COMPOUND DATABASE

Synthetic versions of the primary male sex hormone and the essential "base" for almost all cycles to prevent the symptoms of low testosterone caused by other suppressive compounds.

A 19-nor derivative with 5x the anabolic potency of testosterone. It is considered the most powerful physique-altering steroid available, providing extreme hardening, strength, and nutrient partitioning.

A DHT-based steroid favored for its high safety profile and low side-effect burden. Often used in high doses for lean mass preservation. Long rumored in bodybuilding lore to have been Arnold Schwarzenegger's favorite steroid.

A slow-acting 19-nor steroid famous for mass gains and joint lubrication. Provides significant hypertrophic effects while offering therapeutic benefits for joint and connective tissue health.

A DHT-derived compound used primarily as a cosmetic finisher for competition. Provides muscle hardness, dryness, and acts as a mild anti-estrogen.

A legendary oral steroid used for rapid "kickstarting" of mass cycles. Known for dramatic strength and size gains within the first few weeks of use.

A "cleaner" oral version of Dianabol that does not cause water retention. Developed by East German scientists for their Olympic athletes, providing lean mass and performance enhancement without detection.

A mild oral steroid often used for fat loss and by female athletes. Known for its favorable safety profile and ability to preserve strength during caloric deficits.

A notoriously toxic and potent oral steroid known for "dry" but extreme mass gains. Provides dramatic strength and size increases but carries severe hepatotoxicity.

A synthetic androgen 10 times more potent than testosterone, initially developed for male contraception. Can serve as a replacement for testosterone as a cycle base due to its conversion to estrogen (unlike other 19-nors).

An oral androgen used to increase free testosterone and enhance libido. Unlike most orals, it is not 17-alpha-alkylated and is not hepatotoxic.

An extreme androgenic oral steroid used for raw strength and aggression without weight gain. One of the strongest androgens available, used almost exclusively by powerlifters and combat athletes.

A veterinary-grade injectable anabolic steroid derived from testosterone with a unique double-bond structure. Originally developed for horses, EQ provides steady, quality gains with enhanced vascularity, appetite stimulation, and significant increases in red blood cell production.

One of the most powerful oral anabolic steroids ever created, with an anabolic rating of 320 (vs testosterone at 100). Originally developed to treat anemia and muscle-wasting diseases. Known for producing rapid, dramatic gains in size and strength, but with significant side effects including unique estrogenic effects despite being a DHT derivative.

A DHT-derived anabolic steroid famous for its use in competitive sports (notably causing Ben Johnson to lose his 1988 Olympic gold medal). Known for producing a dry, hard, vascular look without water retention. Available in both oral and injectable forms, though the injectable is an aqueous suspension, not oil-based.

A fast-acting version of nandrolone (Deca) on the short phenylpropionate ester. Delivers the same joint-friendly mass gains as Deca but clears the system far quicker, making it easier to dial in and to bail out of if sides appear.

A non-aromatizing injectable steroid (the 5-alpha-reduced metabolite of boldenone/Equipoise) prized for strong, lean, dry gains and strength. Its reputation is defined as much by brutal post-injection pain and harsh effects on lipids and endurance as by its results.

A single injectable that blends four testosterone esters (propionate, phenylpropionate, isocaproate and decanoate) in one oil. It is the same hormone as any other testosterone, the four esters just release it over different timeframes from a single shot.

An extraordinarily potent oral steroid (a 17-alpha-methylated trenbolone analogue) that was abandoned in development for being too toxic to use. Today it exists mainly as the androgen-receptor research ligand R1881, and, recklessly, as a microgram-dosed pre-contest compound. It is widely regarded as one of the most hepatotoxic androgens ever made.

One of the first orally active anabolic steroids, a 17α-methylated form of testosterone that survives first-pass liver metabolism. FDA-approved for male hypogonadism, delayed puberty and advanced breast cancer, it is now largely superseded but still illustrates the classic trade-off of oral 17-alkylated androgens: convenience at the cost of liver strain and strong estrogenicity.

A veterinary anabolic steroid: marketed by Upjohn as "Cheque Drops" to prevent estrus (heat) in female dogs, that became an infamous pre-contest drug in bodybuilding. Extremely potent at the androgen receptor and taken in microgram doses, it is used almost entirely for a short-term aggression and hardness "psych-up" before lifting or stepping on stage, not to build muscle.

A potent oral designer steroid from the prohormone era, the 17α-methyl derivative of 1-testosterone (dihydroboldenone/DHB). It delivers hard, dry strength and mass at small doses but is notorious for severe liver toxicity, debilitating lethargy and lipid damage. Sold over-the-counter as a "prohormone" until it was scheduled as a controlled substance.

An oral prohormone (1-DHEA) that converts in the body to 1-testosterone (dihydroboldenone/DHB) and other 1-dehydrogenated androstanes. Marketed for years: and still sold OTC by some retailers today, as a "legal" dry-gains supplement, because 1-androsterone itself was not explicitly added to the DEA's Schedule III list, unlike the DHB/1-testosterone it converts into. It produces lean, hard mass because its active product is a non-aromatizing androgen.

An oral prohormone (4-DHEA), a positional isomer of DHEA, that converts in the body to testosterone via 4-androstenedione. Because its active product aromatizes, 4-Andro gives fuller, "wet" bulking gains and is often paired with the dry-converting 1-Andro. It is marketed as a "legal" prohormone/dietary supplement, but its legal status is unsettled. The ketone form is not explicitly named on the federal Schedule III anabolic-steroid list the way the related "4-androstenediol" is, though the FDA has challenged similar DHEA-isomer prohormones as unlawful dietary ingredients.

An oral "nor" prohormone marketed as a dietary supplement. Wikipedia describes it as a combined derivative of the anabolic steroid nandrolone (19-nortestosterone) and the prohormone DHEA, and groups it with the known orally active prohormones of nandrolone. It is intended to raise nandrolone levels in the body, delivering nandrolone-like lean-mass effects along with nandrolone's progestogenic side-effect profile.

A naturally occurring 5α-reduced androstane steroid (3β-hydroxy-5α-androstan-17-one) sold as an oral "prohormone." Wikipedia describes it as a metabolite of testosterone and DHT with weak androgenic activity, produced from the adrenal hormone DHEA by the enzyme 5α-reductase. Because it is already 5α-reduced (saturated A-ring) it sits on the DHT side of steroid metabolism, which is why it is marketed as a non-aromatizing, "dry"/hardening compound rather than a mass builder.

Designed to provide the benefits of testosterone in muscle and bone without prostatic effects. One of the most potent SARMs available, providing significant lean mass and strength gains.

A non-steroidal SARM highly effective for mass accrual. One of the most studied SARMs with clinical trial data supporting its muscle-building effects.

The most popular "beginner" SARM, used for maintenance and healing. Provides mild muscle preservation effects with a favorable safety profile compared to more potent SARMs.

A SARM valued for muscle "dryness"/hardening and modest strength gains, generally regarded as milder than SARMs like LGD-4033 or RAD-140 and often stacked with them. Notable for its unique visual side effects that can occur at higher doses.

A synthetic steroidal SARM that also acts as a myostatin inhibitor. Theoretically allows for bypassing genetic muscle limits via follistatin upregulation.

Considered the most potent SARM, often yielding results comparable to steroids. Provides extreme muscle hardening and strength with complete testosterone shutdown.

A grey-market "SARM" sold as RAD-150 or TLB-150 and described by vendors as the benzoate ester of RAD-140 (testolone), an ester prodrug intended to be longer-acting. Once cleaved, it is presumed to act as RAD-140, a nonsteroidal selective androgen receptor modulator. Important caveat: there is essentially no peer-reviewed literature on RAD-150 specifically, so almost everything below is extrapolated from its parent compound RAD-140.

A nonsteroidal selective androgen receptor modulator (SARM) with good oral bioavailability, originally investigated as a possible treatment for osteoporosis. Wikipedia notes it functions as a selective androgen-receptor agonist with functional selectivity, a partial agonist for androgenic effects but a full agonist for anabolic effects. It is a distinct compound from LGD-4033 (Ligandrol): a different molecule (PubChem CID 25195253) whose evidence base is preclinical, whereas LGD-4033 has actual human trial data.

A SERM that boosts natural testosterone without suppressing fertility. The trans-isomer of clomiphene, it stimulates LH and FSH production more effectively with fewer side effects than Clomid.

A first-generation non-steroidal Selective Estrogen Receptor Modulator (SERM) that has been the gold standard for PCT since the 1970s. Acts as an estrogen antagonist in breast tissue and the hypothalamus/pituitary (stimulating LH/FSH release) while acting as an agonist in bone (protective) and liver. The cornerstone of most PCT protocols.

A first-generation SERM that is a mixture of two isomers: 62% enclomiphene (trans, antagonist) and 38% zuclomiphene (cis, agonist). Works primarily at the hypothalamus to block estrogen negative feedback, increasing GnRH pulsatility and subsequent LH/FSH release. Produces a stronger initial LH/FSH spike than tamoxifen but with more side effects, particularly vision issues.

A second-generation SERM (benzothiophene class) that is clinically superior to tamoxifen specifically for treating and reversing gynecomastia. Studies show 86% of patients achieve >50% breast tissue reduction vs only 41% with tamoxifen. Acts as an estrogen antagonist in breast tissue while being an agonist in bone. NOT recommended for PCT due to weak testosterone stimulation.

A first-generation triphenylethylene SERM, structurally almost identical to tamoxifen (Nolvadex), differing by a single chlorine substitution. Like tamoxifen it is an estrogen antagonist in breast tissue and at the hypothalamus/pituitary (raising LH/FSH) while acting estrogenically in bone and liver. It is used off-label for post-cycle therapy and gynecomastia. Its main practical distinctions from tamoxifen are a stronger positive effect on blood lipids, a lower blood-clot risk, metabolism by a different liver enzyme (so it dodges tamoxifen's SSRI interaction problem), and a QT-prolongation warning that tamoxifen lacks.

A third-generation non-steroidal aromatase inhibitor (AI) that competitively and reversibly inhibits the aromatase enzyme. The most commonly used AI for estrogen control during steroid cycles due to its balance of efficacy and manageability. At 1mg/day, reduces estradiol by ~80% (per FDA labeling), with aromatase inhibition around 97% in clinical studies.

A third-generation non-steroidal aromatase inhibitor that is 10-30x more potent than anastrozole in intact-cell assays. Achieves >99% whole-body aromatase inhibition at the standard 2.5mg/day oncology dose. Considered the "nuclear option" for emergency gynecomastia intervention or when anastrozole proves insufficient. Due to its extreme potency, it has a very low margin for error and easily crashes estrogen.

A steroidal, irreversible "suicidal" aromatase inactivator (Type I AI) that permanently destroys aromatase enzymes rather than temporarily blocking them. Unlike anastrozole and letrozole, exemestane causes no estrogen rebound when discontinued, has a more favorable lipid profile, and possesses mild androgenic activity through its active metabolite.

Arimistane (androsta-3,5-diene-7,17-dione, CID 150910, CAS 1420-49-1) is a steroidal androstadienedione sold over-the-counter as a supplement and marketed as an aromatase inhibitor for controlling estrogen and for post-cycle therapy. It belongs to the steroidal (irreversible, "suicidal") class of aromatase inhibitors by structure. It is popular precisely because it is marketed as a legal, OTC estrogen-control option, but the FDA disputes that framing (it has issued warning letters stating the ingredient does not meet the legal definition of a dietary ingredient), and it is far less studied and generally regarded as weaker/less predictable than pharmaceutical AIs like anastrozole, letrozole or exemestane.

A fragment of the GH molecule (amino acids 176-191) that targets fat loss without affecting insulin or blood glucose. Provides the lipolytic benefits of GH without the typical GH side effects.

A peptide derived from a protein found in stomach acid with profound tissue-healing properties. Used for healing tendons, ligaments, gut inflammation, and various injuries.

Focuses on systemic healing, cell migration, and flexibility. A naturally occurring peptide present in almost all human cells that plays a key role in tissue repair and regeneration.

A natural copper complex that rejuvenates skin and hair follicles. Found naturally in human plasma, GHK-Cu levels decline with age, and supplementation may restore youthful tissue function.

A pineal gland peptide studied for telomere lengthening and longevity. Synthesized version of the naturally occurring Epithalamin, it may slow cellular aging.

A myostatin inhibitor designed to promote extreme muscle growth. By inhibiting myostatin, it theoretically removes the natural limit on muscle growth.

A 70-amino acid polypeptide hormone that serves as the primary mediator of Growth Hormone effects. The most commonly used variants in bodybuilding are IGF-1 LR3 (extended half-life, systemic effects) and IGF-1 DES (10x potency, localized site enhancement). Works through the PI3K/Akt/mTOR pathway to stimulate muscle protein synthesis and potentially hyperplasia (new muscle fiber creation).

An anti-inflammatory tripeptide (Lysine-Proline-Valine) derived from the C-terminus of alpha-melanocyte-stimulating hormone (α-MSH). It carries α-MSH's anti-inflammatory activity without its pigmentary (tanning) or other melanocortin-receptor effects. KPV is the "K" that is added to the GLOW stack to make the KLOW stack, contributing inflammation control and gut/mucosal healing.

A melanocortin agonist used for sexual dysfunction. FDA-approved (as Vyleesi) for hypoactive sexual desire disorder in premenopausal women; also used off-label by some men for sexual dysfunction, though it carries no FDA approval or official dosing guidance for that use.

A peptide that stimulates melanin production for tanning. Also increases libido as a side effect through melanocortin receptor activation.

A modified C-terminal fragment of human growth hormone (amino acids 177-191 with N-terminal tyrosine) that isolates the fat-burning properties of hGH without metabolic or growth-promoting effects. Does NOT increase IGF-1 or affect blood glucose. An early 12-week trial showed ~2.6kg weight loss vs 0.8kg placebo at the 1mg dose, but the larger, pivotal 24-week Phase IIb trial (~500+ subjects) failed to meet its primary endpoint and development was discontinued in 2007. More stable than standard HGH Fragment 176-191. Not approved by the FDA, TGA, or any regulator for any therapeutic indication; in Australia it is a Schedule 4 restricted poison, not an approved medicine.

A 28-amino acid immunomodulatory peptide derived from thymus gland. Functions as immune modulator (not stimulant) - shifts responses toward homeostasis rather than amplifying. Promotes T cell maturation, enhances NK cell cytotoxicity, stimulates dendritic cell function via TLR signaling. Extensive clinical use internationally for hepatitis B/C, cancer adjunct, sepsis, and immunodeficiency. Excellent safety profile with minimal side effects.

A 9-amino acid neuropeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu, ~849 Da) first isolated from rabbit cerebral venous blood in 1974 and chemically characterized by Schoenenberger & Monnier in 1977. Promotes delta wave (slow-wave) sleep stages 3-4 NREM. Modulates GABA and serotonin systems. Animal studies report increased nocturnal GH pulses and altered stress-hormone responses, but the controlled human trials that tested this directly found no effect on GH/prolactin (Giusti et al. 1993) or on CRH-/meal-induced ACTH/cortisol (Späth-Schwalbe et al. 1995): so the often-repeated GH and cortisol claims are largely unproven in humans. Research peaked in the 1980s-90s but development stalled due to very short half-life and inconsistent clinical results. Evidence quality is low-moderate with mostly small, outdated studies.

A synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) developed by combining tuftsin (immunomodulatory peptide) with Pro-Gly-Pro for stability. Anxiolytic comparable to benzodiazepines but WITHOUT sedation, tolerance, dependence, or cognitive impairment. Allosteric GABA-A modulation, increases BDNF expression, and provides immunomodulatory effects. A Russian randomized trial (Zozulia et al., 2008) found its anxiolytic effect on GAD/neurasthenia comparable to the benzodiazepine medazepam over ~14 days. Non-stimulating alternative to Semax.

A synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) derived from ACTH(4-10) with a Pro-Gly-Pro tail for stability. Primary nootropic with cognitive enhancement, focus, and neuroprotection. Significantly upregulates BDNF (1.4x protein, up to 3x mRNA per Dolotov et al. 2006) and modulates NGF expression. Unlike full ACTH, it lacks steroidogenic (adrenal) and melanocyte-stimulating activity, so it does not produce cortisol/HPA stimulation or tanning; some more recent reviews suggest it may still interact with central MC4/MC5 melanocortin receptors, so "no melanocortin activity at all" overstates current evidence. Available as standard Semax, N-Acetyl Semax, and NASA (Amidate) - each progressively more stable.

A 37-amino acid endogenous antimicrobial peptide (begins with two leucines - hence "LL") cleaved from hCAP18 by proteinase 3. Broad-spectrum antimicrobial against bacteria, fungi, and enveloped viruses. MIC 1-32mcg/mL. Promotes wound healing via EGFR transactivation, angiogenesis, and keratinocyte migration. Potent immunomodulator - attracts immune cells, neutralizes LPS endotoxin. Very short half-life limits systemic utility. Associated with psoriasis, rosacea, lupus when dysregulated.

A locally-acting splice variant of IGF-1 (IGF-1Ec) that skeletal muscle produces in response to mechanical strain and damage, hence "Mechano Growth Factor." It consists of the mature IGF-1 domain plus a unique 24-amino-acid E-domain; the cleaved E-peptide is the biologically distinctive part, believed to activate satellite (muscle stem) cells that donate new nuclei to repairing and growing fibers. Native MGF acts locally for only minutes, so a PEGylated version (PEG-MGF) was created to extend its half-life for systemic use.

A 16-amino-acid peptide encoded not in the nuclear genome but within the mitochondrial 12S rRNA region, one of the first-described "mitochondrial-derived peptides." MOTS-c behaves as an exercise mimetic: it activates the AMPK energy-sensing pathway, improves insulin sensitivity and glucose disposal, promotes fat oxidation, and in animals restores age-related declines in physical capacity. It is studied for metabolic health, longevity, and endurance rather than muscle growth.

A four-amino-acid, cell-penetrating peptide (sequence D-Arg-Dmt-Lys-Phe-NH2) from the Szeto-Schiller class that concentrates in the inner mitochondrial membrane and binds the phospholipid cardiolipin. By stabilising cardiolipin and the cristae architecture, it reduces oxidative stress and electron leak and helps mitochondria keep producing ATP efficiently. It is studied across mitochondrial dysfunction, heart failure, eye disease, and aging, and its pharmaceutical form was FDA-approved in 2025 for the rare disease Barth syndrome.

An 11-amino-acid peptide engineered from the helix-B surface of erythropoietin (EPO). EPO has two separable activities: raising red blood cells, and protecting/repairing tissue. ARA-290 was designed to trigger only the second. It selectively activates the innate repair receptor without engaging the classical EPO receptor that drives erythropoiesis. The result is EPO's anti-inflammatory, anti-apoptotic, and regenerative signalling with none of the hematocrit rise (and none of the clotting/cardiovascular risk) that makes EPO a dangerous doping agent.

A tridecapeptide analogue of alpha-melanocyte stimulating hormone (alpha-MSH), also written [Nle4,D-Phe7]-alpha-MSH or NDP-MSH. It is the tanning peptide sold grey-market as "Melanotan-1," and is chemically the same molecule as afamelanotide, the drug approved by the FDA in October 2019 (brand Scenesse) to increase pain-free light exposure in adults with erythropoietic protoporphyria (EPP). It is distinct from the separately developed Melanotan II.

A pegylated version of Mechano Growth Factor (MGF). MGF is a naturally occurring 24-amino-acid peptide - the C-terminal fragment produced when insulin-like growth factor 1 (IGF-1) is spliced/cleaved to the "IGF-1Ec" isoform - which muscle expresses during repair after physical activity and which has anabolic effects. Because native MGF is rapidly broken down in the body, synthetic versions attach polyethylene glycol (PEG) to the peptide (and often use D-amino acid substitutions in the central QRRK region) to resist metabolism, so PEG-MGF can act systemically rather than only locally.

A selective agonist of the melanocortin-4 receptor (MC4R), marketed as Imcivree. It was approved by the FDA in November 2020 as a first-in-class treatment for chronic weight management in patients aged 6 and older with obesity due to genetically confirmed pro-opiomelanocortin (POMC) deficiency, proprotein convertase subtilisin/kexin type 1 (PCSK1) deficiency, or leptin receptor (LEPR) deficiency, and was later approved (FDA 2022, EMA 2021) for weight management in Bardet-Biedl syndrome (BBS). In March 2026 the FDA further approved it for acquired hypothalamic obesity (age 4+) - hypothalamic damage, most often from a brain tumor or its treatment, that disrupts the same MC4R pathway - which unlike the other indications does not require genetic testing. It remains not approved for common/general (polygenic) obesity.

A nine-amino-acid peptide hormone (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH2, a disulfide-bridged nonapeptide) produced in the hypothalamus and released by the posterior pituitary. Medically it is an FDA-approved injectable used to induce/augment labor and control postpartum bleeding. Popularly nicknamed the 'love' or 'bonding' hormone, it is studied intranasally for its effects on social behavior, trust, and anxiety. None of which are performance-enhancing in the athletic sense.

An experimental mixture (code name FPF-1070) of enzymatically-treated peptides and amino acids derived from pig brain, manufactured by Ever Pharma (Austria). It is proposed to have neurotrophic/neuroprotective activity and is used abroad, not in the US, for stroke, dementia, and brain injury. It is given by injection and is popular in nootropic circles for cognition and neuro-recovery, but the clinical evidence is weak and mixed.

Direct replacement of the body's growth hormone for recovery, fat loss, and anti-aging. Provides systemic benefits including improved body composition, sleep, skin quality, and healing.

A synthetic analogue of insulin-like growth factor 1 (IGF-1), the main downstream mediator of growth hormone. LR3 ("Long R3") is engineered to bind the IGF binding proteins (IGFBPs) much less than native IGF-1; because most native IGF-1 is normally bound by IGFBPs, cutting that binding leaves more free peptide in circulation and dramatically lengthens its active half-life. It is used in the bodybuilding community for a longer, systemic version of IGF-1's anabolic signalling. Note: the exact LR3 half-life figure widely quoted (~20-30 h) comes from research-reagent/community sources, not an approved-drug label.

An oral ghrelin mimetic that stimulates GH pulses. Technically not a peptide but a non-peptide agonist of the ghrelin receptor that increases growth hormone and IGF-1 levels.

A GHRH analog FDA-approved for reducing visceral adipose tissue. Particularly effective at targeting stubborn abdominal and visceral fat.

A peptide that stimulates the pituitary to release more GH in a natural pattern. One of the earliest and most studied GHRH analogs, commonly used in anti-aging and regenerative medicine.

A synthetic hexapeptide ghrelin mimetic that stimulates growth hormone release by binding to the growth hormone secretagogue receptor (GHS-R1a). More potent than GHRP-6 with fewer side effects, particularly less appetite stimulation. Often combined with GHRH peptides (Mod GRF/CJC-1295) for synergistic GH release.

A synthetic hexapeptide ghrelin mimetic that was one of the first GH secretagogues developed. Stimulates growth hormone release through the GHS-R1a receptor. Known for causing intense appetite stimulation (the "hunger peptide"), which can be beneficial for bulking but problematic for cutting. Less selective than GHRP-2 with higher cortisol and prolactin elevation.

A synthetic pentapeptide and the first truly selective growth hormone secretagogue. Unlike GHRP-2 and GHRP-6, ipamorelin does not significantly raise cortisol, ACTH, or prolactin - even at doses 200x higher than the effective dose for GH release. This makes it the "cleanest" GHRP with the best side effect profile, commonly stacked with CJC-1295 for synergistic GH elevation.

A synthetic 29 amino acid GHRH analog with four amino acid substitutions that extend its half-life from ~5-10 minutes (native GHRH/GRF) to ~30 minutes. Unlike CJC-1295 with DAC (5-8 day half-life), Mod GRF maintains natural pulsatile GH release patterns. Most commonly stacked with GHRPs like Ipamorelin for synergistic GH elevation - peptide-community sources commonly cite combined GH increases of up to ~54-fold, though this figure is not traced to a specific peer-reviewed trial.

A synthetic hexapeptide GHRP long regarded in community/vendor use as the strongest of the class, though the one direct human comparison study found its GH, cortisol and prolactin responses statistically similar to equal doses of GHRP-2 rather than clearly superior. Its standout feature is a unique cardioprotective action via CD36 receptor binding on cardiomyocytes, independent of GH release. It desensitizes faster than alternatives like Ipamorelin and elevates cortisol/prolactin more than that selective peptide. Better suited for short-run/pulsed use: a 16-week continuous human trial showed GH responsiveness declining significantly within the first week and continuing to decline through week 16.

A synthetic analogue of growth hormone-releasing hormone (GHRH), developed by ConjuChem as a modified GRF(1-29)/sermorelin bearing a drug affinity complex (DAC). The DAC: a maleimidopropionyl-lysine group added at the C-terminus, bonds to albumin in the bloodstream, protecting the peptide from degradation and stretching its half-life to an estimated 6-8 days. A single dose can raise GH and IGF-1 for days. This long action is the key contrast with CJC-1295 "no DAC" (Modified GRF 1-29), whose ~30-minute half-life preserves natural pulses.

A PPAR-delta agonist that shifts fuel source from glucose to lipids. Provides massive boosts in endurance and fat oxidation but was abandoned in clinical trials due to cancer concerns.

A Rev-Erb agonist that improves metabolic rate and circadian rhythms. Enhances exercise capacity and metabolism without affecting hormones.

A powerful Beta-2 agonist that increases basal metabolic rate and lipolysis. Originally developed as a bronchodilator, now widely used for rapid fat loss.

A mitochondrial toxin that uncouples oxidative phosphorylation, creating pure heat from calories. Extremely effective for fat loss but potentially lethal.

The most biologically active thyroid hormone, roughly 3-4x more potent than T4 at the cellular level. Used in bodybuilding to dramatically accelerate metabolic rate and fat loss during cutting phases. Powerful but carries significant risks including muscle catabolism and thyroid suppression if used improperly.

A sympathomimetic amine that works through both direct beta-receptor activation and indirect norepinephrine release to increase thermogenesis and metabolic rate. The classic fat burner, often stacked with caffeine and aspirin (ECA stack). The JAMA meta-analysis of ephedra/ephedrine trials shows ~0.9 kg/month weight loss above placebo. Carries significant cardiovascular risks.

An alpha-2 adrenergic receptor antagonist extracted from Pausinystalia yohimbe bark. Works by blocking alpha-2 receptors on fat cells, particularly effective for "stubborn fat" areas (lower abdomen, hips, thighs) which have high alpha-2 receptor density. MUST be taken fasted - insulin completely negates its effects. Soccer player study showed body fat decrease from 9.3% to 7.1% in 21 days.

A selective beta-2 adrenergic agonist, roughly 29-fold more selective for beta-2 vs beta-1 receptors. Often considered a safer alternative to clenbuterol due to a much shorter half-life (5-6 hrs vs ~26-48 hrs) and better cardiac profile. Works through the cAMP pathway to promote lipolysis and exhibits anti-catabolic effects by inhibiting calpain (a muscle protein-degradation enzyme). Rat studies show a 19% muscle mass increase and 12-39% fat reduction; the effect in humans is real but far more modest.

The main hormone secreted by the thyroid gland and the standard replacement therapy for hypothyroidism. T4 is essentially a prohormone: it is largely inactive until deiodinase enzymes convert it into the far more potent T3 inside peripheral tissues. In a physique context it is used to raise metabolic rate and support fat loss, but it works slower and more gently than T3 and is generally viewed as the milder, more physiological way to run thyroid.

A centrally acting triple monoamine reuptake inhibitor originally developed for Parkinson's and Alzheimer's disease, where patients unexpectedly lost weight. It was repurposed as an anti-obesity agent and produced some of the strongest weight-loss numbers seen for a single small-molecule drug in phase 2 trials. It works mainly by suppressing appetite, with a smaller effect on energy expenditure, and carries a stimulant-type side-effect profile (raised heart rate and blood pressure).

An experimental synthetic agonist of the estrogen-related receptors (ERRalpha/beta/gamma), a family of orphan nuclear receptors that govern mitochondrial biogenesis and oxidative metabolism. Nicknamed an "exercise mimetic" because in rodents it reproduces some of the metabolic adaptations of endurance training (more mitochondria, greater fat oxidation and improved endurance) without exercise. It is an early-stage research compound: essentially all data is from mice, and honest evaluation means treating human benefit and safety as unproven.

An endogenous diiodothyronine thyroid-hormone metabolite (two iodine atoms at the 3 and 5 positions) that is marketed as a fat-loss supplement. Its distinguishing feature versus T3 is a rapid, non-genomic action directly at the mitochondria to raise metabolic rate. In rodents it increases energy expenditure and reduces fat mass without some of the classic thyrotoxic effects seen with T3, but that "cardiac-sparing" profile is contested, and in humans it has only been tested in a single tiny pilot study (n=2), so robust controlled data are essentially lacking.

A thyroid-hormone analogue (triiodothyroacetic acid) that is an analogue of a naturally circulating metabolite of T3. It acts as a thyroid-hormone receptor agonist and, unlike T3/T4, can enter cells independently of the MCT8 transporter, which is why it is used to treat MCT8 deficiency (Allan-Herndon-Dudley syndrome). It has also been used for thyroid-hormone resistance syndrome and, in France, as adjuvant thyroid-cancer therapy. Separately, it has been widely (and improperly) marketed as a weight-loss aid on the strength of its thyroid-receptor agonism, prompting FDA/Health Canada regulatory warnings, but controlled trials found its central (pituitary TSH-suppressing) potency does not reliably translate into the peripheral, metabolic-rate-raising effect that would actually drive fat loss, so the marketed benefit is scientifically shaky even before weighing the thyrotoxic risk.

A prescription appetite-suppressant stimulant approved for short-term treatment of obesity alongside diet and exercise. Structurally an amphetamine relative, it acts as a norepinephrine-dopamine releasing agent (an 'anorectic'). Approved in the US in 1959 and still one of the most prescribed weight-loss drugs, it is meant for short-term use only.

The most widely used performance drug in the world, and one of the few whose ergogenic effect is beyond dispute. It belongs in this archive both because it genuinely improves training and because it is the missing third component of the classic ECA fat-loss stack alongside ephedrine and aspirin.

A GLP-1 receptor agonist used for weight loss, appetite suppression, and type 2 diabetes management. Originally developed and approved as Ozempic for diabetes, the same drug is now FDA-approved as Wegovy for chronic weight management (injectable and, since December 2025, an oral tablet) and as Rybelsus for oral diabetes treatment. Also carries FDA approvals for reducing major cardiovascular events (SELECT trial) and slowing chronic kidney disease progression in type 2 diabetics (FLOW trial).

A "triple agonist" targeting GLP-1, GIP, and Glucagon receptors. Still investigational (Phase 3 TRIUMPH trials, primary completion reached April 2026), Phase 2 data showed ~24% mean body-weight loss at 48 weeks on the 12mg dose - beyond single or dual GLP-1/GIP agonists.

A first-in-class dual GLP-1/GIP receptor agonist (sometimes called a "twincretin"). This 39-amino acid synthetic peptide activates both incretin receptors, producing superior weight loss and glycemic control compared to GLP-1-only agonists like semaglutide. The most effective FDA-approved pharmaceutical weight loss agent currently on the market (investigational triple agonists like retatrutide show larger effects in trials but are not yet approved).

The original GLP-1 receptor agonist for weight management, with 97% amino acid homology to human GLP-1. Less potent than semaglutide (~8% vs ~16% weight loss) and requires daily injection vs weekly, but now available as generic making it a more affordable option. Works through appetite suppression, delayed gastric emptying, and central satiety signals.

A long-acting amylin analog developed by Novo Nordisk. Amylin is a satiety hormone released alongside insulin after meals, and it works through a different pathway than GLP-1, so cagrilintide complements GLP-1 agonists rather than duplicating them. It is best known as the amylin half of CagriSema, the fixed-dose once-weekly combination of cagrilintide 2.4mg and semaglutide 2.4mg, which produced 22.7% mean weight loss at 68 weeks in the REDEFINE 1 trial assuming full adherence (the treatment-policy estimate, which counts everyone regardless of adherence, was 20.4%).

A dual GLP-1 / glucagon receptor agonist from Boehringer Ingelheim in Phase 3 development for obesity and metabolic dysfunction-associated steatohepatitis (MASH). By adding glucagon-receptor activity to GLP-1, it pairs appetite suppression with increased energy expenditure and hepatic fat burning, which makes it particularly interesting for fatty liver disease. The SYNCHRONIZE-1 Phase 3 obesity trial (NEJM 2026) reported -12.2% (3.6mg dose) to -13.0% (6.0mg dose) mean weight loss at 76 weeks vs -5.4% on placebo, with roughly 72% of treated participants losing at least 5% of body weight vs 46% on placebo.

An oral, non-peptide (small-molecule) GLP-1 receptor agonist from Eli Lilly, FDA-approved in April 2026 under the brand name Foundayo. Unlike peptide GLP-1 drugs, which must be injected or taken as a highly restricted oral tablet, orforglipron is a chemically stable small molecule that can be taken once daily as a pill with no food restrictions. In the ATTAIN-1 Phase 3 obesity trial the highest dose (36mg) produced -11.2% mean weight loss at 72 weeks (treatment-regimen estimand) versus -2.1% for placebo. The big deal is the format: an easy-to-manufacture oral GLP-1 with the potential to scale globally.

A dual GLP-1 / glucagon (GCG) receptor agonist, notably developed and first approved in China (Innovent Biologics, co-developed with Eli Lilly). Built on the mammalian oxyntomodulin (OXM) peptide, it combines appetite suppression with increased energy expenditure and improved hepatic fat metabolism. In the pivotal GLORY-1 Phase 3 trial (n=610, 48 weeks), the 4mg and 6mg doses produced ~12% and ~15% weight loss respectively, and GLORY-2 showed up to ~20.1% weight loss at the 9mg dose in participants without diabetes.

A once-weekly GLP-1 receptor agonist sold as Trulicity, originally developed for type 2 diabetes and also approved to reduce cardiovascular events in diabetics with cardiovascular disease. Structurally it is the GLP-1(7-37) peptide fused to a human IgG4 Fc fragment, which extends its half-life enough for once-weekly subcutaneous dosing. It produces appetite reduction and modest weight loss as a class effect, but less than semaglutide or tirzepatide.

An injectable synthetic analog of the beta-cell hormone amylin, sold as Symlin. It is FDA-approved as an adjunct to mealtime insulin in type 1 and type 2 diabetics who have not reached glucose targets on insulin alone. It slows gastric emptying, promotes satiety and blunts post-meal glucagon, smoothing post-meal glucose spikes and producing modest weight loss. Notably, pramlintide is the amylin analog that is actually FDA-approved for human use, unlike cagrilintide, the newer long-acting amylin analog still in development for obesity.

One of the first GLP-1 receptor agonists, exenatide is a synthetic version of exendin-4, a peptide originally found in the venom of the Gila monster. It is FDA-approved for type 2 diabetes. The immediate-release form (Byetta) is injected twice daily; an extended-release microsphere formulation (Bydureon / Bydureon BCise) was injected once weekly but has been discontinued in the US as of 2024 and is no longer on the market (generic immediate-release exenatide remains available). It lowers blood glucose and causes gradual, modest weight loss, though generally less than newer agents like semaglutide or tirzepatide.

A glycoprotein hormone that mimics luteinizing hormone (LH), directly stimulating the Leydig cells in the testes to produce testosterone. Essential for maintaining testicular function during steroid cycles and facilitating recovery during PCT. The alpha subunit is identical to LH, FSH, and TSH.

A bile acid used for extreme liver protection during oral steroid cycles. Provides hepatoprotection by improving bile flow and reducing cellular stress.

A coenzyme essential for cellular energy and DNA repair. NAD+ levels decline with age, and supplementation may support cellular health and energy production.

The body's "master antioxidant" used for detoxification and oxidative stress reduction. Critical for liver health and cellular protection.

A potent dopamine D2 receptor agonist (ergot derivative) used to control elevated prolactin levels. Essential ancillary during cycles containing 19-nor steroids (trenbolone, nandrolone) which elevate prolactin. Known for its exceptionally long half-life allowing twice-weekly dosing and its superior tolerability compared to bromocriptine.

A biguanide antidiabetic drug that improves insulin sensitivity through AMPK activation. Used in bodybuilding to manage blood sugar during high-carb bulking phases and to counteract insulin resistance from HGH/insulin use. Also researched extensively for longevity/anti-aging applications (TAME trial). IMPORTANT: May blunt muscle hypertrophy adaptations from training.

A 5-alpha reductase inhibitor that blocks the conversion of testosterone to DHT, reducing serum DHT by 65-70%. Used during testosterone cycles to prevent DHT-related hair loss. CRITICAL: Only works with testosterone-based compounds. Does NOT work with DHT derivatives (Masteron, Winstrol, Anavar). Makes hair loss WORSE with nandrolone compounds.

A dual 5-alpha reductase inhibitor that blocks both Type I and Type II isoenzymes, reducing serum DHT by roughly 90-94% at steady state (FDA trial median; some sources cite up to ~98%), versus ~70% with finasteride. More potent than finasteride for hair loss prevention but with a very long half-life of ~5 weeks. Clinically superior to finasteride for hair count and growth in head-to-head trials. Same caveats apply: only works with testosterone-based compounds, not DHT derivatives, and worsens nandrolone-related hair loss.

A synthetic decapeptide identical to endogenous GnRH that stimulates the pituitary to release LH and FSH. Unlike HCG (which directly mimics LH at testicular level), gonadorelin works upstream by stimulating natural pituitary signaling. Very short half-life (2-40 min) is a major limitation. May help maintain testicular function during TRT but HCG is superior for fertility preservation. Often used as HCG alternative when HCG is unavailable.

A urinary-derived medication containing both FSH and LH activity (typically 1:1 ratio, 75 IU each per vial). Unlike HCG which only mimics LH, HMG provides FSH activity that directly supports spermatogenesis through Sertoli cells. Often combined with HCG for comprehensive fertility restoration after AAS use. Clinical case studies show successful reversal of steroid-induced azoospermia even after 1+ year of infertility.

A hypothalamic neuropeptide that acts as the master upstream regulator of the HPG axis by stimulating GnRH release. Binds to KISS1R (GPR54) on GnRH neurons, triggering pulsatile GnRH secretion. Available as Kisspeptin-10 (shorter half-life) and Kisspeptin-54 (longer half-life). Acutely increases LH roughly 2- to 3-fold, with more modest FSH and testosterone rises, in men. Theoretically attractive for PCT due to upstream mechanism, but short half-life and research status limit practical application.

A non-ergot dopamine agonist with high D3 selectivity (7-10x over D2). Used off-label for prolactin control during 19-nor steroid cycles. Key advantage over cabergoline: NO cardiac valve fibrosis risk (no ergot derivation). Key disadvantage: higher impulse control disorder risk (gambling, hypersexuality, compulsive behaviors) and requires daily dosing. Less potent than cabergoline for prolactin suppression but safer cardiac profile.

A stilbene polyphenol best known as a longevity and cardiometabolic supplement and a sirtuin (SIRT1) activator. Frequently stacked with NAD+ precursors on the theory that NAD+ fuels the sirtuins resveratrol activates. Its most important practical caveat for lifters is that it is a strong antioxidant, which is exactly why it can be a double-edged sword around training.

The most reproducibly life-extending pharmaceutical in mammals and the flagship of the longevity-drug community. Rapamycin is an mTOR inhibitor: at the low, intermittent (typically weekly) doses used for healthspan it is intended to inhibit mTORC1, a nutrient/growth sensor, to trigger autophagy and mimic aspects of caloric restriction, while sparing mTORC2. This is a fundamentally different use case from the daily immunosuppressive dosing it is FDA-approved for. Its most important practical caveat for lifters is that the very pathway it inhibits (mTOR) is the master switch for muscle protein synthesis, a real tension when the goal is muscle.

One of the two most popular oral NAD+ precursors (alongside NR). NMN sits one step closer to NAD+ than nicotinamide riboside in the salvage pathway and is taken to restore declining age-related NAD+ levels for longevity and cellular-energy goals. It raises blood NAD+ in humans without the flushing that high-dose niacin causes. See the NAD+ page for the shared biology, and TMG for the (mostly theoretical, for NMN) methyl-donor support angle.

A form of vitamin B3 and one of the two leading oral NAD+ precursors (alongside NMN). NR has the deepest human dataset of any NAD+ precursor. Multiple RCTs confirm it raises blood NAD+ safely and without the flushing of high-dose niacin. It is the precursor to reach for when you want the best-characterised human evidence. See the NAD+ page for the shared biology.

A yellow plant alkaloid best known for lowering blood glucose and improving lipids, popularly dubbed "nature's metformin" because it activates the same AMPK energy-sensing pathway. In head-to-head trials it rivals metformin for glycemic control. In the physique world its key role is as the support supplement for compounds that raise blood sugar, most notably MK-677, and as a general metabolic/longevity adjunct.

Trimethylglycine (betaine) is a naturally occurring methyl donor. It plays two roles that make it popular: it lowers homocysteine (via the BHMT remethylation pathway) supporting cardiovascular/methylation health, and it acts as an osmolyte with a modest ergogenic reputation for power and strength. In the longevity world it is the default "methyl support" paired with NAD+ precursors, though, honestly, that specific need is strongest with high-dose niacin rather than NMN/NR.

A polyamine present in all living cells and in many foods, spermidine is one of the few dietary compounds that reliably induces autophagy, the cellular "self-cleaning" process that declines with age. That autophagy link, plus epidemiological data associating higher dietary spermidine with lower cardiovascular and all-cause mortality, has made it a staple longevity supplement. Most supplements are wheat-germ-derived.

A calcium salt of alpha-ketoglutarate (AKG), a central intermediate of the TCA/Krebs cycle that also serves as a co-substrate for a large family of dioxygenase enzymes (including DNA and histone demethylases). Endogenous AKG levels fall with age, which is the rationale for supplementation. It is marketed as a longevity/biological-age supplement (e.g. Rejuvant). Be clear-eyed: the headline lifespan and 'biological age reversal' findings come from mouse studies and a small uncontrolled human dataset, not rigorous human trials.

A flavonol polyphenol best known as the leading candidate senolytic, a compound that selectively clears senescent ('zombie') cells that accumulate with age and secrete inflammatory signals. It is also a general antioxidant and anti-inflammatory. The distinctive practical feature is dosing: rather than daily use, senolytic protocols use short, high-dose pulses ('hit-and-run'), reflecting how senescent cells are cleared. Human evidence is early. Most of the strong data are still in mice.

A long-acting angiotensin II receptor blocker (ARB) used to lower blood pressure. Among ARBs it is uniquely also a partial agonist of PPAR-gamma, the target of the 'glitazone' insulin-sensitising drugs. That dual action: blood-pressure control plus favourable effects on insulin sensitivity and lipids, is exactly why it became the community-favourite blood-pressure drug for people on cycle, where androgens routinely drive blood pressure up.

A long-acting phosphodiesterase type-5 (PDE5) inhibitor, the drug in Cialis. It relaxes vascular smooth muscle, improving blood flow to the penis (erections), the prostate/bladder (urinary symptoms), and the vasculature generally (endothelial function, modestly lower blood pressure). Its long half-life makes it well suited to low-dose daily use, which is popular on cycle for erectile function, cardiovascular support, and 'better pumps.'

The most powerful acne drug available: an oral retinoid (13-cis-retinoic acid) that can produce long-term or permanent acne remission. In the PED context it is used for the severe acne that high androgen loads cause, particularly from strongly androgenic and DHT-derived compounds that overdrive the sebaceous glands. It is extremely effective, but it carries serious risks (severe birth defects, lipid and liver changes, mucocutaneous dryness, and debated mood effects) and demands monitoring.

A second-generation H1-antihistamine and mast-cell stabiliser used medically for allergy and asthma. Its relevance to physique athletes is a side property: it restores and upregulates beta-2 adrenergic receptor density. Because clenbuterol and other beta-2 agonists lose effect as those receptors downregulate within a couple of weeks, ketotifen is run to reset the receptors and extend the useful window of a clenbuterol cycle. It is sedating, so it is taken at night.

A compound formed when the body breaks down indole-3-carbinol (I3C) from cruciferous vegetables (broccoli, cabbage, kale). It is marketed as a natural way to 'control estrogen,' and it does influence estrogen, but by changing which estrogen metabolites are produced, not by lowering total estrogen. This distinction is the entire point: DIM is an estrogen-metabolism modulator, not an anti-estrogen, and it does not replace an aromatase inhibitor when a cycle actually needs estrogen suppressed.

An endogenous steroid hormone produced by the adrenal glands, gonads and brain, and one of the most abundant circulating steroids in humans. DHEA is a precursor ("parent") hormone: it is a metabolic intermediate in the biosynthesis of both the androgen and estrogen sex steroids, converting locally in tissues toward testosterone, DHT and estradiol. In the US it is sold over the counter as a dietary supplement and is also available as the drug prasterone.

A short-acting phosphodiesterase type-5 (PDE5) inhibitor, the drug in Viagra (erectile dysfunction) and Revatio (pulmonary arterial hypertension). It relaxes vascular smooth muscle and enhances blood flow, most famously to the penis. Its ~4-hour half-life makes it a fast-on, as-needed drug rather than a low-dose daily one like tadalafil. On cycle it is used for erectile function, 'pumps' and vascular/blood-pressure support.

N-Acetylcysteine (NAC) is a prodrug of L-cysteine, the rate-limiting building block the body uses to make glutathione, its master antioxidant. In medicine it is FDA-approved as the intravenous/oral antidote for paracetamol (acetaminophen) overdose and as an inhaled/oral mucolytic that thins mucus. In the enhancement world it is used on-cycle as cheap liver and antioxidant support, especially alongside oral steroids.

Nebivolol (brand name Bystolic) is a highly beta-1-selective beta-blocker with an added nitric-oxide-mediated vasodilating effect. It is FDA-approved for hypertension. Among enhanced users it is a favoured blood-pressure tool on cycle because, unlike older beta-blockers, its NO-driven vasodilation and beta-1 selectivity are associated with fewer reports of erectile dysfunction, fatigue and adverse lipid/metabolic effects.

Milk thistle is the common name for Silybum marianum, whose seed extract is silymarin, a standardised mixture of flavonolignans (silibinin/silybin, isosilibinin, silychristin, silidianin and others), of which silibinin is the major active constituent. It is one of the most popular liver-support supplements and is commonly run on-cycle alongside oral (17-alpha-alkylated) steroids. Honest caveat: for most liver conditions the clinical evidence is mixed and limited.

Pregnenolone is an endogenous steroid, synthesised from cholesterol, that sits at the very top of the steroid-hormone pathway. It is the precursor/metabolic intermediate for most steroid hormones (progestogens, androgens, estrogens, glucocorticoids and mineralocorticoids). It is also a neurosteroid with its own activity in the brain. In the US it is sold over-the-counter as a supplement, mainly promoted for mood, memory and cognition, claims that rest on weak, preliminary evidence.

A traditional Southeast Asian herbal remedy prepared from the root of Eurycoma longifolia. Marketed to bodybuilders and men as a natural testosterone booster, libido enhancer and anti-stress ("adaptogen") supplement. Honest caveat: available clinical research has found no significant effect of the supplement, so the popular hormonal claims are weakly supported at best.

One of the most studied adaptogenic herbs, used for centuries in Ayurvedic medicine and now sold widely (often as the standardised root extract "KSM-66") to reduce stress and anxiety, support sleep, and, in fitness circles, to modestly aid strength and recovery. It has more real human RCT data than most "natural test boosters," but the effects are modest and the overall evidence base is still described as tentative/insufficient.

A phytoecdysteroid (a subclass of ecdysteroids: steroidal compounds structurally related to cholesterol) found in plants such as Ajuga turkestanica, Vitex species and wheat. Heavily marketed as a natural muscle-building supplement, often with bigger claims than the better-studied ecdysterone. Human trial data specific to turkesterone is still minimal, the first published human trial (2024) tested only acute (single-dose) administration and found no significant anabolic signal.

Ecdysterone (20-hydroxyecdysone) is an ecdysteroid, a steroid hormone that controls moulting and metamorphosis in arthropods, also found in plants such as Rhaponticum carthamoides, Cyanotis vaga and Ajuga turkestanica. Sold as a "natural anabolic" supplement. Unlike most such products it has some human data, but that data is mixed and its strongest positive study is disputed.

A traditional West African (notably Nigerian, where the Hausa name "bakin gagai" is often translated as "black aphrodisiac") plant used as an aphrodisiac, sold today, often stacked with Tongkat Ali, as a natural testosterone booster. Its reputation rests on rodent experiments showing increased blood testosterone and sexual behaviour; there are no human trials, and the same research group reported adverse effects on the testes, liver, and kidneys at the same doses in follow-up studies.

A potassium-channel-opening vasodilator that is the only non-hormonal drug with FDA approval for androgenetic alopecia. It grows hair by pushing follicles out of the resting phase and extending the growth phase. It does NOT block DHT, so it treats the symptom rather than the cause. That makes it the one hair drug that works regardless of which compound is driving the loss, including the DHT-derivatives and 19-nors that finasteride cannot help with.

An antifungal shampoo that became a hair-loss adjunct after a 1998 study found the 2% formulation improved hair density comparably to 2% minoxidil. It is the third leg of the community "big three" (minoxidil, finasteride, ketoconazole), but the evidence behind it is genuinely thin compared with the other two, and the authors of the key study said as much themselves.

A non-steroidal topical androgen receptor antagonist originally developed by Roussel Uclaf for androgen-dependent skin conditions. It is the community answer to the one problem finasteride cannot solve, because it blocks the receptor itself rather than the enzyme that makes DHT, it theoretically works against ANY androgen, including DHT-derivatives and trenbolone, where 5-AR inhibitors are useless. That theory rests almost entirely on animal data. There is no published human trial.

A topical androgen receptor antagonist: the same mechanistic idea as RU58841, but actually taken through formal clinical trials. That makes it the most credible member of the topical-antiandrogen category. The results, however, are genuinely mixed: its US Phase 2 failed to separate from placebo, while later and longer Chinese trials reported clear statistically significant benefit.

The most clinically advanced topical antiandrogen for hair loss. Unlike RU58841 and pyrilutamide, clascoterone already has FDA approval in a related indication (acne, as Winlevi), and its hair-loss program has reported positive Phase III results from large trials run in the US and Europe rather than a single region.

The most commonly used "natural finasteride": a berry extract that inhibits 5-alpha-reductase weakly. The one head-to-head trial against finasteride is the honest summary of its value: it works, and it works considerably less well. It exists in this archive because people ask whether they can avoid finasteride, and the answer deserves a real number rather than a shrug.

One of the most potent statins available and the standard pharmaceutical answer to the lipid damage that steroid cycles cause. Oral 17-alpha-alkylated compounds in particular can crater HDL and drive LDL up sharply within weeks, an effect no amount of fish oil meaningfully offsets. This is the intervention that actually moves those numbers, and it is prescription medicine rather than a supplement.

The second-line lipid drug: used when a statin alone is not enough, or when statin muscle side effects limit the dose. It works on a completely different mechanism (blocking intestinal cholesterol absorption rather than hepatic synthesis), which is why it stacks additively with a statin rather than overlapping with it.

The most commonly taken supplement in this entire archive, and one where the honest evidence is narrower than the reputation. It genuinely and reliably lowers triglycerides in a dose-dependent way. Whether it reduces cardiovascular events is a far more contested question, two large trials of the same broad idea reached opposite conclusions.

The most popular "natural statin alternative" in bodybuilding circles, and the one people reach for when they want to address cycle-damaged lipids without a prescription. It has genuine randomized trial support, and the size of the effect it produces is roughly a fifth of what a statin does, which is the part that usually goes unmentioned.

The standard companion supplement to statin therapy. The rationale is mechanistically sound, statins suppress the pathway that produces CoQ10 as well as cholesterol, but the trial evidence on whether replacing it actually relieves statin muscle symptoms is genuinely split, with credible meta-analyses reaching opposite conclusions.

The most effective legal supplement in sports nutrition, and the yardstick this entire scale is calibrated against. If you take creatine, train hard and eat well, you are natty. The compound raises what your natural physiology can express without changing the physiology itself. Included here so the scale has an honest floor.

The most commonly used sleep aid, and relevant here because sleep is where recovery actually happens. The compounds people obsess over do far less than a consistently good night. It is also directly useful against the sleep disruption caused by several compounds in this archive, from late caffeine to trenbolone night sweats.

Best known here as the "A" in the ECA stack, where it was traditionally included to prolong the thermogenic effect. Its more important role for this population is cardiovascular, though the guidance on taking it preventively has moved substantially, and taking it because you are "on cycle" is not a supported reason.

The supplement industry's most heavily marketed "natural test booster" of the last decade, and one of the clearest cases in this archive where the controlled evidence went against the marketing. It is included specifically so the record is straight: in resistance-trained men, the trials show nothing, and the higher dose may be counterproductive.

One of the oldest and most persistent "natural test booster" ingredients, still found in a large share of testosterone support products. The systematic review evidence does not support the testosterone claim. It is included here so that anyone considering it can see what the trials actually found rather than what the label says.

A peptide hormone that is one of the most dangerous performance-enhancing drugs used in bodybuilding. Unlike steroids which cause health issues over time, insulin can kill within hours of a single miscalculated dose. Used by advanced bodybuilders to shuttle nutrients into muscle cells, but the margin for error is essentially zero.

An orally-active small molecule that inhibits nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed in fat tissue in obesity. NNMT normally clears nicotinamide by methylating it (spending a methyl group from SAM); blocking it is intended to recycle more nicotinamide back into NAD+, raise cellular NAD+, and increase metabolic rate in fat cells. It sits on the same NAD+/methylation axis as NAD precursors but works from the opposite direction, reducing NAD breakdown rather than adding raw material.

A wakefulness-promoting medication approved for excessive sleepiness from narcolepsy, obstructive sleep apnea and shift work sleep disorder. Described as a CNS stimulant / atypical dopamine reuptake inhibitor, it is widely used off-label as a cognitive enhancer. Approved in the US in 1998 and sold as Provigil among other brands.

A natural choline compound found in the brain that acts as an acetylcholine precursor. Alpha-GPC rapidly delivers choline across the blood-brain barrier, where it is used to make acetylcholine. It is sold as a nootropic/pre-workout supplement and, in several countries, prescribed as choline alfoscerate for cognitive decline.

A synthetic dipeptide (N-phenylacetyl-L-prolylglycine ethyl ester) developed in Russia and promoted as a nootropic. It is a prodrug of cyclic glycine-proline (cycloprolylglycine) and is an analog of piracetam. It is not FDA-approved; human evidence is limited.

A stimulant nootropic that is the 4-phenyl-substituted analogue of piracetam. It was developed in 1983 as a medication for Soviet cosmonauts (Russian Academy of Sciences, Institute of Biomedical Problems). It is characterised as a selective atypical dopamine reuptake inhibitor and is used for cognition, stress tolerance and fatigue - and is prohibited in-competition by WADA.

An oligopeptide drug derived from angiotensin IV (full name N-hexanoic-Tyr-Ile-(6) aminohexanoic amide), developed in Joseph Harding's laboratory at Washington State University. In animal models it is an extraordinarily potent procognitive and synaptogenic agent, working through the hepatocyte growth factor (HGF) / c-Met receptor system. It is preclinical only, no completed human trials, and is sold online as an unregulated "nootropic" research chemical.

Methylthioninium chloride, methylene blue, is a phenothiazine-derived dye and medication (a dark green powder that dissolves to a deep blue solution). Medically it is the FDA-approved antidote for methemoglobinemia. It has become a fashionable low-dose nootropic and 'longevity' supplement because it can act as an alternative electron carrier in mitochondria. Its established medical use is solid; its cognitive/anti-aging use is trend-driven and unproven, and it carries genuine interaction risks.