My Favorite
Peptides
A deep-dive into the compounds I find most compelling — from metabolic powerhouses to full-body regeneration stacks. These are personal notes, not medical advice.
Tirzepatide
(Tirz)
Tirzepatide is, in my opinion, the most potent metabolic agent available right now. It's a dual GIP/GLP-1 receptor agonist — meaning it hits two hunger and insulin pathways simultaneously — and the results in clinical trials have been genuinely staggering. The SURMOUNT trials showed average weight loss exceeding 20–22% of body weight over 72 weeks, which puts it ahead of anything else in its class.
What sets Tirz apart for me is the psychological dimension of appetite suppression. This isn't just about slowing gastric emptying. GIP receptor agonism appears to modulate reward circuitry and the hedonic drive to eat — that constant background noise of food-related thoughts that makes dieting exhausting gets quieter. Dramatically quieter.
Blood glucose regulation is exceptional, insulin sensitivity improves meaningfully, and the reduction in visceral adipose tissue is arguably its most important long-term benefit. For anyone with metabolic syndrome tendencies, Tirz addresses root causes, not just symptoms.
Retatrutide
(Reta)
Triple Receptor Action
Reta adds glucagon receptor agonism to the GIP/GLP-1 dual action, creating a genuinely novel triple-hormone approach. Glucagon activation drives thermogenesis and directly increases energy expenditure — a mechanism Tirzepatide lacks entirely.
Lipid & Liver Benefits
The glucagon component has meaningful hepatic effects — driving fat oxidation in the liver and making Reta particularly interesting for fatty liver disease. Lipid panels improve significantly, often more than with GLP-1 monotherapy.
Energy Expenditure
Where Tirz primarily reduces intake, Reta also increases the output side of the equation. This thermogenic boost is measurable and likely explains why Phase 2 trial results (up to ~24% weight loss at 48 weeks) look competitive with Tirz.
Retatrutide is the next evolution — a GIP/GLP-1/glucagon tri-agonist developed by Eli Lilly. The addition of glucagon receptor agonism is what makes it genuinely different from Tirzepatide rather than merely "more of the same."
The appetite suppression on Reta is strong, but it has a slightly different character than Tirz. The psychological food-noise reduction is less pronounced, but the metabolic upregulation compensates — your body is burning more, not just consuming less.
Reta also shows interesting preliminary data around cardiovascular protection and potentially liver disease, making it potentially useful for a broader range of metabolic conditions beyond simple weight management.
The Tirz + Reta
Stack
This is where it gets interesting personally. Tirz and Reta each bring something the other doesn't — and combining them at thoughtful doses creates a more balanced metabolic effect than going heavy on either compound alone.
The Core Philosophy
Tirzepatide is the psychological powerhouse — it silences the hedonic drive to eat, the food obsession, the reward-seeking behavior that undermines every diet. That GIP receptor action on the brain is genuinely remarkable. But Tirzepatide doesn't meaningfully increase energy expenditure. Retatrutide fills that gap perfectly. By adding Reta's glucagon-driven thermogenesis, you're simultaneously reducing input AND increasing output — and doing it with lower doses of each compound, which generally means a cleaner side-effect profile.
Why This Combination Works
The psychological hunger suppression from Tirz is its strongest differentiator — it's noticeably more powerful than anything Reta provides on that dimension. But by using a moderate dose of Tirz rather than maxing it out, you get 80% of that benefit while leaving room to add Reta for the glucagon component.
Reta's thermogenic effect means the body isn't just consuming fewer calories — it's running hotter, burning more fat as fuel, and improving hepatic lipid metabolism. The two compounds address completely different mechanisms, which is why they can be genuinely synergistic rather than redundant.
What Each Brings
Psychological food-noise reduction · Hedonic appetite suppression · GIP-mediated reward circuit modulation · Strong glucose control
Glucagon-driven thermogenesis · Increased energy expenditure · Hepatic fat oxidation · Lipid panel improvement
The KLOW
Stack
KLOW is a four-peptide blend that I think of as a comprehensive tissue repair and anti-inflammatory protocol. It combines BPC-157, TB-500, GHK-Cu, and KPV into a single vial — and the reason this combination is intelligent is that each compound attacks a different part of the healing cascade.
The difference from the older GLOW stack (BPC-157 + TB-500 + GHK-Cu) is the addition of KPV. That addition matters more than it might seem: healing doesn't work efficiently when systemic inflammation is elevated. KPV removes that biochemical roadblock, letting the repair peptides actually do their jobs.
GHK-Cu — 50mg
A copper-binding tripeptide naturally present in human plasma. Stimulates collagen and elastin synthesis, activates antioxidant gene expression, and drives tissue remodeling. Works during the remodeling phase to ensure tissue heals with quality, not just speed. Also notable for skin, hair follicle, and neurological support.
BPC-157 — 10mg
Body Protection Compound, derived from gastric juice. Accelerates tendon, ligament, and muscle healing via VEGF and nitric oxide pathway modulation. Also has robust gut lining repair effects and neuroprotective properties. Often called "Wolverine in a vial" for good reason — it's the repair catalyst.
TB-500 — 10mg
Synthetic Thymosin Beta-4. The heavy hitter for tissues with poor blood supply — tendons, ligaments, fascia, scar tissue, chronic injuries. Drives angiogenesis (new vessel formation), improves cell migration, reduces fibrosis, and restores tissue flexibility. Essential for stubborn or deep injuries.
KPV — 10mg
A tripeptide fragment of alpha-MSH. The inflammation controller — it inhibits NF-κB and MAPK pathways, the master switches for inflammatory signaling. Stabilizes mast cells, reduces histamine response, and is particularly powerful for gut-related inflammation. Without KPV, elevated inflammation limits what BPC-157 and TB-500 can accomplish.
The Layered Healing Sequence
When these peptides work together, a clear sequence emerges: KPV and GHK-Cu first control the inflammatory environment and protect against oxidative stress. Then TB-500 improves blood flow and cell access to the damaged area. BPC-157 directs the active repair. Finally, GHK-Cu drives the remodeling phase to ensure collagen quality and long-term durability. Users consistently also report improvements in sleep quality, mood, libido, and stress resilience — which makes sense given the systemic inflammatory load being reduced.
NMN & the
NAD+ Pathway
Nicotinamide Mononucleotide (NMN) is a precursor to NAD+ (nicotinamide adenine dinucleotide), one of the most critical coenzymes in cellular biology. NAD+ levels decline significantly with age — often dropping 50% or more between young adulthood and midlife — and this decline is implicated in virtually every hallmark of aging.
NMN is efficiently converted to NAD+ in cells and has emerged as one of the most practical ways to restore declining NAD+ levels. Unlike direct NAD+ supplementation, NMN crosses cell membranes effectively and the conversion is rapid. David Sinclair's lab at Harvard has published extensively on NAD+ restoration and its effects on sirtuin activation, DNA repair, and mitochondrial function.
What makes the NAD+ pathway particularly compelling is its role as a master regulator — it doesn't do one thing, it's involved in hundreds of enzymatic reactions across energy metabolism, inflammation response, and genetic stability.
Mitochondrial Function
NAD+ is essential for the electron transport chain. Restoring NAD+ levels directly improves cellular energy production and mitochondrial efficiency — measurable as improved physical endurance and reduced fatigue.
Sirtuin Activation
Sirtuins (SIRT1-7) are NAD+-dependent enzymes involved in DNA repair, inflammation control, and metabolic regulation. SIRT1 in particular is often called a "longevity gene" — and NMN is one of the most direct ways to fuel it.
DNA Repair & Inflammation
PARP enzymes that repair DNA damage are NAD+-dependent. With adequate NAD+, cells can respond to DNA damage efficiently. Reduced NAD+ is associated with the chronic low-grade inflammation often called "inflammaging."
Other Compelling
Compounds
These are the other peptides and compounds I find genuinely backed by solid science — not hype. Each has meaningful preclinical or clinical data and addresses something the earlier sections don't cover.
MOTS-c
MOTS-c is encoded within mitochondrial DNA — a completely different origin than most peptides. It's been called a "mitochondrial hormone" and acts as a metabolic regulator that travels to the nucleus and activates AMPK, the energy-sensing master switch.
Research shows it improves insulin sensitivity, reduces fat accumulation, and enhances exercise capacity. A remarkable 2021 study in Nature Communications found MOTS-c levels in centenarians were significantly higher than in younger adults — and supplementation in older mice reversed age-related metabolic decline. The exercise-mimetic effects are real and measurable.
5-Amino-1MQ
5-Amino-1MQ inhibits NNMT (Nicotinamide N-methyltransferase), an enzyme highly expressed in adipose tissue that consumes methyl groups and reduces NAD+ availability specifically in fat cells. By blocking NNMT, 5-Amino-1MQ effectively raises NAD+ in adipocytes and activates SIRT1 locally.
The result is increased fat cell metabolism and a reduction in adipogenesis — the creation of new fat cells. Studies show significant reduction in fat mass without muscle loss. It pairs interestingly with NMN since they both elevate NAD+ but through entirely different mechanisms and in different tissue compartments.
Epithalon
Epithalon (Epitalon) is a tetrapeptide — Ala-Glu-Asp-Gly — developed by Vladimir Khavinson's group in Russia, with decades of research behind it. Its primary mechanism is activation of telomerase, the enzyme that lengthens telomeres. Telomere shortening is one of the core hallmarks of aging.
Khavinson's studies with a peptide bioregulator approach showed measurable telomere lengthening, improved melatonin secretion, enhanced antioxidant capacity, and in animal studies, meaningful lifespan extension. The human data is less robust by Western standards but the mechanistic rationale is solid and the safety profile appears excellent.
Selank / Semax
These Russian-developed peptides are among the most compelling nootropics with actual mechanistic data. Selank is an anxiolytic and BDNF-enhancing peptide that reduces anxiety without the sedation or dependence risk of benzodiazepines. It modulates GABA and serotonin systems and has been studied in anxiety disorders and immune function.
Semax is an ACTH-derived peptide that powerfully upregulates BDNF (brain-derived neurotrophic factor) — critical for neuroplasticity, learning, and mood. Used clinically in Russia for stroke recovery and cognitive decline. The cognitive sharpening effects have good mechanistic backing and a long history of use.
Thymosin Alpha-1
TA-1 is an FDA-approved compound (Thymalfasin/Zadaxin) in many countries for immune dysfunction. It's a naturally occurring peptide produced by the thymus that declines with age. It modulates T-cell function, enhances NK cell activity, and has been studied in cancer immunotherapy, chronic viral infections, and as a general immune optimizer.
For longevity purposes, thymic involution — the shrinking of the thymus with age — is one of the key drivers of immune senescence. TA-1 partially compensates for this decline and has an excellent long-term safety record given its clinical use across multiple countries since the 1980s.
Tesamorelin
Tesamorelin is an FDA-approved GHRH (growth hormone releasing hormone) analogue. Unlike direct GH injection, it works through your own pituitary — resulting in pulsatile, physiological GH release rather than pharmacological flooding. This matters for safety and long-term use.
The primary studied benefit is visceral fat reduction, particularly in HIV-associated lipodystrophy, but its metabolic effects extend to improved lean body mass, IGF-1 elevation, better sleep quality, and potentially cognitive benefits. It's one of the most evidence-backed GH-axis interventions with a controlled release mechanism that avoids many of the issues with exogenous GH.
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The information on this page represents personal research notes and opinions. Nothing here constitutes medical advice, diagnosis, or treatment recommendation. All peptides and compounds discussed are for research use only in many jurisdictions. Always consult a qualified physician before using any of these compounds. Dosing, interactions, and individual responses vary significantly.