I know this is all over the place and feel free to dump links - I'm looking for YOUR stack and protocol and I will adjust accordingly. I just received a mini-shipment of excess from a colleague to have my go, before I buy retail or reseller. 2x CJC+IPA 5mg/5mg (research tells me 200mcg a night?) 2xMOTS-C 10mg (2mg daily in the morning, 5x a week?) 2x Reta 10mg (I'm coming off Tirzepatide @ 7.5mg. It's been working without going up in dose, hunger is at bay, weight loss is flat now, but feel great. I just want to try Reta for a couple months. Thought 2mg a week and titrate up?) Background: I am 3 weeks off TRT (reasons) and hope to get back on it soon. The effects are definitely noticeable though, brain fog, loss of energy, just feel like I can give 100% in my workouts, but I'm realistically at 60%.

❇️ Most peptides are synthesized elsewhere and shipped to their targets — MOTS-c is different. It's encoded directly in mitochondrial DNA, making it one of the first mitochondria-derived peptides ever identified. That origin story alone makes it worth paying close attention to, but the research behind it makes the case even stronger. ❇️ First described in 2015 by Lee et al. at USC, MOTS-c has quickly become one of the more exciting compounds in metabolic and longevity research. If you've been sleeping on it, now's a good time to catch up. 🧬 The Science: Nerding out! MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA Type-c) is a 16-amino acid peptide encoded in the 12S rRNA region of mitochondrial DNA. When cells sense metabolic stress — things like high glucose, low energy availability, or oxidative load — mitochondria release MOTS-c into the cytoplasm and eventually the bloodstream. 👉🏼 Once circulating, MOTS-c acts on skeletal muscle and metabolic tissues to enhance insulin sensitivity, promote glucose uptake, and shift the cell toward fat oxidation. It does this partly by activating AMPK (AMP-activated protein kinase), the same master metabolic switch targeted by exercise and metformin. Think of it as your cells' built-in "exercise signal" — triggered by stress, optimizing energy use. ✅ More recent work has also shown MOTS-c translocates to the nucleus under stress, where it interacts directly with gene regulatory elements to modulate stress-response pathways. This nuclear activity suggests it plays a broader role in cellular resilience than initially understood. ✅ Research Highlights • Improved insulin sensitivity in mouse models of type 2 diabetes — MOTS-c administration reversed diet-induced insulin resistance and reduced fat accumulation in skeletal muscle (Lee et al., Cell Metabolism, 2015). • Exercise-mimetic effects — circulating MOTS-c levels rise with physical exercise in humans, suggesting it mediates some of the metabolic benefits of training; exogenous MOTS-c reproduced similar effects in sedentary animals.

❇️ If you've been following the metabolic peptide space lately, you've probably seen 5-Amino-1MQ pop up more and more. It's not a traditional peptide — it's a small molecule — but it's earned its place in research circles for one very compelling reason: it targets an enzyme called NNMT, and the downstream effects are seriously interesting. ❇️So What Is NNMT, and Why Does It Matter? NNMT stands for Nicotinamide N-Methyltransferase — an enzyme that methylates nicotinamide (a form of vitamin B3), effectively pulling methyl groups away from the metabolic pool and reducing NAD+ availability. When NNMT is overactive (which it tends to be in obese and insulin-resistant individuals), it acts like a metabolic brake. You get lower NAD+, slower mitochondrial function, and a harder time burning fat. 👉🏼 5-Amino-1MQ blocks NNMT. That's its whole job — and by doing so, it lets NAD+ levels rise naturally. ❇️ What the Research Shows 🔸 Preclinical studies have highlighted some notable effects: ➡ Fat loss without caloric restriction: In mouse models, NNMT inhibition led to significant reductions in body fat, even without changes to diet. The mechanism appears tied to increased energy expenditure at the cellular level. ➡ NAD+ elevation: Higher NAD+ means more fuel for sirtuins (especially SIRT1) and improved mitochondrial efficiency — both linked to longevity and metabolic health. ➡ Muscle preservation: Unlike aggressive caloric deficits that chew through lean mass, NNMT inhibition appears to preferentially target adipose tissue. ➡ Improved insulin sensitivity: Early data suggests better glucose handling, which is particularly relevant for metabolic syndrome research. ❇️How It's Different From NAD+ Precursors: You might be thinking: "Why not just take NMN or NR?" Fair question. Those work by directly adding NAD+ precursors to the system. 5-Amino-1MQ works differently — it removes the enzyme that's draining NAD+ in the first place. Think of it less like adding water to a leaky bucket and more like patching the hole. Some researchers believe this makes it especially relevant for metabolically compromised models where NNMT is chronically upregulated.

❇️ Introduction Most peptides get attention for physical performance — muscle, fat loss, recovery. Selank flips the script. Developed by the Institute of Molecular Genetics in Russia, this heptapeptide analog of tuftsin has been generating serious interest for its dual ability to reduce anxiety and enhance cognitive function — without the sedation or dependency risks associated with traditional anxiolytics. If you're exploring peptides beyond the gym, Selank deserves a closer look. 🧬 The Science Selank (sequence: TKPRPGP) is a synthetic analog of the naturally occurring immunomodulatory peptide tuftsin. Its primary mechanism involves modulating the expression of BDNF (brain-derived neurotrophic factor) and stabilizing enkephalin — endogenous opioid peptides that regulate mood and stress responses. Crucially, Selank doesn't simply suppress anxiety by sedating the CNS; it appears to recalibrate the GABAergic system in a more balanced way than benzodiazepines. Beyond mood, Selank also influences serotonin metabolism and has shown the ability to modulate expression of genes related to immune function, making it one of the few research compounds that bridges neurology and immunology. It has a very short half-life (minutes in plasma), which is why intranasal delivery is the most studied administration route — it allows rapid CNS access via the olfactory pathway. 👉🏼 Animal studies have consistently shown Selank to improve learning, memory consolidation, and attention. These cognitive benefits appear to be distinct from its anxiolytic effects, suggesting multiple independent mechanisms at play. 🔸 Research Highlights • In Russian clinical trials, Selank showed anxiolytic efficacy comparable to medazepam (a benzodiazepine), with significantly fewer side effects and no reported dependency. • A 2008 study found Selank significantly increased BDNF expression in rat hippocampus — a key marker for neuroplasticity and memory formation. • Research published in the Bulletin of Experimental Biology and Medicine found Selank stabilized enkephalin degradation, prolonging natural opioid mood regulation without exogenous opioid activity.

Dosing Protocol Why Most Protocols Online Do Not Make Sense The mouse study used doses that translate to roughly 400 mg per day for humans using allometric scaling. Online you will find recommendations ranging from 150 to 600 micrograms per day (microdosing) up to 50 to 150 mg per day. That is a 2,500x difference between the low end and what the science suggests should work. For a drug to actually do its job, you need enough of it in your bloodstream to block at least 50% of the target enzyme. This is called IC50 coverage. If you are below that threshold, the drug is not doing much. Based on pharmacokinetic analysis using metformin as a structural analog (similar molecular weight, charge, oral bioavailability, and half-life), to achieve 50% NNMT inhibition you need roughly 50 to 100 mg per day. To achieve near-complete inhibition you need 400 to 600 mg per day. Microdoses of 150 to 600 micrograms per day get you roughly 400 times below the threshold needed for 50% inhibition. You cannot outsmart pharmacology. Either you are achieving effective concentration or you are not. There is another reason microdose protocols do not make sense. The enzyme that actually makes NAD+ from nicotinamide is called NAMPT, and NAMPT has 430 times higher affinity for nicotinamide than NNMT does. Under normal conditions, nicotinamide preferentially flows toward NAD+ synthesis anyway. NNMT only becomes a significant drain when it is massively overexpressed. If you want NAD+ support, taking a direct precursor like NMN or using injectable NAD+ makes more sense than taking a microdose of an enzyme inhibitor that does not achieve meaningful tissue concentrations. Why do these smaller protocols exist? Follow the economics. A 10 mg vial at 150 micrograms per day lasts about 66 days. That same vial at 5 mg per day lasts 2 days. The true effective dose never gets tested because it is economically prohibitive outside of funded clinical trials.