I working through a couple kits of PGB 26mg, I see lots of interest on other groups that will be testing the 100mg Uther kits and if I decide to order, I will run it through PTDS before I use it. So confident there will be quite a few independent tests in a month or two.
Then we can start asking for 200mg kits!
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Fantastic news! I love when someone else will do the work for me 
Run it through ‘Ptds’?
PTDS is a testing group. They mostly focus on testing of degradation of peptides, and tend to test more than GLP1s. They’ve also tested Indian pharma products. To be considered active, you have to contribute financially to at least 1 test every 4 months
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Thx for that @qBx123Yk
I only know what I learned from watching the Janoshik YouTube. He made it sound like degradation is nothing to worry about… I had the feeling he quietly giggles at the thought of storing them in a freezer.
Having said that, can I assume if people are paying to test, it is in fact ‘a thing’?
Fwiw, mine are in a thermos in the freezer
When talking about degradation, we are mostly talking after reconstitution. Like how long does reconstituted tirzepatide stay potent without significant degradation. Or how much potency loss does retatrutide suffer after freezing the reconstituted solution and thawing it back.
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Some useful information for veterans and neophytes.
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This is mostly fine, except I would not recommend khole for newbies. Khole has successfully been used by scammers to take people’s money (via her vendor “interviews” ).
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Thanks for posting this in response to the article I posted. I thought this was something that required a prescription.
Has your father tried it?
It’s available via grey market sources. The prescription version is extremely expensive. I have not yet obtained the peptide yet. It’s on my to do list.
Degradation testing for reconstituted thymosine alpha 1 is finally underway for up to a 30 days. Should find out soon how stable that peptide is.
I’m not sure what that will imply for Zadaxin. Probably nothing, since they are probably using another formulation (could different buffering agent, solution, temp stability, etc) for it. Similar to tesamorelin and Egrifta.
@John_Hemming You’re all about the mitochondria but I’ve not seen you speak much about SS-31/ Elamipretide.
Have you got any thoughts on it? Have you tried it or are you thinking of trying it?
What does it do?
My view on short proteins is that if I need them my protocol in the round should provide them. My priority if anything is selective mitophagy.
SS-31 aka Elamipretide
“Mitochondria are cellular hubs integral for metabolism, signaling, and survival. Mitochondrial dysfunction is centrally involved in the aging process and an expansive array of disease states. Elamipretide is a novel mitochondria-targeting peptide that is under investigation for treating several disorders related to mitochondrial dysfunction. This review summarizes recent data that expand our understanding of the mechanism of action (MOA) of elamipretide. Elamipretide is a potential first-in-class therapeutic that targets the inner mitochondrial membrane. Despite initial descriptions of elamipretide’s MOA involving reactive oxygen species scavenging, the last ten years have provided a significant expansion of how this peptide influences mitochondrial bioenergetics. The cardiolipin binding properties of elamipretide have been corroborated by different investigative teams with new findings about the consequences of elamipretide-cardiolipin interactions. In particular, new studies have shown elamipretide-mediated modulation of mitochondrial membrane electrostatic potentials and assembly of cardiolipin-dependent proteins that are centrally involved in mitochondrial physiology. These effects contribute to elamipretide’s ability to improve mitochondrial function, structure, and bioenergetics. In animal studies, elamipretide-mediated amelioration of organ dysfunction has been observed in models of cardiac and skeletal muscle myopathies as well as ocular pathologies. A number of clinical trials with elamipretide have been recently completed, and a summary of the results focusing on Barth syndrome, primary mitochondrial myopathy, and age-related macular degeneration, is also provided herein. Elamipretide continues to show promise as a potential therapy for mitochondrial disorders. New basic science advances have improved understanding of elamipretide’s MOA, enabling a better understanding of the molecular consequences of elamipretide-cardiolipin interactions.”
"By localizing to the IMM and associating with CL, elamipretide improves assembly of ETS complexes into respiratory supercomplexes and as a result, respiratory efficiency [55,56], thereby improving bioenergetics, reducing ROS production, and improving mitochondrial morphology in dysfunctional mitochondria.
Recent studies show that elamipretide interacts with proteins that are associated with the IMM, interact with CL, and are involved in oxidative phosphorylation. Elamipretide has also been recently shown to modulate mitochondrial membrane surface electrostatic properties, which may underpin its modulation of electron carrier properties and its ability to interact with ANT and ETS supercomplexes. These changes of membrane physical properties can themselves elicit improvements in overall mitochondrial function that are independent of alterations in constituent protein structure and function, and therefore reinforces elaimpretide’s ability to target mitochondrial health at multiple levels within the organelle itself.
Preclinical models of disease also show that elamipretide improves mitochondrial structure and function, enhances mitochondrial bioenergetics, and is associated with improvements in physiologic functions, such as cardiac and skeletal muscle performance, as well as improvements in age-related retinal dysfunction. Clinical trials also support elamipretide’s efficacy in mitochondrial-related diseases (eg, BTHS, mitochondrial myopathy, and AMD), although the results have been mixed, which may be due to a variety of factors including the difficulty in identifying appropriate endpoints, small patient populations, and inadequate treatment duration."
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This is exactly how the gray market community does it for the GLP 1 peptides.
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Playing around with the new Google Gemini video generator. How SS-31 works:
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Is this free to use?
“Mitochondrial dysfunction contributes to impaired myocardial energetics and performance in heart failure with preserved ejection fraction (HFpEF). Elamipretide (Ela) enhances mitochondrial bioenergetics in preclinical models, yet its relevance in HFpEF remains unclear. This study examined the effects of Ela on cardiac mitochondrial function, structure, and cardiovascular performance in a rodent HFpEF model…
…Ela modestly improved complex I and II respiration, whereas mitochondrial ultrastructure, cardiolipin composition, and tafazzin expression were unchanged. Diastolic dysfunction persisted, reflected by unchanged E/é, ventricular stiffness factor β, and titin phosphorylation. Compared to untreated HFpEF, systolic performance showed a mild decline, with small reductions in LV ejection fraction and end-systolic elastance. Accordingly, cardiac remodeling, including hypertrophy, fibrosis, and inflammatory activation, remained unaltered. Vascular stiffness slightly increased, while carotid reactivity and morphology were preserved. In conclusion, despite enhanced mitochondrial respiration following Ela treatment, no functional or structural benefits were observed in experimental HFpEF, suggesting limited therapeutic efficacy once HFpEF is established.”
Mitochondrial Targeting by Elamipretide Improves Myocardial Bioenergetics Without Translating into Functional Benefits in HFpEF Mitochondrial Targeting by Elamipretide Improves Myocardial Bioenergetics Without Translating into Functional Benefits in HFpEF - PMC
“SS-31 could effectively improve post-CA brain injury, in which the mechanism was potentially related to the inhibition of microglial ferroptosis and polarization through the regulation of Sesn2 signaling pathway.”
SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization - PMC
“Excessive production of reactive oxygen species during in vitro embryo production can impair mitochondrial defense mechanisms, thereby reducing embryonic developmental competence. We investigated the effects of elamipretide, a mitochondrial-targeted antioxidant, on porcine oocyte maturation and subsequent embryo development in vitro. The results demonstrated that SS-31 enhanced the antioxidative capacity of oocytes by reducing intracellular reactive oxygen species levels, increasing glutathione content, improving mitochondrial membrane potential, and reducing DNA fragmentation, resulting in higher rates of oocyte maturation and blastocyst formation.”
Mitochondrial-Targeted Protective Potential of Elamipretide for the In Vitro Production of Porcine Embryos Mitochondrial-Targeted Protective Potential of Elamipretide for the In Vitro Production of Porcine Embryos - PMC
“This study found that PINK1/Parkin-mediated mitophagy was activated during tendon ossification, and the regulation of mitophagy could impact the osteogenesis of injured tendon-derived progenitor cells (inTPCs). Loss of Slc25a4 inhibited tendon ossification by downregulating the excessive mitophagy. Elamipretide, a targeted drug for ANT1, showed significant efficacy in treating Heterotopic ossification (HO).”
Targeting ANT1 to regulate PINK1/Parkin-mediated mitophagy is an effective treatment of trauma-induced tendon heterotopic ossification Targeting ANT1 to regulate PINK1/Parkin-mediated mitophagy is an effective treatment of trauma-induced tendon heterotopic ossification - PMC
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If anybody knows a legit source for 100mg/vial × 10 vials for max 180 USD, please let me know.
Not a chance. Cheapest I’ve seen is 50-mg vials x 10 for $320 plus shipping. Many online sources.
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I saw 50mg kit for 225, which looked pretty good from what I was told. Out of stock now, unfortunately.
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