Peptides are short chains of amino acids (typically 2 to 50) linked by peptide bonds. Functioning as biological messengers, they signal cells to perform vital functions such as producing collagen, regulating hormones, and repairing tissue. Smaller and more easily absorbed than full-sized proteins, peptides are the essential "instruction manuals" that coordinate many of the body's most critical physiological processes.
The foundation of any "recover better" stack. BPC-157 and TB-500 are the cornerstone duo; the rest extend or specialize the same machinery.
The Swiss army knife of healing peptides. Gut, joints, tendons, inflammation. One-off cycles when something needs healing.
BPC-157 is a synthetic peptide derived from a protein found in stomach acid. It calms gut inflammation (helps with reflux, IBS, gastritis), speeds tendon and ligament healing, reduces systemic inflammation, and shows mild neuroprotective effects in the literature. One of the most versatile soft-tissue tools available.
Soft-tissue healing peptide. Tells injured tissue to rebuild faster. One-off course alongside BPC for injury repair.
TB-500 is a synthetic version of thymosin beta-4, a peptide the body uses for cell migration during tissue repair. Injected, it speeds recovery from muscle, tendon, and ligament injuries, improves blood flow to damaged tissue, and produces a systemic background-healing effect that's useful even without a specific injury.
A short 7-residue active fragment of TB-500 — same actin/migration signaling, smaller molecule, faster onset.
The full 43-residue parent protein of TB-500 — broadest regenerative signaling, but harder to source and overkill for most users.
Which TB to take
All three signal the same actin/cell-migration repair pathway. They differ in molecule size, half-life, cost, and how systemic the effect is.
The Wolverine Stack uses standard TB-500 (the 17-residue active fragment), paired with BPC-157. That's the default. Start there.
The body's "architectural reset button." A copper-bound peptide that signals the system to tighten skin, regrow hair, and repair soft tissue by mimicking the high-speed regenerative chemistry of youth.
GHK-Cu is a naturally occurring copper complex found in human plasma that acts as a primary survival and repair signal. While abundant in our teens, levels drop by over 60% by age 60, slowing the ability to bounce back from injury and aging. Injecting GHK-Cu essentially "tricks" the body into returning to a high-performance regenerative state. It is a multi-system remodeling agent that works far beyond the surface:
Peptides that turn down the volume on inflammation — useful for gut issues, skin conditions, chronic infections.
KPV is a potent anti-inflammatory peptide. It specializes in shutting down the inflammatory fire and regulating the immune system.
KPV works by entering the cell and interacting directly with NF-κB, which is essentially the "master switch" for inflammation in your body. It stops the production of pro-inflammatory cytokines.
Why add KPV to your stack?
If you have an injury that feels "hot," "throbbing," or "angry," KPV is the missing piece. While BPC and TB-500 help the structure heal, they sometimes struggle if the "inflammatory storm" in that area is too high. KPV clears the path.
LL-37 is a potent, naturally occurring antimicrobial peptide that serves as the "heavy artillery" for your innate immune system.
It works by physically puncturing the cell walls of harmful bacteria, fungi, and viruses, while simultaneously dissolving the protective biofilms that chronic pathogens use to hide from your white blood cells. A healthy optimizer would run a short, two-week cycle twice a year to perform a "biological deep clean" — pruning the gut microbiome of pro-inflammatory bacteria and clearing out any dormant, low-grade infections that may be subtly draining the nervous system. This "pulse" approach ensures your internal environment remains pristine and your immune system stays sharp without the risk of over-stimulation or chronic inflammation associated with long-term use.
A specialized "nervous system shield" — modified from the protein that builds red blood cells, focused entirely on repair.
ARA-290 targets the Innate Repair Receptor, a "master switch" that usually only turns on when the body detects significant tissue distress or nerve damage. It's an 11-amino-acid peptide that provides the healing and protective benefits of Erythropoietin (EPO) without the dangerous side effect of thickening the blood. Think of it as a "calming signal" designed specifically for your nerves and internal organs.
Why a normal person would take it
For a healthy optimizer, ARA-290 is the ultimate tool for Autonomic Nervous System (ANS) recovery.
The bottom line: a normal person uses ARA-290 for 4 weeks to "re-wire" a stressed nervous system, silence systemic inflammation, and restore a high-performance Heart Rate Variability.
These push your pituitary to release its own GH in pulses. Mix a GHRH (CJC, Tesa, Sermorelin) with a GHRP (Ipa, Hexarelin, GHRP-2/6) for the synergistic effect — neither does much alone.
Selective GHRP that triggers a clean GH pulse without spiking cortisol, prolactin, or hunger.
Ipamorelin tells your pituitary to release a pulse of your own growth hormone by mimicking ghrelin at the GH-secretagogue receptor. What made it the community favourite is its selectivity: older GHRPs also dragged up cortisol (stress) and prolactin and switched on hunger, whereas Ipamorelin does almost none of that. You get the deeper sleep, faster recovery, and slow body-composition improvement of a GH bump without the side baggage. It's the "clean" half of the standard GH stack and the one most people start with.
Short-acting GHRH analog — the GHRH half of the standard GHRP+GHRH stack. Restores natural pulse architecture.
CJC-1295 No DAC (also sold as Mod-GRF 1-29) is a stabilised copy of the natural signal your hypothalamus sends to tell the pituitary "release GH now." On its own it does little — its job is to amplify the pulse that a GHRP like Ipamorelin triggers. Think of the GHRP as flooring the accelerator and the GHRH as widening the road: together the pulse is several times bigger than either makes alone. "No DAC" means it clears in about half an hour, producing a sharp, natural-shaped pulse rather than a flat all-day elevation — which is why it's the preferred GHRH for anyone who wants to keep their own rhythm intact.
Long-acting GHRH analog (albumin-bound) that elevates GH baseline for ~6 days per dose.
This is the same GHRH signal as No-DAC, but with a "Drug Affinity Complex" that binds it to albumin in your blood so it lingers for days instead of minutes. The appeal is convenience — one or two shots a week instead of daily — plus a steady lift in GH and IGF-1. The trade-off is that it replaces your body's natural pulsing rhythm with a constant low "bleed" of GH, which is less physiologic and can dull your own pulse generator over time. People who want to do it "by the book" pick No-DAC; DAC is the choice when sticking to a simple schedule matters more than mimicking nature.
Stabilized GHRH analog (Egrifta) — FDA-approved for visceral fat reduction in HIV lipodystrophy.
Tesamorelin is the most clinically proven member of the GHRH family — an actual approved drug (Egrifta) with real trial data, originally for shrinking the deep visceral fat that builds up in HIV patients on older medications. That visceral-fat effect is exactly what makes it interesting to everyone else: it's one of the few peptides shown to target the dangerous fat packed around your organs rather than just the soft fat under the skin. It also raises IGF-1 and has shown cognitive signals in mild-cognitive-impairment trials. Stronger and far better documented than Sermorelin, it's the GHRH of choice when fat loss is the real goal.
GHRH(1-29) — the original, gentler GHRH research peptide. Milder than Tesamorelin.
Sermorelin is the original GHRH fragment — just the first 29 amino acids of natural growth-hormone-releasing hormone, the minimum needed to do the job. It's the gentlest, most physiologic option in the family: it nudges your pituitary rather than hammering it, which makes it a popular entry point for people who mainly want better sleep and recovery without pushing GH hard. The flip side of that gentleness is a very short half-life and milder effects than Tesamorelin, so it's best understood as the easy-going starter GHRH.
Most potent of the classic GHRPs — strong GH pulse plus direct cardiac/CD36 effects.
Hexarelin is the hardest-hitting of the old-school GHRPs — it produces the biggest single GH pulse of the group and has its own direct effects on heart tissue (via the CD36 receptor) that the others don't. The catch is rapid desensitisation: within a few weeks the receptor stops responding, so it has to be pulsed in short bursts rather than run continuously. It's a specialist tool — reach for it when you want a strong, short GH kick or are specifically interested in its cardioprotective signalling, not as a daily driver.
Older ghrelin-receptor agonist — strong GH release with mild appetite stimulation and some cortisol.
GHRP-2 is a previous-generation GH secretagogue: it reliably fires off a strong GH release, but because it's less selective than Ipamorelin it also bumps cortisol and prolactin slightly and switches on appetite. That appetite effect is mild next to GHRP-6 and can be a feature if you're trying to eat more. It still works perfectly well paired with a GHRH — it's simply been superseded by Ipamorelin for anyone who wants the cleanest possible pulse.
Strongly appetite-stimulating GHRP — used in research when GH and weight gain are both wanted.
GHRP-6 is the GHRP with the most pronounced "ghrelin" effect — it triggers intense hunger within minutes, alongside the GH release. For most optimizers that hunger is an unwanted side effect, but it's exactly why GHRP-6 has a niche: research into appetite, recovery from wasting conditions, and bulking protocols where eating more is the point. If you don't want to be ravenous, pick Ipamorelin; if stimulating appetite is the goal, GHRP-6 is the right tool.
These bypass the pituitary and signal directly at IGF-1 or related anabolic receptors. Stronger and more pointed than the secretagogues, with bigger trade-offs.
Long-acting IGF-1 analog with reduced binding-protein affinity — direct anabolic signaling, much stronger than native IGF-1.
IGF-1 is the hormone that does most of growth hormone's actual muscle-building work — GH largely just tells the liver to make IGF-1. This version (Long R3) is engineered to dodge the binding proteins that normally switch native IGF-1 off within minutes, so it stays active for a day or more and signals far more powerfully. The payoff is strong, direct muscle growth — bigger fibres and more of them — plus fast recovery. The catch is that you've bypassed the body's own safety dial: it pushes growth in everything it reaches, which is why it carries the real risks below.
Mechano Growth Factor — short-acting IGF-1 splice variant that activates local satellite cells right at the injection site.
MGF is the splice variant of IGF-1 your muscles make locally right after they've been mechanically stressed — i.e., after a hard set. It's the "repair this exact spot" signal that wakes up satellite cells (muscle stem cells) to rebuild the fibres you just worked. Injected straight into a trained muscle immediately post-workout, it concentrates that repair signal where you want it. Its half-life is only minutes, so timing is everything — and that brevity is also a safety feature, keeping the effect local instead of systemic.
PEGylated MGF — pegylation extends half-life so it signals systemically, not just locally.
PEG-MGF takes the same mechano-growth-factor signal and attaches a polyethylene-glycol "tail" that shields it from rapid breakdown, stretching its life from minutes to days. The point is to turn a hyper-local, per-workout peptide into one that works body-wide on a once- or twice-weekly schedule. You trade the precise "this muscle, right now" targeting of plain MGF for convenience and systemic reach — useful if you want a general anabolic background signal rather than spot repair.
Modified HGH(176-191) C-terminal fragment studied for fat oxidation without raising GH or IGF-1.
AOD-9604 is the tail end of the growth hormone molecule — the specific fragment responsible for GH's fat-burning action, snipped away from the parts that raise blood sugar or grow tissue. The idea is to get GH's lipolytic (fat-releasing) effect without elevating GH or IGF-1 at all, so none of the growth-related risks apply. In practice the fat-loss effect is modest and the human data is thin, but its very clean safety profile makes it a low-stakes option, and there are early hints of joint and cartilage benefit too.
Myostatin-binding analog studied for muscle hypertrophy by removing the genetic "growth brake."
Your body caps how much muscle you can build using a protein called myostatin — the genetic "brake pedal" on growth. Follistatin binds and neutralises myostatin, effectively lifting your foot off that brake, which in animal models produces dramatic, rapid muscle gain. It's one of the most powerful anabolic concepts in the catalogue — and one of the least proven in humans. The risks below (tendons that can't keep pace with the new muscle, possible heart-muscle overgrowth, very high cost) are exactly why it stays firmly in experimental territory.
Libido, arousal, and natural HPG-axis support. The melanocortins (PT-141, MT1, MT2) work centrally; Kisspeptin and Enclomiphene restore upstream hormone signaling.
Melanocortin agonist that triggers libido and arousal via the central nervous system — works for both sexes.
Most ED drugs (Viagra, Cialis) work on the plumbing — blood flow. PT-141 works on the wiring instead: it activates melanocortin receptors in the brain to switch on desire and arousal at the source. That's why it helps low libido in both men and women, and why it can still work when the problem isn't circulation. It's an approved drug for women (Vyleesi). You take it situationally, around 45 minutes ahead — the nausea and flushing in the risks below are the price of that central activation.
Selective MC1R agonist for skin pigmentation — FDA-approved as Scenesse for porphyria.
Melanotan I tells your skin's pigment cells to make melanin without needing sun, producing a real tan and meaningful UV protection. Because it's selective for the pigment receptor (MC1R) only, it's the cleaner and more predictable of the two melanotans — without the libido and nausea baggage of MT2. It's an actual approved drug (Scenesse) for people with a painful sun-sensitivity disorder. For everyone else the appeal is a protective base tan; get a skin check first, since it darkens existing moles.
Non-selective melanocortin agonist — stronger tanning, plus libido (PT-141 was derived from it).
MT2 hits several melanocortin receptors at once, so you get a faster, deeper tan and a libido kick from the same molecule (PT-141 was literally carved out of it to isolate the libido half). That two-for-one is the appeal — and the catch: hitting multiple receptors means more nausea, blood-pressure swings, spontaneous erections, and a harder push on moles and freckles than MT1. It works well; it's just less tidy. Mole monitoring matters more here than with MT1.
Hypothalamic neuropeptide that triggers GnRH release — restores natural sex-hormone signaling upstream.
Kisspeptin sits at the very top of the hormone chain — it's the signal that tells your brain to kick off the whole cascade that ends in testosterone (or estrogen) production. Instead of replacing a hormone, it restarts your own factory from upstream, which is why it's used to restore natural testosterone, support fertility, and recover the HPG axis after it's been suppressed (e.g., post-cycle). It also lifts libido without the melanocortin side effects of the tanning peptides — a cleaner "switch the system back on" approach.
Hypothalamic nonapeptide for bonding, trust, social anxiety, and pair-bonding research.
Oxytocin is the body's "bonding" hormone — the one that surges with touch, intimacy, and childbirth. Dosed (usually intranasally), people use it to take the edge off social anxiety, deepen feelings of trust and connection, and sometimes to wind down before sleep; it's also studied for PTSD and autism. The effect is real but subtle and short-lived (it clears in minutes), and chronic daily use can backfire by downregulating receptors — so it's best used situationally, not every day.
SERM (not a peptide) that blocks estrogen at the pituitary to raise endogenous LH and testosterone.
Enclomiphene isn't a peptide — it's a selective estrogen receptor modulator (the "active" isomer of clomiphene). It blocks estrogen's feedback signal at the pituitary, fooling the brain into thinking estrogen is low and ramping up LH and FSH — your body's own instructions to make more testosterone. The big draw versus TRT is that it raises testosterone while preserving fertility and testicular function rather than shutting them down. It's a daily oral, popular for natural-T optimisation and for recovering the axis after a cycle.
Russian-origin nootropics dominate this category. The N-acetylated forms are stable upgrades of the originals; P21 is the experimental neurogenic outlier.
Russian ACTH(4-10)-derived heptapeptide studied as a fast-acting nootropic and BDNF elevator.
Semax is a Russian-developed fragment of the ACTH hormone, stripped of its hormonal action so only the brain effects remain. It's a genuine prescription drug there — for stroke recovery, cognitive complaints, and attention — and works largely by raising BDNF, the protein that helps neurons grow and form new connections. Users describe a clean lift in focus, verbal fluency, and mental stamina without the jittery edge of stimulants. It's taken intranasally so it reaches the brain quickly, with effects inside an hour.
Acetylated Semax — longer half-life and stronger BDNF effect than the base molecule.
This is base Semax with an acetyl group added to the front, which shields it from being broken down so fast. You get the same focus-and-BDNF profile, but longer-lasting and somewhat stronger from a single dose — usually the version people settle on once they know they respond well to Semax. If plain Semax wears off too quickly for you, this is the fix.
Russian Tuftsin-derived heptapeptide studied as a non-sedating anxiolytic with GABA-modulating effects.
Selank is the "calm" counterpart to Semax — derived from tuftsin, an immune peptide, and developed in Russia as an anti-anxiety treatment. Its trick is taking the edge off anxiety without sedation, brain fog, or the dependence risk of benzodiazepines, partly by modulating GABA and serotonin and steadying the brain's stress chemistry. People reach for it during high-pressure stretches when they need to stay calm but sharp. It pairs naturally with Semax for "calm focus."
Acetylated Selank — longer half-life, more stable, same anxiolytic profile.
Same logic as N-Acetyl Semax: an acetyl group makes Selank more stable and longer-acting, so one daily intranasal dose carries the calm-focus effect through the day instead of needing re-dosing. Same profile, more convenient — the form most regular Selank users prefer.
Neurogenic peptide derived from the CNTF active region — promotes new neuron growth and reduces tau pathology.
P21 is an experimental compound built from the active piece of CNTF (a nerve growth factor) and engineered to actually cross into the brain. In animal studies it does two striking things: it stimulates the birth of new neurons in the hippocampus (the memory centre) and reduces the tau tangles tied to Alzheimer's. That makes it a real neurogenesis-and-neuroprotection candidate rather than just a focus aid — but human data is essentially nonexistent and it's expensive, so it sits firmly in the experimental tier.
Khavinson tripeptide (Glu-Asp-Arg) that crosses the blood–brain barrier and regulates brain tissue.
Pinealon is one of the short Russian "bioregulator" peptides — a three-amino-acid sequence small enough to slip across the blood–brain barrier and act directly on brain tissue. It's used as a gentle neuroprotectant and cognitive support, especially in older users, with antioxidant effects that help shield neurons from oxidative stress. Think maintenance and protection rather than acute focus — it's run in short courses, often alongside Epitalon in the Khavinson longevity protocols.
Delta Sleep-Inducing Peptide — short nonapeptide isolated from rabbit cerebral blood during sleep.
DSIP was first isolated from the blood of sleeping rabbits — a naturally occurring signal tied to the deep, slow-wave stage of sleep. Rather than knocking you out like a sedative, it seems to nudge sleep architecture toward more restorative deep sleep and helps buffer the body against stress. Response is genuinely variable — some people find it transformative, others feel nothing — so it's worth a short trial to see which camp you fall in. It clears in minutes, but the downstream sleep effect carries through the night.
Thymic peptides for T-cell maturation, antiviral defense, and post-infection recovery. The Khavinson immune trio (Thymalin, Thymogen, Vilon) overlaps but each has a different center of gravity.
Synthetic thymic peptide approved in many countries (Zadaxin) for hepatitis and immune modulation.
Your thymus is the gland that trains immune cells — and it shrinks with age, part of why immunity weakens over time. Thymosin Alpha-1 is a synthetic copy of one of its key signalling peptides; it helps T-cells mature and sharpens the immune system's ability to recognise threats. It's an approved drug in dozens of countries (Zadaxin) for hepatitis and as an immune adjunct, and saw heavy use during COVID. Reach for it when you want to genuinely tune up immune function — frequent infections, post-viral recovery, research-stage cancer adjunct — rather than just react to a cold.
Polypeptide complex extracted from calf thymus — immune-system restoration in aging and infection.
Thymalin is a natural extract of thymus tissue (rather than a single synthetic peptide), used in Russia for decades to restore immune function in older and chronically ill people. It's best known from the long-running Khavinson aging cohorts, where elderly subjects given periodic Thymalin courses showed better immune markers and, strikingly, lower mortality over years of follow-up. Think of it as a periodic "immune reset" run a couple of times a year — and one half of the classic Epitalon + Thymalin longevity pairing.
Synthetic 5-residue active fragment of thymopoietin — pharmaceutical-grade immune modulator.
TP-5 is the five-amino-acid active core of thymopoietin, another thymic hormone — the smallest piece that still carries the immune-signalling effect. It's a pharmaceutical-grade immunomodulator used clinically for conditions where the immune system is misfiring or worn down: rheumatoid arthritis, severe eczema, chronic infection. More targeted and clinical in feel than the broad "tune-up" peptides — reached for when there's a specific immune dysfunction to correct.
Khavinson dipeptide (Glu-Trp) — a lower-dose, intranasal-friendly cousin of Thymalin.
Thymogen is the minimalist of the thymic family — just two amino acids — which makes it potent at tiny doses and convenient as an intranasal spray. It's the practical "cold-and-flu-season" option: a short course to shore up immune defences and cut the number of infections you pick up, as shown in Russian clinical studies. Lower-commitment than injectable Thymalin — the easy way to get thymic immune support through the high-risk months.
Epitalon is the flagship; FOXO4-DRI is the experimental senolytic; Humanin is the emerging mitochondrial-protective option.
Khavinson tetrapeptide (Ala-Glu-Asp-Gly) that activates telomerase and regulates the pineal gland — the flagship longevity peptide.
Epitalon is the headline act of the longevity peptides. Each time a cell divides, the protective caps on its chromosomes (telomeres) get a little shorter — run them out and the cell ages and stops dividing. Epitalon switches on telomerase, the enzyme that rebuilds those caps, and it also restores the pineal gland's melatonin rhythm, which flattens with age. The Russian Khavinson cohorts that ran it periodically over years showed improved aging biomarkers and better sleep. It's taken as a short course once or twice a year, not continuously.
Senolytic peptide that disrupts FOXO4–p53 binding, selectively triggering apoptosis in senescent cells.
As you age, some cells stop dividing but refuse to die — these "zombie" (senescent) cells linger and pump out inflammatory signals that age the tissue around them. FOXO4-DRI is a senolytic: it breaks a protein interaction keeping those zombie cells alive, nudging them to self-destruct while leaving healthy cells untouched. In mice the results were dramatic — restored fur, fitness, and kidney function. In humans it's almost entirely untested, expensive, and used in pulsed protocols, so it remains a research tool rather than a wellness staple.
Mitochondrial-derived 24-residue peptide that protects neurons and improves insulin sensitivity.
Humanin belongs to a small class of peptides encoded not in the cell's main DNA but inside the mitochondria themselves — tiny signals the powerhouses send out to protect the body under stress. It guards neurons against the kind of damage seen in Alzheimer's, improves insulin sensitivity, and protects heart tissue in models; levels naturally decline with age, tracking with rising disease risk. It's an emerging longevity option built around mitochondrial resilience, and pairs conceptually with MOTS-C, the other mitochondrial-derived peptide.
Energy production, fat oxidation, antioxidant defense. Run MOTS-C as a "primer" cycle before tissue-repair stacks to clean up mitochondrial function first.
Mitochondrial-derived 16-residue peptide that activates AMPK — the closest thing to an injectable exercise mimetic.
MOTS-C is a signal your mitochondria release during exercise and metabolic stress — it flips on AMPK, the cellular "energy sensor" that tells the body to burn fuel, take up glucose, and clean house. Injecting it essentially mimics some of the metabolic signalling of a workout: better insulin sensitivity, more fat oxidation, improved endurance. Because it tunes up mitochondrial function at the source, it's an ideal "primer" run a month before a fat-loss or repair stack — clean up the engine before you ask more of it.
Mitochondria-targeted peptide that binds cardiolipin and rescues inner-membrane function.
Where MOTS-C signals the mitochondria, SS-31 physically goes inside them. It binds cardiolipin, a fat that holds the inner membrane's energy-producing machinery in the right shape; in aged or damaged cells that machinery turns sloppy and leaky, and SS-31 restores it. The payoff is more efficient energy production with less oxidative "exhaust" — which is why it's been studied for heart failure, mitochondrial muscle disease, and the age-related decline in muscle power. It's a repair tool for tired cellular engines.
Critical redox coenzyme and sirtuin/PARP substrate — fuel for mitochondrial and DNA-repair machinery.
NAD+ is a coenzyme every cell needs to turn food into energy — and it's also the raw material your longevity enzymes (sirtuins) and DNA-repair crews (PARPs) burn through to do their jobs. Levels fall steeply with age, so those repair and energy systems effectively run short on fuel. Topping it up (injected or IV) aims to restore cellular energy, support DNA repair, and may carry anti-aging benefits. Fair warning: it stings going subQ, and an IV push that's too fast causes flushing and chest pressure — a slow drip is mandatory.
Master intracellular antioxidant tripeptide (Glu-Cys-Gly) — detox, liver, oxidative-stress defense.
Glutathione is the body's "master antioxidant" — the molecule cells use to neutralise free radicals and the liver uses to bind and clear toxins (Phase II detox). You make it naturally, but stores get drained by alcohol, illness, pollution, and age. Supplementing it (IV/IM works best, since oral absorbs poorly) supports detox, lowers oxidative stress, and is popular for skin clarity and hangover recovery. It's the natural antioxidant partner to NAD+'s energy role — hence the common NAD+ + GSH pairing.
Quaternary amine that shuttles fatty acids into mitochondria for energy production.
L-Carnitine isn't a peptide — it's the molecular "ferry" that carries fatty acids across the mitochondrial membrane so they can actually be burned for fuel. Without enough of it, fat can't reach the furnace. Used (injected, for far better uptake than oral) to support fat oxidation, exercise endurance, and recovery; the acetyl form (ALCAR) also crosses into the brain for a cognitive and energy effect. A simple, well-established metabolic helper rather than an exotic peptide.
NNMT inhibitor (small molecule, not a peptide) studied for fat loss and muscle anabolism via methylation balance.
This is a small molecule, not a peptide. It blocks an enzyme called NNMT that runs overactive in fat tissue; when NNMT is high, fat cells store energy lazily and waste the cell's methylation currency. Inhibiting it pushes fat cells to burn more energy and frees up resources for muscle — so in research it shows fat loss alongside a mild anabolic effect. Taken orally, it's an experimental "metabolic flexibility" tool with limited human data so far.
AMPK activator nucleotide analog studied as an "exercise mimetic" for endurance and glucose uptake.
AICAR is a nucleotide analogue that flips on AMPK directly — the same energy-sensing switch MOTS-C hits — fooling the cell into thinking it's just exercised. In animal studies it boosted endurance and glucose uptake without any training, which earned it the "exercise in a bottle" reputation (and a ban in competitive sport). The practical brakes are cost and hypoglycemia risk: effective in theory, but expensive and finicky enough to stay niche.
Pan-ERR agonist studied as "exercise in a pill" — mitochondrial biogenesis and endurance signaling.
SLU-PP-332 activates the ERR family of receptors, which govern how many mitochondria a cell builds and how strongly it shifts toward fat-burning, endurance-type metabolism. In mice it pushed the body to make more mitochondria and improved running endurance with no actual exercise — the headline "exercise in a pill" result. It's strictly preclinical for now, taken orally, with essentially no human safety data, so it sits in the speculative tier.
The incretin and incretin-plus class. Semaglutide is the conservative baseline, Tirzepatide the standard upgrade, Retatrutide the strongest emerging option. Cagrilintide is the amylin booster you add to extend effects.
GLP-1 receptor agonist (Ozempic / Wegovy) — the baseline incretin therapy.
Semaglutide mimics GLP-1, a gut hormone your body releases after eating that tells the brain you're full and slows how fast the stomach empties. Dosed weekly, it dramatically quiets appetite and "food noise," which is what drives the ~15% weight loss — alongside better blood sugar and real cardiovascular benefit. It's the well-established, conservative baseline of the whole class (Ozempic for diabetes, Wegovy for weight). The trade-offs are the GI side effects early on and meaningful muscle loss if you're not lifting and eating enough protein.
Dual GIP / GLP-1 receptor agonist (Mounjaro / Zepbound) — stronger weight loss than Semaglutide.
Tirzepatide hits two gut-hormone receptors instead of one — GLP-1 plus GIP — and the combination produces stronger appetite suppression and weight loss (~20%) than Semaglutide, often with better GI tolerance at equivalent results. It's become the standard "upgrade" for people who plateau on or don't tolerate Sema. Same class cautions apply: titrate up slowly, and protect lean mass with protein and resistance training.
Triple agonist (GLP-1 + GIP + glucagon) in late-stage trials — strongest weight loss in development.
Retatrutide adds a third target — glucagon — on top of GLP-1 and GIP. That glucagon arm directly raises energy expenditure and pushes the liver to burn fat, so it doesn't just curb appetite, it turns up the metabolic burn. The result is the largest weight loss seen in any obesity-drug trial to date: ~24% in Phase 2, and up to ~28.7% at the top dose in the Phase 3 TRIUMPH program — territory that rivals bariatric surgery. It's still investigational (no approval yet; a filing is expected late 2026), and the glucagon mechanism is exactly what drives its distinctive risks below.
Dual GLP-1 / glucagon agonist (Eli Lilly / Innovent) — emphasis on fat-mass loss and NASH.
Mazdutide pairs GLP-1 with glucagon — the appetite-suppressing arm plus the energy-burning, liver-fat-clearing arm. Originating in Lilly's labs and developed for the Chinese market by Innovent, it became the world's first approved GLP-1/glucagon dual agonist when China's regulator cleared it for weight management in mid-2025. The glucagon component gives it a particular edge on fat-mass loss and liver fat (NAFLD/MASH), with up to ~20% weight loss in its Phase 3 GLORY-2 trial. Lilly retains the rights outside China, where it isn't yet approved.
Dual GLP-1 / glucagon agonist (Boehringer Ingelheim / Zealand) — studied for weight loss and NASH.
Survodutide is another GLP-1/glucagon dual agonist, from Boehringer Ingelheim and Zealand. Its standout feature is what the glucagon arm does to body composition: in the Phase 3 SYNCHRONIZE-1 trial it produced ~16.6% weight loss while preferentially burning fat and sparing lean mass — a benefit pure GLP-1 drugs don't share. It's also a leading candidate for liver disease, with dedicated Phase 3 MASH trials (LIVERAGE) reading out in 2026. Still investigational for now.
Long-acting amylin analog — extends GLP-1 effects via additional satiety and gastric-emptying signals.
Cagrilintide copies amylin, a second satiety hormone the pancreas releases alongside insulin — a different "you're full" pathway from GLP-1. On its own it's a decent appetite suppressant, but its real role is as a multiplier: stacked with a GLP-1 drug it deepens the weight loss and often softens the nausea, because two satiety signals let you get more effect at a lower GLP dose. That's the logic behind CagriSema (with Semaglutide) and the researched Retatrutide and Tirzepatide combos.
Pro-apoptotic peptidomimetic targeting fat-vasculature prohibitin — rapid weight loss in primate models.
Adipotide works on a completely different principle from the GLP class. Instead of curbing appetite, it targets the blood vessels that feed fat tissue and triggers them to die, effectively starving the fat cells of their supply. In primate studies it caused fast, dramatic fat loss — but it also caused kidney toxicity, which is the dealbreaker. It's a genuinely dangerous, deeply experimental compound, included here for completeness rather than as a realistic option.
Russian-developed tetrapeptides targeted at specific organ tissues. Mechanism is largely epigenetic gene-expression modulation. Common protocol across all: 20 mg vial reconstituted with 4 mL bac water = 5 mg/mL, 0.5–1 mg subQ daily (10 units = 0.5 mg), 10–20 day course 1–2× per year, AM, short half-life. Side-effect profile is uniformly mild.
Tripeptide signaling cartilage cell regeneration — joint and osteoarthritis support.
Cartalax is the cartilage-specific bioregulator — its sequence is meant to nudge the cells that build and maintain joint cartilage back toward a younger pattern of activity. In practice it's run as a periodic course by people with wear-and-tear joints or early osteoarthritis, usually alongside the heavier-hitting joint peptides (BPC-157, TB-500) rather than instead of them.
Tetrapeptide directed at myocardial tissue regulation.
Cardiogen targets heart muscle, signalling cardiomyocytes to keep functioning the way they did at a younger age. It's used as a preventive "tune-up" for cardiovascular aging — gentle background support for heart-tissue health rather than treatment for any acute condition.
Tripeptide targeting bronchial epithelium.
Chonluten is aimed at the lining of the airways and lungs. People run it for respiratory resilience — recovery from chronic irritation, age-related decline in lung function, or seasonal support — backing the bronchial tissue's own repair rather than acting like a bronchodilator.
Tetrapeptide directed at the adrenal cortex and peripheral nerves.
Cortagen targets the adrenal cortex and peripheral nerves. It's used for nerve-regeneration support and to help steady the body's stress and cortisol response — a niche pick for people recovering from nerve issues or chronic stress, run in short periodic courses.
Tripeptide aimed at liver and intestinal tissues.
Ovagen is directed at the liver and intestinal lining. It's run as a periodic "gut and liver" maintenance course — backing the regeneration of tissues that take a daily beating from food, alcohol, and toxins — and complements the gut-repair peptides like BPC-157 and KPV.
Tetrapeptide directed at prostate tissue.
Prostamax targets prostate tissue. It's used by older men as preventive support for prostate-cell function and to help keep BPH-related markers in check — a gentle, periodic addition to a men's-health protocol rather than a treatment.
Tetrapeptide aimed at testicular tissue and reproductive function.
Testagen is aimed at testicular and reproductive tissue, intended to support healthy gene expression in the cells involved in testosterone production and fertility as they age. It sits alongside the upstream hormone tools (Kisspeptin, Enclomiphene) as tissue-level support rather than a hormone driver in its own right.
Tripeptide (Lys-Glu-Asp) targeting vascular endothelium.
Vesugen targets the endothelium — the delicate inner lining of your blood vessels that governs circulation and vascular health. It's run as preventive support for healthy blood flow and vascular aging, and pairs naturally with the cardiac (Cardiogen) and longevity peptides.
Dipeptide (Lys-Glu) studied as an immune bioregulator.
Vilon is the immune bioregulator of the set, directed at the thymus and lymphoid tissue. It's used to counter immunosenescence — the gradual weakening of immunity with age — as a short periodic course, overlapping in purpose with Thymalin and Thymogen but at the simplest, two-amino-acid end of the family.
Topical-only research peptides for compounding into creams and serums. None of these get injected — formulate at the stated concentrations into a base (HA, niacinamide serum, simple cream).
SNAP-25 mimetic that interferes with neurotransmitter release at neuromuscular junctions — botox-like expression-line reducer.
Argireline is the original "topical Botox" peptide. It works on the same target as Botox — the SNARE machinery nerves use to fire muscles — but applied to the skin's surface it only mildly dampens the tiny muscle contractions that etch expression lines over time. The effect is real but gradual and far gentler than injections: softening of forehead and crow's-feet lines with daily use, not freezing.
Extended-sequence relative of Argireline with the same SNARE-targeting mechanism.
SNAP-8 is Argireline's longer cousin — an extended sequence that targets the same nerve-to-muscle signalling but is generally considered a bit more effective at relaxing expression lines. It's the pick when you want a stronger topical "muscle-relaxing" peptide, and it's often layered with Argireline in the same serum.
Lipidated procollagen fragment (KTTKS) that stimulates collagen I, III, and fibronectin synthesis. The original Matrixyl.
Matrixyl is the workhorse collagen-building peptide. It's a fragment of collagen itself, attached to a fatty tail so it can penetrate the skin; once there it tricks the skin into thinking its own collagen has broken down and needs replacing, switching on fresh collagen and fibronectin production. It's one of the best-evidenced anti-aging actives for firmness and fine lines, and the backbone of countless serums.
Anti-inflammatory dermal peptide that downregulates IL-6 and glycation-related inflammation.
Pal Tetrapeptide-7 is the anti-inflammatory half of the famous Matrixyl 3000 duo. It calms the low-grade inflammation and glycation (sugar-damage) that quietly degrade collagen over time, so it's less about building and more about protecting what you have. It's almost always paired with Pal-GHK rather than used alone.
Lipidated form of GHK paired with Pal-Tetrapeptide-7 to form the Matrixyl 3000 cosmetic blend.
This is GHK — the same copper-peptide repair signal from the healing section — in a lipid-wrapped topical form, combined with Pal Tetrapeptide-7 to make Matrixyl 3000. Together they tell the skin to rebuild its matrix while damping the inflammation that breaks it down: a build-plus-protect pairing that's one of the most popular anti-aging blends in skincare.
Lipidated tripeptide that stimulates six dermal matrix components including collagens I, III, IV, and laminin 5.
Pal Tripeptide-38 is the most comprehensive of the Matrixyl family — instead of stimulating one or two matrix components, it boosts six (collagens I, III and IV, fibronectin, hyaluronic acid, and laminin 5). The result is more all-round structural rebuilding, particularly studied for smoothing deeper lines. Think of it as the upgraded, broader-spectrum version of the original Matrixyl.
Synthetic tripeptide mimicking a Temple Viper venom component — nAChR antagonist that relaxes facial muscles.
SYN-AKE is a synthetic mimic of a component of Temple Viper venom — minus any toxicity. The venom paralyses prey by blocking the receptor that tells muscles to contract; the cosmetic version borrows that exact mechanism, very gently, to relax facial muscles and soften expression lines. It's a topical alternative to Argireline with a slightly different target, sometimes used in rotation or combination.
Why combine peptides? The right combo hits complementary mechanisms with the same dosing schedule — a single shot that delivers both peptides at their ideal frequency. The wrong combo forces one peptide into a sub-optimal protocol just so they can share a vial.
The classic example: BPC-157 wants daily injections, but TB-500 only needs twice a week. A BPC + TB blend means you're injecting TB daily — not harmful, just wasteful, and not how TB was actually studied. You're paying for the convenience of one shot with a less-efficient TB schedule.
Each combo below carries one of two tags. Optimal dose means the blend respects both peptides' ideal frequency and dosing. Non-optimal · Convenient means you're trading dosing efficiency for one-shot simplicity — the alternative (separate vials, separate schedules) is noted in each entry.
GHRP + GHRH synergy. A GHRP alone gives a weak pulse; a GHRH alone gives nothing without the GHRP signal. Together: ~5–10× the GH pulse of either alone, with physiologic pulse shape. Both peptides are taken at the same time (pre-bed, fasted) at matching doses — perfect blend candidate.
Calm-focus pairing. Selank delivers non-sedating anxiolytic effects; Semax is a fast-acting nootropic / BDNF elevator. Same intranasal route, same daily dosing, complementary effects — frequently combined in Russian clinical literature.
BPC drives anti-inflammatory and angiogenic signaling; TB drives actin / cell migration. Together they cover both major repair axes — the most evidence-supported pairing in the healing category. The catch is dosing frequency: BPC wants daily, TB wants twice a week, but the blend forces one schedule.
Aesthetic + repair stack. GHK-Cu drives collagen / skin / hair; BPC + TB cover tissue repair. One injection delivers all three. Same TB-frequency tradeoff as BPC + TB.
GLOW + KPV. Adds gut/skin anti-inflammatory action via KPV's α-MSH mechanism — covers inflammation, repair, and aesthetics in one injection. Of all the healing blends, this one comes closest to dose-balanced for daily injection.
KLOW without the copper. Anti-inflammatory + repair without GHK-Cu accumulation concerns — useful if you already run topical GHK-Cu separately.
Which peptides go first, which follow, and what to do once a cycle ends. Running everything at once is rarely the right move.
The catalogue above tells you what each peptide does. This section is about order. A handful of principles cover most situations: prime the system before you tax it, clean before you repair, calm inflammation before you rebuild structure, and always cycle off long enough to stay sensitive. Below are the sequences that come up most often, then a sample year showing how they fit together.
Prime, then build
Run a MOTS-C cycle for ~4 weeks before a tissue-repair stack (GLOW / KLOW / BPC+TB) or a fat-loss phase. MOTS-C tunes up mitochondrial function and insulin sensitivity, so the cells you're about to ask to repair tissue or burn fat are already working efficiently. Clean the engine, then ask more of it.
Clean, then repair
These send opposing immune signals, so they run in sequence, never together. LL-37 first to clear pathogens and biofilms; then ARA-290 to quiet the nervous system and repair what's left. Trying to "clean" and "calm" at the same time just cancels out.
Same logic applies more loosely whenever you're clearing an infection or gut overgrowth before a rebuild: knock down the bad actors first, then switch to repair mode.
Cool, then mend
If an injury is hot, throbbing, or angry, the inflammatory storm blunts BPC-157 and TB-500. Lead with a few days of KPV to take the heat out, then bring in the structural-repair peptides — or run KPV alongside them from the start. (The KLOW blend bakes this in by including KPV from day one.)
Build, then consolidate
Growth-hormone stacks (Ipamorelin + CJC) run in 12–16 week blocks followed by ~4 weeks off so the pituitary resensitises. The strong anabolics (IGF-1 LR3, Follistatin) are deliberately short 4-week pulses for the same reason — and because the risk climbs the longer you run them. After a build block, drop to maintenance or rotate to a different modality rather than simply re-dosing into a desensitised system.
Suppress, then restore
After a cycle that suppresses natural testosterone — or any time the HPG axis needs restarting — Kisspeptin and Enclomiphene restart the system from the top. Run them as a dedicated recovery block after the suppressive protocol ends, not during it.
A sample year
Most of these are short seasonal courses, not continuous use. A sane annual rhythm leaves recovery gaps between the heavy lifters:
The point isn't this exact calendar — it's spacing the demanding stacks apart, pulsing the longevity and immune peptides a couple of times a year, and never running two resensitisation-dependent stacks back to back.
What not to put in the same protocol — combinations that are redundant, that cancel each other out, that stack risk, or that are flatly unsafe given a condition.
Three kinds of bad combination show up again and again: redundancy (two peptides fighting over the same receptor, so the second adds cost and side effects but no extra effect), opposing signals (two peptides pulling the body in contradictory directions), and additive risk (two peptides whose side effects compound). On top of those sit a few hard stops tied to your health status, not to another peptide.
Worked example — if you're running Retatrutide
A triple agonist already maxes out appetite suppression and fat-burning. Most things people are tempted to bolt on are redundant, and a few pull in the wrong direction: