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Author: kodiac

Methamphetamine (Research)

Plain-language summaryIntrigue 60 / 100

Methamphetamine is the N-methylated cousin of amphetamine. The extra methyl group makes it more lipophilic and substantially better at crossing into the brain, so d-methamphetamine releases central dopamine roughly five times more potently than d-amphetamine on a per-milligram basis. It actually has FDA approval as Desoxyn (1944) for ADHD and obesity, though prescriptions are vanishingly rare; the public knows it primarily as the illicit Schedule II drug. Same mechanism as amphetamine: reverses the monoamine transporters to force release rather than blocking reuptake. The l-enantiomer is the active component of Vicks Vapor Inhaler, which is a strange historical footnote. Used in research as a high-potency reference monoamine releaser. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundFederally scheduled

38/100

Textbook monoamine releaser with real reference value but settled science and Schedule II friction throughout

Look, methamphetamine occupies a genuinely strange position in a research library. It’s Schedule II, massively studied, FDA-approved since 1944, and its pharmacology is about as well-characterized as any small molecule in existence. That combination of thorough understanding and intense regulatory burden makes it a difficult call for most programs.

The mechanism isn’t interesting from a discovery standpoint. Reverse transport at DAT, NET, and SERT with preferential dopamine release is chapter one of stimulant pharmacology. The N-methyl group relative to amphetamine confers greater CNS penetration and a roughly 5-fold potency advantage at central dopamine release, but the N-methylation story was settled decades ago. There’s no unexplored receptor interaction here, no second target that opens up new biology, no emerging indication that changes the calculus. We’ve read every chapter of this book.

Where methamphetamine retains genuine bench value is as a reference standard. If your program involves characterizing novel DAT substrates or inhibitors, running abuse-liability profiling on candidate stimulants, or building monoaminergic neurotoxicity models, meth is the positive control you benchmark against. The striatal dopaminergic neurotoxicity it produces in rodents is a real and reproducible research model, used extensively by the Ricaurte lab and others to probe the limits of monoaminergic resilience and recovery. That role doesn’t go away just because the compound is old.

But here’s the thing: d-amphetamine sulfate does most of the same jobs. For a research program that needs a monoamine releaser reference, amphetamine serves nearly all the same functions with a slightly cleaner regulatory profile (still Schedule II, but more familiar to institutional DEA coordinators). Meths advantages, specifically the enhanced CNS penetration and longer 9-12 hour half-life, matter in specific experimental designs but don’t build a compelling case for general library inclusion.

The evidence quality is excellent in the sense that everything about this compound is known. That’s actually the scoring problem. You can’t rate high on novelty, mechanism promise, or differentiation when the science is essentially finished. The translational signal is clear and thoroughly replicated, but there’s nothing new being translated. Where researchers are doing interesting work adjacent to this compound, they’re typically using it as a tool, not studying it as a discovery target.

What we’d say to bench scientists: procure it if your specific research program requires a high-potency monoamine release reference or an addiction neurobiology stimulus with decades of precedent literature. Don’t add it speculatively. The DEA Schedule II overhead, storage requirements, and institutional scrutiny are real costs, and they aren’t worth paying unless the experimental question specifically demands this compound rather than a functional analog with fewer compliance hurdles.

Novelty

10

Mechanism promise

18

In-category differentiation

32

Evidence quality

78

Translational signal

60

Research bench value

50

Rationale Methamphetamine scores low on novelty and mechanism because its pharmacology is essentially finished knowledge, but retains meaningful bench utility as a DAT/NET reference standard and addiction neuroscience model compound. The Schedule II cap of 65 does not bind because the weighted score lands at 38 on its own merits.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

N-methylated phenethylamine stimulant

The N-methylated analog of amphetamine; FDA-approved (Desoxyn) for ADHD and obesity but principally encountered as an illicit drug; a research-grade pharmacology probe.

Abstract

Methamphetamine (N-methyl-1-phenylpropan-2-amine; CAS 537-46-2; molecular formula C10H15N; molecular weight 149.23) is the N-methylated analog of amphetamine, approved by the FDA in 1944 (Desoxyn) for narcolepsy, ADHD, and obesity. Mechanism is the same as amphetamine (monoamine release via reverse transport) with greater CNS penetration owing to the increased lipophilicity from N-methylation. The d-enantiomer (d-methamphetamine) is approximately 5-fold more potent than d-amphetamine at central dopamine release; the l-enantiomer (l-methamphetamine) is the active component of Vicks Vapor Inhaler. Plasma half-life is approximately 9 to 12 hours. Schedule II prescription drug; principally encountered as illicit Schedule II. Used as a research-grade reference compound for monoamine release pharmacology and as a clinical (rare) ADHD medication.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 9, 2026
Mazindol

Plain-language summaryIntrigue 50 / 100

Mazindol is a tetracyclic compound that inhibits norepinephrine reuptake (NET, with potency around 30 nM) plus weaker dopamine and serotonin reuptake. Critically, it is a true reuptake inhibitor, not a transporter-reversing releaser like amphetamine. FDA-approved in 1973 (Sanorex, Mazanor) as a short-term obesity drug, withdrawn from the US market in 2001 when the appetite-suppressant category collapsed. Recently NLS Pharmaceutics has revived it as a controlled-release formulation for narcolepsy with cataplexy and ADHD. Useful as a non-amphetamine reference NRI/DRI in pharmacology research, particularly for investigators who want monoamine-uptake inhibition without the release pharmacology. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

39/100

A half-century-old withdrawn anorectic with modest renewed interest in narcolepsy and ADHD

Look, mazindol has a story, but it’s mostly a story about what used to matter. FDA approved in 1973 as Sanorex and Mazanor, withdrawn from the US market in 2001 when the anorectic category got picked apart by post-fen-phen regulatory scrutiny. What remained is a tetracyclic scaffold with a genuinely interesting pharmacological property: it inhibits NET (Ki around 30 nM), hits DAT weakly, and touches SERT even more weakly, but it does all of this as a true reuptake inhibitor rather than a transporter-reverser like the amphetamines. That distinction matters mechanistically. Amphetamines force transporters into reverse gear; mazindol just sits in them. The behavioral and abuse-liability profiles diverge from that mechanistic difference, and thats the main reason it remains a useful reference compound for investigators who need to parse reuptake inhibition from release in catecholamine pharmacology studies.

The contemporary angle is NLS Pharmaceutics, a Swiss company that has been running controlled-release mazindol through trials for narcolepsy with cataplexy and ADHD. Their phase 2 and phase 3 work represents the most credible recent human data for this compound. The narcolepsy signal is real enough that it generated legitimate clinical interest, and the non-amphetamine, non-releasing profile is exactly what that indication needs from a regulatory and tolerability standpoint. So it’s not dead. But we have to be honest about what the ceiling is here: the mechanism is NE/DA reuptake inhibition in 2024, a category that already has atomoxetine, methylphenidate, viloxazine, and modafinil competing for attention. Mazindol doesn’t dominate any of those comparisons on mechanism promise or differentiation.

What we actually like about it is the bench tool angle. As a high-affinity NET ligand with known transporter selectivity, it remains a credible probe for investigators studying sympathomimetic vs. releasing-agent effects, or for studies that need a non-releasing NRI control arm. It’s not exciting in the way that a triple agonist or a mitochondrial peptide is exciting, but it earns its slot in a research library as a reference compound with a long pharmacological history and a clear mechanistic profile.

What we don’t like: the evidence base is aging and fragmented. Historical obesity data is mostly low-quality by modern standards. The NLS trials are the most current and rigorous data, but they’re narrow in indication scope. Replication outside that consortium is thin. The compound is Schedule IV, which adds procurement overhead for any lab that wants to work with it seriously. For most research programs, atomoxetine or methylphenidate will answer the same questions with less regulatory friction. Mazindol earns a place as a niche tool, not as a priority target.

Novelty

25

Mechanism promise

35

In-category differentiation

35

Evidence quality

50

Translational signal

52

Research bench value

45

Rationale Mazindol is a 1973-approved, 2001-withdrawn Schedule IV anorectic. The NLS Pharmaceutics controlled-release narcolepsy program gives it some contemporary signal, but the compound itself is old, the mechanism (NRI/weak DRI) is mechanistically unremarkable by today’s standards, and differentiation from existing approved options is thin. Schedule IV cap (75) does not bind at the calculated score of 39.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Tetracyclic norepinephrine reuptake inhibitor (anorectic)

A tetracyclic NRI with weak DAT and SERT activity; a discontinued anorectic agent investigated for narcolepsy and ADHD.

Abstract

Mazindol ((R/S)-5-(4-chlorophenyl)-2,5-dihydro-3H-imidazo[2,1-a]isoindol-5-ol; CAS 22232-71-9; molecular formula C16H13ClN2O; molecular weight 284.74) is a tetracyclic norepinephrine reuptake inhibitor with secondary dopamine transporter inhibition, originally approved by the FDA in 1973 (Sanorex, Mazanor) for short-term obesity treatment. Withdrawn from the US market in 2001. Mechanism: NET inhibition (Ki approximately 30 nM) with weak DAT and SERT inhibition; distinct from amphetamines by being a true reuptake inhibitor rather than a transporter-reversing releaser. Plasma half-life is approximately 10 hours. Recent development by NLS Pharmaceutics has investigated mazindol controlled-release for narcolepsy with cataplexy and ADHD. Used as a non-amphetamine reference NRI/DRI compound.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 9, 2026
Synephrine

Plain-language summaryIntrigue 42 / 100

Synephrine is an alkaloid from bitter orange peel (Citrus aurantium) that became a bestselling thermogenic supplement after the FDA banned ephedra in 2004. Structurally it resembles phenylephrine, but it preferentially activates beta-3 adrenergic receptors over the alpha-1 and beta-1 receptors that drive blood pressure changes. The beta-3 activity stimulates fat oxidation and thermogenesis in adipose tissue, which is the basis of the weight-loss claims. Clinical evidence for actual fat loss is modest at best. Plasma half-life is about two hours. Used as a beta-3-preferring adrenergic agonist in metabolic research and as the workhorse stimulant ingredient in many over-the-counter weight-loss formulas. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

27/100

Outcompeted beta-3 agonist with modest evidence, useful only as a reference standard

Look, synephrine got its moment in the sun after the 2004 ephedra ban, and that moment is over. It’s a phenylethanolamine alkaloid from bitter orange with a preference for beta-3 adrenergic receptors over the alpha-1 and beta-1 activity that got ephedra pulled in the first place. That selectivity profile was genuinely interesting in the supplement context circa 2005. In 2026, it’s a textbook example of a compound the research frontier has lapped.

The mechanism isn’t wrong. Beta-3 adrenergic receptors are real targets expressed in adipose tissue and other metabolic compartments, and agonism there does drive thermogenesis via cAMP-mediated lipolysis. The problem is synephrine does this modestly, and we now have far better tools for studying this receptor system. Mirabegron, a pharmaceutical-grade selective beta-3 agonist with solid PK data and actual receptor selectivity characterization, is the obvious bench choice for any serious beta-3 adrenergic research program. Synephrine’s selectivity is partial at best, its potency is low, and the signal-to-noise ratio for controlled experiments is poor compared to purpose-built probes.

The clinical literature reflects exactly this. Multiple small trials have looked at synephrine for thermogenesis and body weight endpoints. The honest read: effect sizes are small, the data isnt compelling by any rigorous standard, and no serious phase 2 or 3 program is chasing it. The broader adrenergic and metabolic pharmacology space has moved to GLP-1 biology, beta-3 selective drugs with actual selectivity data, and mitochondrial targets with novel mechanisms. Synephrine is watching from the parking lot.

What we don’t like about it as a research compound is the ceiling problem. Even a clean, well-powered synephrine study in 2026 just confirms what’s already known about a mechanism that’s already been characterized in depth. The evidence base is decent by supplement standards (multiple small clinical studies, some methodological replication), but that bar is low and the information value per experiment is low. A landmark paper is not coming out of this compound.

The only scenario where it earns bench time today is narrow: comparative pharmacology where you need a weak beta-3 agonist as a reference alongside something more interesting, or structure-activity work in the phenylethanolamine chemical series. That’s a limited application, and most programs would reach for mirabegron or a custom ligand instead. We score it where it belongs: well-understood, outcompeted, modest evidence, and limited utility for anything a frontier investigator would care about right now.

Novelty

20

Mechanism promise

28

In-category differentiation

22

Evidence quality

38

Translational signal

32

Research bench value

25

Rationale Synephrine’s beta-3 adrenergic selectivity was genuinely interesting post-ephedra but is now thoroughly characterized and outcompeted by purpose-built pharmaceutical probes like mirabegron; clinical evidence exists but effect sizes are small, replication is weak by serious trial standards, and the information yield per experiment is too low for anything on the current research frontier.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Adrenergic agonist (bitter orange alkaloid)

p-Synephrine; a phenylethanolamine alkaloid from Citrus aurantium (bitter orange); a beta-3 adrenergic-preferring agonist used as a thermogenic supplement.

Abstract

Synephrine (p-synephrine, (R/S)-4-[1-hydroxy-2-(methylamino)ethyl]phenol; CAS 94-07-5; molecular formula C9H13NO2; molecular weight 167.21) is a phenylethanolamine alkaloid from Citrus aurantium (bitter orange) and other Citrus species. The compound is a structural analog of phenylephrine (the m-isomer) with a beta-3 adrenergic preference (relative to alpha-1 and beta-1) that distinguishes its pharmacology. The beta-3 activity drives thermogenesis and fat oxidation in adipose tissue, the basis for its supplement use as a weight-loss aid. Synephrine became prominent after the 2004 FDA ban on ephedra (which contained the more potent ephedrine). Clinical evidence for weight-loss effect is modest. Plasma half-life is approximately 2 hours. Used as a beta-3-preferring adrenergic agonist in metabolic research and supplement formulations.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 9, 2026
Higenamine

Plain-language summaryIntrigue 38 / 100

Higenamine is a benzylisoquinoline alkaloid found in lotus, aconite, and several traditional Chinese medicine herbs. It acts as a beta-2-preferring adrenergic agonist (with weaker beta-1 activity), giving it a pharmacological profile loosely similar to clenbuterol but at much lower potency. Marketed in pre-workout supplements for vasodilation and mild stimulant effects. WADA banned it in competition. The plasma half-life is extremely short, on the order of 6 to 18 minutes, which limits how long any effect lasts. The actual clinical evidence in humans is sparse and the supplement industry uses are mostly extrapolated from beta-agonist class effects. Botanical beta-adrenergic reference compound. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

26/100

Weak botanical beta-2 agonist outcompeted by synthetics on every relevant research dimension

Look, higenamine has enough pharmacology to take seriously as a compound. It’s a benzylisoquinoline alkaloid with genuine beta-2 adrenergic agonist activity, WADA bans it in competition, and the TCM tradition around Aconitum and Nelumbo nucifera isn’t nothing. But real pharmacology isn’t the same as an interesting research target, and on the dimensions we actually care about, higenamine doesn’t clear the bar.

The mechanism story is familiar to the point of being boring. Beta-2 adrenergic agonism is one of the best-characterized receptor biology stories in all of pharmacology. Clenbuterol, albuterol, salmeterol, formoterol: the synthetic beta-2 agonist space is extraordinarily well-trodden. Higenamine adds secondary beta-1 and trace beta-3 activity, but at substantially lower potency than the synthetic tools and with a plasma half-life sitting somewhere between 0.1 and 0.3 hours. That kinetic profile is a real problem for bench work. You can barely establish a steady-state exposure before you’re already measuring decay.

On differentiation, higenamine loses to its synthetic counterparts on almost every axis. If you want to probe beta-2 receptor biology, isoproterenol and clenbuterol are more potent, better characterized, and carry vastly more supporting literature. If you want a botanical probe for ethnopharmacology or alkaloid chemistry, the compound is interesting as one alkaloid in a complex botanical matrix, but thats a narrow use case that doesn’t justify prioritizing it as a primary research object. The idea that natural origin confers special research value over synthetic alternatives has limited support once you examine the pharmacokinetics honestly.

The evidence base reflects its supplement-industry trajectory more than rigorous science. Case reports of cardiovascular adverse events, a handful of pharmacokinetic characterization studies, and receptor-binding data constitute most of the serious literature. The WADA ban confirms real physiological activity, but banning something in sport isn’t a substitute for a replicated mechanistic evidence base. There are no multi-lab mechanistic studies, no phase 2 data, no serious signal that this compound does something synthetic alternatives or the underlying botanical pharmacology doesn’t address better.

We think higenamine has narrow value as a reference probe for investigators specifically interested in the adrenergic pharmacology of benzylisoquinoline alkaloids, and not much beyond that. The half-life is a liability, the potency is modest, and the literature is thin enough that almost any other direction in beta-adrenergic research would be more productive. It’s not junk. But it’s not a priority, and a bench scientist looking for a worthwhile allocation of time should pass.

Novelty

25

Mechanism promise

22

In-category differentiation

20

Evidence quality

27

Translational signal

32

Research bench value

35

Rationale Higenamine scores low on novelty and differentiation because beta-2 adrenergic agonism is an extremely saturated mechanism space, and higenamine is outperformed on potency, half-life, and literature depth by synthetic alternatives. Bench value is minimal outside narrow alkaloid pharmacology niches.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Beta-2 adrenergic agonist (botanical)

A benzylisoquinoline alkaloid found in lotus and aconite; a beta-2 adrenergic agonist used in pre-workout supplements.

Abstract

Higenamine ((R/S)-1-(4-hydroxybenzyl)-1,2,3,4-tetrahydroisoquinoline-6,7-diol; CAS 5843-65-2; molecular formula C16H17NO3; molecular weight 271.31) is a benzylisoquinoline alkaloid found in Aconitum, Tinospora cordifolia, Nelumbo nucifera (lotus), and other plants. The compound is a beta-2-preferring adrenergic agonist with secondary beta-1 and limited beta-3 activity; the agonist profile is qualitatively similar to clenbuterol with substantially lower potency. Used in traditional Chinese medicine for cardiac and respiratory indications. Marketed as a pre-workout supplement ingredient for vasodilation and mild stimulant effects. WADA-banned in competition. Plasma half-life is approximately 0.1 to 0.3 hours, very short. Used as a botanical beta-adrenergic agonist in research.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 9, 2026
Hordenine

Plain-language summaryIntrigue 35 / 100

Hordenine (N,N-dimethyl-tyramine) is a phenethylamine alkaloid found in germinating barley and several cacti. It is a weak MAO-B inhibitor and a weak monoamine reuptake inhibitor, and the combination slows the breakdown of dopamine and short-lived trace amines like beta-phenylethylamine (PEA). The supplement use angle is to pair it with PEA, where the MAO-B inhibition extends PEA’s normally minutes-long duration into something noticeable. Plasma half-life is one to two hours. The actual pharmacological effects in humans at supplement doses are modest, and most enthusiasm comes from extrapolation rather than human trials. Botanical MAO-B reference compound. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

22/100

Weak botanical MAO-B inhibitor with a narrow PEA-extension niche and no compelling independent research case

Look, hordenine isn’t a bad compound. It’s just not an interesting one, and those are different problems. N,N-dimethyl-tyramine has been in the literature long enough that its pharmacological ceiling is well-understood, and that ceiling is low. Weak MAO-B inhibition, weak monoamine reuptake inhibition, plasma half-life around 1-2 hours. Nothing there surprises anyone who’s read the trace amine literature from the last two decades.

The mechanism isn’t without logic. MAO-B catabolizes beta-phenylethylamine aggressively, which is why PEA’s endogenous half-life is measured in minutes despite its potent monoaminergic effects. Hordenine slows that degradation, so stacking it with PEA extends PEA’s window of action. That’s the entire scientific case for hordenine as a research-relevant compound, and its essentially a delivery-extension story, not a primary mechanism story. We like that the trace amine/TAAR1 space has gotten serious attention in the last decade, but hordenine isnt the probe you reach for when you want to study it properly.

On differentiation, hordenine loses badly to actual pharmacological MAO-B inhibitors. Selegiline is selective, potent, and has a massive preclinical and clinical literature. Rasagiline similarly. Safinamide adds a sodium channel component that gives it real mechanistic depth. Hordenine against those tools is like using a butter knife for something that needs a scalpel. Its botanical origin is sometimes cited as a feature, and we suppose it is if you’re running naturalistic formulation studies, but that’s a thin reason to prioritize it on a serious bench program.

Evidence quality is limited. Theres reasonable in vitro and rodent preclinical data supporting the MAO-B inhibitory activity, but multi-lab replication is sparse and human-facing data at supplement-relevant doses is essentially observational and anecdotal. The pharmacodynamic effects in humans are described uniformly as modest, which is consistent with the weak binding affinities measured in vitro. No robust phase 1 or 2 clinical work anchors the human translation.

Honestly, the only scenario where hordenine earns a place in an active research program is if the program specifically needs a botanical source of mild MAO-B modulation, or if PEA pharmacokinetics are the direct object of study. Both are narrow. Outside those cases, its a mature, well-understood adjunct compound that doesn’t open new questions, doesnt offer unique probe value, and doesn’t differentiate from better tools. A serious investigator would deprioritize this in favor of almost anything else in the phenethylamine or trace amine space.

Novelty

22

Mechanism promise

22

In-category differentiation

18

Evidence quality

25

Translational signal

20

Research bench value

28

Rationale Hordenine scores low across every axis because it’s a decades-old, well-characterized botanical alkaloid whose pharmacology is unremarkable: weak MAO-B inhibition, weak monoamine reuptake inhibition, modest human effect size at supplement doses, and zero differentiation from superior pharmacological tools in its class. Its only credible research angle is as a botanical adjunct extending PEA’s short half-life, which is a narrow probe application rather than a standalone research program.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Phenethylamine MAO-B inhibitor / mild stimulant

N,N-dimethyl-tyramine; a phenethylamine alkaloid found in barley sprouts; a weak MAO-B inhibitor used as a stimulant adjunct.

Abstract

Hordenine (N,N-dimethyl-tyramine; CAS 539-15-1; molecular formula C10H15NO; molecular weight 165.23) is a phenethylamine alkaloid found in germinating barley (Hordeum vulgare) and several cacti. The compound is a weak monoamine oxidase B inhibitor and a weak monoamine reuptake inhibitor; the combined activity slows the degradation of dopamine and trace amines including beta-phenylethylamine (PEA), prolonging their action. Used as a supplement, particularly in combination with PEA where the MAO-B inhibition extends PEA’s normally minutes-long duration. Plasma half-life is approximately 1 to 2 hours. The pharmacological effects in humans at supplement doses are modest. Used as a botanical MAO-B inhibitor in research and in supplement formulations.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 9, 2026
Testosterone (Research)

Plain-language summaryIntrigue 75 / 100

Testosterone is the principal androgen in humans, made from cholesterol in the testes (men) and ovaries plus adrenals (women). It is the foundational compound of androgen pharmacology and the active ingredient in essentially all testosterone replacement therapy plus the backbone of most non-medical anabolic steroid stacks. It binds the androgen receptor directly and is also converted on the fly into dihydrotestosterone (more potent androgen) by 5-alpha-reductase, and into estradiol by aromatase. Sold as cypionate, enanthate, propionate, undecanoate, plus gels and patches, with each ester releasing testosterone over different timescales. Schedule III in the US. The reference androgen receptor agonist for nearly all related research. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundResearch workhorse

44/100

Canonical AR reference compound; foundational but thoroughly mapped, with frontier interest squarely elsewhere

Look, testosterone occupies a genuinely strange position in any research library. It’s the foundational androgen – first isolated by David, Dingemanse, Freud, and Laqueur in 1935, structure confirmed by Butenandt and Ruzicka (Nobel, 1939), and under continuous clinical deployment ever since. At this point, the AR pharmacology is about as well-characterized as receptor biology gets. Ki of roughly 0.5 nM at AR, 5-alpha-reductase conversion to the more potent DHT, aromatase conversion to estradiol. We know this chemistry cold. Thats not a criticism; its just the reality of a compound that has been under rigorous investigation for ninety years across thousands of labs.

The mechanism doesn’t earn novelty points here. Single-receptor agonism in the most saturated steroid class in pharmacology. The interesting research questions around androgen biology, tissue selectivity, AR coactivator recruitment, non-genomic signaling pathways: those are now answered more cleanly with SARMs and selective AR modulators designed specifically to probe those dimensions. If you want to study differential anabolic-to-androgenic ratios, LGD-4033 or RAD-140 are sharper instruments. If you want AR pathway studies without aromatization confound, you need to block aromatase anyway. Testosterone does AR agonism and aromatization simultaneously, which is a physiological feature but a research design confounder.

What actually scores well here is evidence quality and translational signal, and those scores are real. FDA approval for hypogonadism across multiple ester formulations (cypionate, enanthate, propionate, undecanoate). Decades of replicated RCTs, well-characterized PK across routes of administration, solid safety profiling across hematocrit, lipid, and hormonal endpoints. If you’re building a disease model around male hypogonadism or studying androgen-mediated muscle protein synthesis in a clinical context, this is your reference compound, full stop.

Where we find genuine bench value is specifically in the reference probe role. AR binding competition assays, androgen-responsive cell line studies (LNCaP, LAPC4), steroidogenesis pathway models, castration-and-replacement designs in rodents: testosterone is the canonical standard against which everything else is calibrated. That role keeps the bench value score from collapsing. But it’s not a compound you reach for because you’re curious about what it does. You reach for it because you need to establish what something else does relative to it.

Honestly, the overall score here reflects one simple fact: testosterone is so thoroughly understood that the primary research questions it can answer are mostly already answered. The frontier in androgen biology has moved to selective modulators, non-steroidal AR ligands, the androgen receptor splice variants driving castration-resistant prostate cancer, and the complex crosstalk between androgen signaling and metabolic pathways. Testosterone stays in the library as a reference standard and clinical backbone. As an object of primary investigation in 2026, its not where serious investigators are finding new ground.

Novelty

10

Mechanism promise

20

In-category differentiation

42

Evidence quality

80

Translational signal

74

Research bench value

68

Rationale Testosterone scores high on evidence quality and translational signal (FDA-approved, multi-decade RCT base) but bottoms out on novelty and mechanism promise; it’s the prototype AR agonist in the most saturated steroid pharmacology class in existence, and the live research questions in androgen biology are now prosecuted more precisely with SARMs and selective probes. The Schedule III cap (75) does not bind because the weighted score lands well below it.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Endogenous androgen / anabolic-androgenic steroid

The principal endogenous androgen; the foundational compound of androgen pharmacology and the active component of TRT and many AAS regimens.

Abstract

Testosterone (17-beta-hydroxyandrost-4-en-3-one; CAS 58-22-0; molecular formula C19H28O2; molecular weight 288.42) is the principal endogenous androgen, biosynthesized from cholesterol via pregnenolone and progesterone in Leydig cells of the testis (males) and theca cells, ovary, and adrenal cortex (females). The compound is the prototype androgen receptor agonist and the foundation of androgen pharmacology. Pharmacologically, testosterone binds AR (Ki approximately 0.5 nM) and is converted to dihydrotestosterone (DHT) by 5-alpha-reductase (more potent AR agonist) and to estradiol by aromatase (estrogen receptor agonist). Approved as testosterone replacement therapy in male hypogonadism via various ester formulations: cypionate (weekly), enanthate (weekly), propionate (every 2 to 3 days), undecanoate (oral and depot), gels and patches (daily). Schedule III in the US under the CSA. The compound is the foundation of most anabolic-androgenic steroid (AAS) regimens used non-medically for muscle building. Plasma half-life of native testosterone is short (1 to 2 hours); ester formulations release the parent compound over days. Used as the canonical AR agonist in research.

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May 9, 2026
Estradiol (Research)

Plain-language summaryIntrigue 70 / 100

Estradiol (E2) is the principal endogenous estrogen, made from testosterone and androstenedione by the enzyme aromatase in ovary, fat, brain, and bone tissue. It is a high-affinity full agonist at both estrogen receptor subtypes (ER-alpha and ER-beta), driving classic gene-transcription effects plus rapid membrane-level signaling. Approved across many forms (oral, transdermal patch, gel, vaginal, injectable) for menopausal hormone therapy, postmenopausal osteoporosis prevention, hypoestrogenism in conditions like Turner syndrome, and as part of gender-affirming feminizing therapy. Pharmacokinetics depend heavily on route: oral undergoes large first-pass metabolism, while transdermal forms bypass the liver and produce more physiological plasma levels. Reference estrogen receptor agonist for endocrine research. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundResearch workhorse

45/100

The canonical endogenous estrogen: indispensable as a reference probe, biologically too mapped to excite frontier researchers

Look, estradiol isn’t a research compound in the sense the Kodiac library is trying to surface. It’s the endogenous estrogen. It’s been known since Doisy and Butenandt in the 1920s and 30s, it defines estrogen receptor pharmacology the way glucose defines glycolysis, and the mechanism is so thoroughly described that a first-year grad student can recite it: high-affinity full agonism at both ER-alpha and ER-beta (Ki around 0.1 nM at each), genomic effects through estrogen response elements, rapid non-genomic signaling through membrane-associated ER pools, aromatase as the biosynthetic gateway. There is nothing left to discover about what estradiol IS. The question is only ever what it DOES in some specific tissue, population, or formulation context that hasnt been nailed down yet.

That context matters, because the literature is genuinely enormous. The Women’s Health Initiative, the KEEPS trial, the E3N cohort, decades of transdermal vs oral comparative pharmacokinetics, the whole bioidentical vs conjugated equine estrogens debate, the ER-alpha vs ER-beta tissue selectivity question as it applies to bone, breast, cardiovascular, and CNS targets. The evidence base is as strong as anything in endocrine pharmacology. Multiple approved formulations across oral, transdermal, vaginal, and parenteral routes. If evidence quality alone drove the score, estradiol would be at the top of this list. But evidence quality is 15% of the rubric for a reason.

What we like: estradiol remains the reference probe you can’t avoid. Any investigator running ER biology needs it as a positive control and comparator. It’s the benchmark against which every SERM, SERD, and ER-selective agonist is calibrated. In that narrow but important role, its bench value is genuine and non-negotiable. The ongoing translational signal is also real, particularly in the neuroprotection, cardiovascular, and metabolic contexts where estrogen deprivation models are active research territory.

What we don’t like: as a frontier target, theres almost nothing here. The interesting estrogen receptor biology right now is happening in selective tools. ER-alpha vs ER-beta subtype selectivity probes, tissue-selective ER modulators, SERDs in oncology, the brain-specific ER-X question. Estradiol itself activates everything, which makes it blunt as a discriminating probe. If youre building a new research program around estrogen biology, estradiol is your positive control, not your compound of interest. The novelty score reflects that honestly: this is among the most mature, most-mapped pharmacology in the field.

The score of 45 is the right landing zone. High enough to acknowledge that it’s genuinely important and evidence-rich, low enough to be honest that a serious bench scientist wouldn’t pitch this as an exciting new direction. It’s what you reach for when validating an assay, not when designing a study.

Novelty

10

Mechanism promise

18

In-category differentiation

42

Evidence quality

82

Translational signal

78

Research bench value

72

Rationale Estradiol tanks on novelty and mechanism because ER-alpha/ER-beta pharmacology is among the most exhaustively characterized biology in all of endocrinology; it recovers meaningfully on evidence quality and translational signal (decades of RCTs, multiple approvals) and holds respectable bench value as the canonical ER reference probe, but that utility is increasingly eclipsed by selective ER modulators and degraders that can discriminate receptor subtype biology more cleanly.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Endogenous estrogen / ER-alpha and ER-beta agonist

17-beta-estradiol; the principal endogenous estrogen and the foundational compound of estrogen pharmacology.

Abstract

Estradiol (17-beta-estradiol, E2; CAS 50-28-2; molecular formula C18H24O2; molecular weight 272.39) is the principal endogenous estrogen, biosynthesized from testosterone (and androstenedione) by aromatase in ovary, adipose tissue, brain, and bone. The compound is a high-affinity full agonist at estrogen receptors ER-alpha and ER-beta (Ki approximately 0.1 nM at both), with downstream genomic effects on estrogen-responsive gene transcription and rapid non-genomic effects through membrane-associated signaling. Approved indications include menopausal hormone therapy (multiple oral, transdermal, vaginal, and parenteral formulations), prevention of postmenopausal osteoporosis, hypoestrogenism (Turner syndrome), and as part of gender-affirming feminizing hormone therapy. Pharmacokinetics depend strongly on formulation: oral micronized estradiol undergoes substantial first-pass metabolism; transdermal forms (patches, gels, sprays) bypass first-pass and produce more physiological plasma levels. Schedule N (non-controlled). Used as the canonical estrogen receptor agonist in research.

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May 9, 2026
Progesterone (Research)

Plain-language summaryIntrigue 65 / 100

Progesterone is the principal endogenous progestogen, built from cholesterol via pregnenolone in the corpus luteum, adrenal cortex, and (in pregnancy) placenta. It activates the progesterone receptor with high affinity and also has interesting side effects: it antagonizes mineralocorticoid receptors (driving sodium loss) and its metabolite allopregnanolone is a powerful positive modulator of GABA-A receptors (driving sedation). Approved for menopausal hormone therapy paired with estrogen for endometrial protection, IVF luteal support, secondary amenorrhea, and preterm birth prevention. Oral micronized progesterone hits the liver hard and produces sedating allopregnanolone, while vaginal and transdermal forms give cleaner PR effects. Plasma half-life of the parent is short (5 to 20 minutes). Canonical PR agonist. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

48/100

Canonical endogenous PR agonist; mature approved-drug evidence base, low novelty, infrastructure-grade bench tool

Look, progesterone is the compound you already have on the bench before you start designing experiments. It’s the canonical endogenous progestogen, the reference PR agonist against which everything else in its class gets compared. That’s a real and meaningful role. It’s just not what makes something an exciting research target in 2026.

The mechanism is worth unpacking because its actually more layered than the single-receptor framing suggests. High-affinity PR agonism drives the reproductive and endometrial effects everyone knows. Weak glucocorticoid receptor activity produces a mineralocorticoid-antagonist fingerprint that contributes to natriuretic effects. And first-pass hepatic conversion to allopregnanolone produces GABA-A positive allosteric modulation — which is why oral micronized progesterone (Prometrium) reliably produces sedation in a way vaginal forms don’t. That last piece is where the most interesting current biology lives. Brexanolone, which is essentially IV allopregnanolone, got FDA approval for postpartum depression in 2019, and the neurosteroid GABA-A PAM space is genuinely active right now. But the excitement is about synthetic neurosteroid analogs — zuranolone, ganaxolone, next-generation GABA-A selective compounds. Progesterone the compound is upstream infrastructure for that story, not the lead character.

The evidence base is as mature as it gets for a non-blockbuster pharmaceutical. Multiple phase 3 RCTs, approved across HRT, assisted reproductive technology, secondary amenorrhea, and intramuscular preterm birth prevention. The translational arrow is solid for those established uses. Where it gets instructive: the TBI neuroprotection story once looked promising. ProTECT II phase 2 showed signal, the mechanistic rationale was plausible, and then the ProTECT III trial was definitively negative. That failure matters — it’s a clean example of how compelling preclinical work and early phase 2 signal can collapse under a well-powered phase 3, and it appropriately cooled enthusiasm for progesterone as a neuroprotective research target.

For bench use, progesterone is straightforward infrastructure. It’s the reference standard for PR biology, reproductive physiology studies, and neurosteroid pathway work. Sourcing is genuinely easy — multiple suppliers with USP/EP-grade material, well-characterized reference standards widely available. Reconstitution for in vitro work is routine in ethanol or DMSO. Nothing technically demanding here.

What we dont love: novelty is essentially nil for the compound itself in 2026. The frontier science is at the level of synthetic neurosteroid analogs and selective PR modulators, not progesterone as a primary investigational compound. If you’re building a research program, progesterone is part of your toolkit, not your lead. It earns its place as a reference standard and a component of neurosteroid pathway studies, but it’s not where you’d place your exploratory bets. Score accordingly.

Novelty

20

Mechanism promise

40

In-category differentiation

45

Evidence quality

72

Translational signal

68

Research bench value

60

Rationale Progesterone is the reference-standard PR agonist with a thoroughly characterized multi-receptor pharmacology (PR, weak GR, GABA-A via allopregnanolone metabolite) and an approved-drug evidence base spanning HRT, ART, and preterm birth prevention. The interesting neurosteroid science has largely migrated to synthetic analogs like zuranolone and ganaxolone; progesterone itself scores low on novelty and differentiation, pulling the overall to 48 despite solid evidence and translational signal.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

Endogenous progestogen / PR agonist

The principal endogenous progestogen; a progesterone receptor agonist with luteal phase, gestational, and neurosteroid functions.

Abstract

Progesterone (pregn-4-ene-3,20-dione; CAS 57-83-0; molecular formula C21H30O2; molecular weight 314.46) is the principal endogenous progestogen, biosynthesized from cholesterol via pregnenolone in the corpus luteum, adrenal cortex, and (during pregnancy) placenta. The compound is a high-affinity progesterone receptor (PR) agonist with secondary effects at the glucocorticoid receptor (mineralocorticoid antagonism contributing to natriuretic effects) and at GABA-A receptors (the pregnanolone metabolite is a positive allosteric modulator producing sedation). Approved indications: menopausal hormone therapy (combined with estrogen for endometrial protection in women with intact uterus), assisted reproductive technology luteal support, secondary amenorrhea, and prevention of preterm birth (intramuscular formulation). Oral micronized progesterone (Prometrium) is highly subject to first-pass metabolism producing the sedating allopregnanolone metabolite; vaginal and transdermal forms produce more direct PR effects with less sedation. Plasma half-life is short (5 to 20 minutes for parent; metabolites variable). Used as the canonical PR agonist in research.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 9, 2026
Oxandrolone

Plain-language summaryIntrigue 55 / 100

Oxandrolone (Anavar, Oxandrin) is a synthetic anabolic steroid developed by Searle in 1962. The 17-alpha-alkylation makes it orally active by blocking liver breakdown, and the 2-oxa substitution shifts the profile toward anabolic (muscle-building) over androgenic (masculinizing) effects in standard assays. FDA-approved for severe weight loss after surgery, trauma, infection, or chronic illness, plus bone pain in osteoporosis. Burn recovery is the cleanest clinical use case, where AAS protocols have solid evidence. HIV wasting is another approved indication. In the gym world it is one of the most commonly diverted oral AAS because users perceive a relatively favorable side-effect profile. Schedule III. Hepatotoxic at high doses owing to the alkylation. Reference 17-alpha-alkylated oral AAS. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

39/100

Mature clinical AAS with replicated burn-recovery evidence but no novel mechanism or frontier research angle

Look, oxandrolone isnt a mystery. Searle synthesized it in 1962, the FDA approved it as Oxandrin, and its mechanism has been understood for decades. As a research compound it occupies a specific and well-defined niche: the canonical reference 17-alpha-alkylated oral AAS. That role gives it some legitimate bench value even now, but it doesnt make it an exciting primary research target.

The mechanism story is completely unsurprising. AR agonism with a higher anabolic-to-androgenic ratio than testosterone, achieved through the 2-oxa substitution at carbon-2 and the 17-alpha methyl group that confers oral activity by resisting hepatic first-pass metabolism. The Hershberger assay work defining its A:A ratio was done a long time ago. What you’re getting is a well-mapped receptor binding profile with no novel target biology, no dual or multi-target mechanism, and no new pharmacology. Single-receptor agonism in a saturated class is about as far from the frontier as you can get.

The clinical evidence is where this compound actually earns points. Burn recovery is one of the more rigorously studied applications of any AAS; pediatric burn trials and adult catabolic wasting data have been replicated across multiple institutions and form the basis of FDA approval. The HIV wasting indication is similarly evidence-backed. This isnt single-lab data or anecdote. There are genuine RCTs, modest N but replicated, and the translational signal in severe catabolic states is real. For a researcher studying anabolic signaling under physiological stress, oxandrolone is a legitimate clinical reference point with a credible evidentiary floor.

That said, nobody picking up oxandrolone for a new program is doing so because it opens a novel mechanistic door. Its differentiation within the AAS class is real but narrow: it’s the oral 17aa benchmark, the compound you reach for when you need a controlled comparison for hepatotoxicity studies or anabolic-to-androgenic ratio methodology. Thats a niche that matters, but it wont pull a lab into new territory. The interesting open questions, long-term IGF-1 modulation, interaction with the GH axis in burn patients, comparative hepatic impact of 17aa structures, are well-known to AAS specialists already and not the kind of questions attracting broad investigator interest in 2025.

What we like: FDA approval, replicated burn data, clean reference profile for comparative 17aa work. What we dont like: the mechanism has no new angles, the literature is decades old, and Schedule III classification adds real procurement and handling overhead for a compound that is unlikely to produce a surprising result. For a general research program not already invested in anabolic pharmacology, theres not much here that earns bench time over newer targets.

Novelty

18

Mechanism promise

22

In-category differentiation

35

Evidence quality

68

Translational signal

63

Research bench value

45

Rationale Oxandrolone scores low on novelty and mechanism because it is a fully mapped AR agonist from 1962 with no dual-target or novel pharmacology; it recovers modestly on evidence and translational signal through replicated RCTs in burn recovery and HIV wasting, and carries narrow bench value as the canonical reference 17-alpha-alkylated oral AAS. The Schedule III cap at 75 does not bind because the raw weighted score lands at 39.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

17-alpha-alkylated oral anabolic steroid

A 17-alpha-alkylated synthetic anabolic steroid; clinically used in burn recovery and HIV wasting; widely used in non-medical AAS contexts.

Abstract

Oxandrolone (17-beta-hydroxy-17-alpha-methyl-2-oxa-5-alpha-androstan-3-one; CAS 53-39-4; molecular formula C19H30O3; molecular weight 306.44) is a 17-alpha-alkylated synthetic anabolic-androgenic steroid (AAS) developed by Searle in 1962 and approved by the FDA (Anavar, Oxandrin) for severe weight loss following surgery, trauma, infection, or chronic illness; for relief of bone pain in osteoporosis; and for compensation of catabolic states. Mechanism: AR agonism (lower than testosterone but with relatively higher anabolic-to-androgenic ratio in the Hershberger assay). The 2-oxa substitution and 17-alpha alkylation produce oral activity (resistance to first-pass hepatic metabolism) and a more anabolic profile relative to androgenic. Plasma half-life is approximately 9 hours. Schedule III in the US under the CSA. Used in burn recovery (where AAS clinical use is well-established) and in HIV wasting; the most commonly diverted oral AAS for non-medical bodybuilding owing to a perceived favorable side effect profile. Used as a reference 17-alpha-alkylated oral AAS in research.

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May 9, 2026
Stanozolol

Plain-language summaryIntrigue 48 / 100

Stanozolol (Winstrol) is a 17-alpha-alkylated synthetic anabolic steroid developed by Sterling-Winthrop in 1962, distinguished by a pyrazole ring fused to the steroid A-ring. The fusion shifts the anabolic-to-androgenic ratio higher than testosterone and supports oral activity. FDA-approved historically for hereditary angioedema (largely replaced now by C1-inhibitor and icatibant) and a few other niche uses. Its place in popular memory belongs to Ben Johnson, whose 1988 Seoul Olympic 100m gold medal was stripped after a positive stanozolol test. Hepatotoxicity is the main limiting concern, the standard cost of 17-alpha-alkylation. Schedule III. Used in research as a reference oral AAS. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Our opinion on this compoundEstablished workhorse

37/100

A historically significant reference AAS with mature mechanism and declining research relevance

Look, stanozolol is not a mystery. It’s been around since 1962, it made Ben Johnson the most famous disqualified sprinter in history, and the mechanism is what you’d expect: androgen receptor agonism via a pyrazol-fused 17-alpha-alkylated backbone that shifts the anabolic-to-androgenic ratio favorably relative to testosterone. Sterling-Winthrop knew what they were doing structurally. But knowing what something does and finding it interesting in 2026 are different things.

The mechanism story starts and ends with AR binding. The pyrazole fusion at the A-ring is chemically clever for its era, and the oral bioavailability is real. What isn’t real anymore is the clinical urgency. The hereditary angioedema indication that got Winstrol its FDA approval has been largely displaced by C1-inhibitor concentrates and icatibant. Those agents are cleaner, better-tolerated, and don’t carry the hepatotoxicity liability that 17-alpha-alkylated steroids all share to varying degrees. The indication that justified the compound’s existence in the clinic is essentially a historical artifact at this point.

What we’re left with is a Schedule III reference compound. That’s not nothing. If you’re running AAS pharmacology studies, SHBG displacement work, or comparative androgen receptor affinity panels, stanozolol occupies a specific and well-characterized position in the reference set. The literature is extensive enough that you can contextualize your findings against a real body of evidence. That’s the bench value argument, and it’s legitimate but limited. Newer AAS analogs with more interesting selectivity profiles have appeared in the literature if your goal is genuinely advancing the mechanistic frontier.

The evidence quality is actually respectable for what it is. FDA approval, multi-decade use, clear pharmacokinetics, well-characterized toxicity. But high evidence quality on a mature well-understood compound is almost a negative signal for research interest. It means the question has already been answered. There’s no ambiguity left to resolve with stanozolol that hasn’t already been resolved, which is why the novelty score sits at the floor and drags the overall down hard.

Honestly, if you’re building a research program around androgen biology in 2026, the interesting questions are in selective androgen receptor modulators, tissue-selective AAS fragments, or non-steroidal AR modulators. Stanozolol tells you where that field came from, not where it’s going. We think it earns its place in the library as a reference compound, but we’d be doing investigators a disservice if we scored it as if it were an active frontier.

Novelty

18

Mechanism promise

22

In-category differentiation

35

Evidence quality

60

Translational signal

55

Research bench value

48

Rationale Stanozolol scores low on novelty and mechanism because it’s a 1962 oral AAS with well-understood AR agonism and an indication space that modern therapy has largely superseded; evidence quality and translational signal are genuine given FDA approval and decades of clinical use, but those points are offset by near-zero novelty and limited differentiation from a saturated class. Schedule III cap (75) does not bind; the raw weighted score of 37 reflects the compound’s historical-reference-only status.

Editorial commentary from Kodiac biolabs. Not a recommendation, not clinical advice. Research use only.

17-alpha-alkylated heterocyclic AAS

A pyrazol-fused 17-alpha-alkylated AAS; the steroid involved in the Ben Johnson 1988 Olympic doping case; clinically used historically for hereditary angioedema.

Abstract

Stanozolol (17-beta-hydroxy-17-alpha-methyl-5-alpha-androstano[3,2-c]pyrazole; CAS 10418-03-8; molecular formula C21H32N2O; molecular weight 328.49) is a pyrazol-fused 17-alpha-alkylated synthetic AAS developed by Sterling-Winthrop in 1962 and approved by the FDA (Winstrol) for hereditary angioedema and other indications. The pyrazole fusion at the A-ring increases the anabolic-to-androgenic ratio relative to testosterone and supports oral activity. Plasma half-life is approximately 9 hours (oral). Schedule III. The compound’s place in popular culture is dominated by the Ben Johnson case at the 1988 Seoul Olympics, where his 100m gold medal was stripped after positive testing for stanozolol. The clinical use in hereditary angioedema (rare, often replaced by C1-INH or icatibant in modern practice) demonstrates the compound’s effect on hepatic protein synthesis. Hepatotoxicity is the principal limitation. Used as a reference oral AAS in research.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

May 9, 2026

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