimmune diseases such as multiple sclerosis, lupus, or rheumatoid arthritis.

Click to expand...

MOGAD makes it look even shakier:

Gemini said:


Because MOGAD is an antibody-mediated attack on the myelin sheath, "immune boosting" agents—often claimed to be the benefit of peptides like Thymosin Alpha-1—could theoretically increase the production of the very autoantibodies driving the disease.

Click to expand...

A little reading on TA 1 was enough to put me off it pretty quickly, this risk being the reason. Perhaps the upside ends up justifying the danger, but far more digging is needed on my part before any research process with TA1 gets under way.

There is nothing unreasonable about either worry, and I had that same question myself: would this simply make autoimmune problems worse? To my mind it is a fascinating subject and one I have gone into quite deeply. Plenty of the writing amounts to speculation about mechanisms, or straightforward observations, yet the picture becomes more comforting the further into it you go (though it is not a completely settled matter).

Parts of the immune system do get "boosted" by TA1 in the published work. Vaccine antibody responses and Th1 immunity can both be strengthened, which makes the worry about autoimmunity-linked antibodies entirely legitimate. A fair question. What the evidence indicates, though, is that this does not happen - and there is considerably more evidence here than I had assumed.

A simple immune "booster" is not what TA1 looks like. It behaves far more like a regulator. Context decides which parts of immunity get turned up or down, and interestingly both can happen simultaneously. On the mechanism side, the selfsame TLR9 signal that drives antiviral and anti-tumour immunity is also capable of switching on tolerance pathways through IDO, IL-10 and regulatory T-cells. Plainly put, the accelerator is not the only pedal it presses. It also looks like it helps reset the immune system, quietening attacks that ought not to occur.

Nowhere is that clearer than in the multiple sclerosis work. MS involves B-cells, yet "B-cells" are not one uniform population. Some of them help hold autoimmune inflammation on; others are regulatory and act to calm the immune response. Those calming regulatory B-cells look too few in relapsing-remitting MS. When TA1 was added to immune cells from such patients, the underactive regulatory population expanded and calming signals such as IL-10 and IL-35 rose, while "bad" inflammatory signals including IFN-gamma and IL-17 fell. TA1 also reduced the capacity of B-cells to turn into IgM- or IgG-secreting cells, which points away from antibody production rather than towards it. What TA1 was doing was restoring balance, bringing the "bad" response down and the "good" response up at once.

An autoimmune-like model of gut inflammation displays the same broad pattern. Colitis triggered by cancer immunotherapy in mice was held off by TA1, which switched on an IDO-dependent tolerance pathway and protected the gut. Taken with the mechanism, the MS findings and the colitis model, everything therefore points at regulation and recalibration rather than an autoimmune boost.

Calling it "proven safe in every autoimmune condition" would be overstating things, since no such study exists. Nobody has run a clinical trial among people with established autoimmune disease that follows real-world flares over time. Still, the data available is genuinely solid and, in my opinion, more persuasive than the particular items discussed so far.

Nor is TA1 some brand-new compound assessed only on the studies just mentioned. Under the name Zadaxin/thymalfasin it has held approvals in many countries for years, applied to hepatitis B, immune deficiency and improved vaccine response. Routine use in places such as China, notably in intensive-care and oncology settings, goes back years as well.

Two distinct kinds of safety data follow from that. The first is the formal trial data, covering over 11,000 people in more than 30 trials. The second is the much larger real-world clinical experience, in which over 600,000 patients have reportedly been treated since approval. Being less controlled than a trial, that second group cannot establish the absence of rare or subtle risks. It remains informative all the same, since a common tendency for TA1 to produce obvious autoimmune flares ought to have surfaced after that much routine use. It has not. Nor was I able to find any data in which an autoimmune response appeared while TA1 was being used. So again: not a perfect all-clear, but definitely reassuring.

Sources I drew on:

Romani L, et al. Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through Toll-like receptor signalling. Blood. 2004.

Giacomini E, et al. Dual effect of thymosin alpha1 on human monocyte-derived dendritic cells stimulated with viral and bacterial toll-like receptor agonists. Expert Opin Biol Ther. 2015.

Romani L, et al. Thymosin alpha1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance. Blood. 2006.

Giacomini E, et al. Thymosin-alpha1 expands deficient IL-10-producing regulatory B cell subsets in relapsing-remitting multiple sclerosis patients. Multiple Sclerosis. 2018.

Renga G, et al. Thymosin alpha1 protects from CTLA-4 intestinal immunopathology. Life Science Alliance. 2020.

Dinetz E, et al. Comprehensive review of the safety and efficacy of thymosin alpha 1 in human clinical trials. Altern Ther Health Med. 2024.

i googled china oncology usage of Zadaxin/thymalfasin just now and came away impressed! more reading on TA-1 is next on my list