Skip to content

Shop
Scholar
Lab Results
Learn
Vote
Forum
About

Search Kodiac

Sign in Sign up Account

Category: Uncategorized

Maprotiline

Plain-language summaryIntrigue 42 / 100

Maprotiline (Ludiomil) is a tetracyclic antidepressant from Ciba-Geigy, approved in the US in 1980, that blocks the norepinephrine pump selectively while having very little effect on serotonin. That makes it pharmacologically distinct from the standard tricyclic antidepressants of its era, even though its side-effect profile (dry mouth, constipation, sedation) looks similar because it still blocks histamine and acetylcholine receptors as a side hobby. Its most notorious problem is seizure risk, which is the highest of any antidepressant and goes up sharply at high doses or with rapid titration. That alone has pushed it to the back of the prescribing line; few clinicians use it now when newer NRIs like atomoxetine are available. 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 Kodiac editorial, not peer-reviewed.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

28/100

A 1980 selective NRI being steadily replaced by cleaner, safer antidepressants with less seizure risk

Look, maprotiline is one of those compounds that made sense in 1980 and progressively less sense after that. Ciba-Geigy’s bridged anthracene scaffold gave it unusually selective NET inhibition — Ki around 11 nM, essentially silent at SERT — which was a reasonable pharmacological achievement when dual-mechanism TCAs were the baseline. The long plasma half-life, 21 to 52 hours, comes from that same rigid scaffold resisting CYP metabolism, which is actually an interesting structural story. We don’t want to dismiss the chemistry entirely.

But the mechanism, as a research object, isn’t doing anything new. Single-target NET reuptake inhibition is well-understood territory. Reboxetine does it cleaner. Atomoxetine does it cleaner. Viloxazine is the newer re-examination of that same noradrenergic thesis, with a more favorable safety window and growing pediatric/adult ADHD literature. Maprotiline’s H1 affinity (Ki approximately 2 nM) and muscarinic activity pile on a TCA-like side effect burden without any of the putative benefits that make mirtazapine’s noradrenergic plus H1 profile actually useful. It occupies an awkward middle ground: too dirty to be a clean NRI probe, not dirty enough to have the clinical versatility of older TCAs.

The seizure risk is the real problem for a research library context. At approximately 0.4 percent seizure incidence at therapeutic doses — the highest of any commonly used antidepressant — any in vitro or in vivo model involving maprotiline has to account for intrinsic CNS excitability effects that are off-target noise for most noradrenergic questions. That’s not a disqualifier for all studies, but it narrows the bench utility considerably.

Evidence quality is decent in the narrow sense: this is an approved drug with multi-site 1970s-80s clinical data, not a peptide riding on single-lab preclinical. But those trials were conducted under standards that wouldn’t pass modern scrutiny, effect sizes were modest, and there’s been no serious modern clinical reinvestigation. The translational signal exists — it works as an antidepressant, full stop — but that fact is not particularly interesting in 2025 when we have SSRIs, SNRIs, mirtazapine, and increasingly bupropion all offering better benefit-risk profiles for the same indication.

Honestly, the only scenario where maprotiline earns serious bench time is if a researcher specifically needs the long half-life pharmacokinetics as a variable, or is doing historical comparative work on NRI mechanisms. We dont see a compelling reason to prioritize it over cleaner NRI tools. It’s worth documenting in the library for completeness, but the score should reflect that the research conversation has largely moved on.

Novelty

22

Mechanism promise

20

In-category differentiation

12

Evidence quality

45

Translational signal

50

Research bench value

30

Rationale Maprotiline’s selective NET inhibition is mechanistically coherent but unremarkable, and its differentiation is actually negative — the seizure liability and TCA-like adverse profile make it strictly worse than modern comparators on most dimensions. Evidence quality is moderate given its approval-era trial base, but the compound is declining in use, not rising in research interest.

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

Tetracyclic norepinephrine reuptake inhibitor

A tetracyclic NRI with TCA-like side effects but selective noradrenergic action; significant seizure risk at high dose.

Abstract

Maprotiline (N-methyl-9,10-ethanoanthracene-9(10H)-propylamine; CAS 10262-69-8; molecular formula C20H23N; molecular weight 277.40) is a tetracyclic norepinephrine reuptake inhibitor developed at Ciba-Geigy and approved in the US in 1980 under the trade name Ludiomil. NET affinity is approximately 11 nM with very weak SERT activity (Ki greater than 1 microM), making the compound a selective NRI structurally classed with the tetracyclics owing to its bridged anthracene scaffold. Significant H1 (Ki approximately 2 nM) and muscarinic activity produces a side effect profile resembling tricyclic antidepressants: sedation, anticholinergic effects, weight gain. Plasma half-life is 21 to 52 hours, the longest of the antidepressant class, owing to the bridged scaffold’s resistance to CYP metabolism. The compound carries the highest seizure risk of any commonly used antidepressant (approximately 0.4 percent at therapeutic doses, increasing sharply in overdose). The seizure risk and TCA-like adverse profile have led to declining use in favor of mirtazapine and SSRIs.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-215Open in new tab →

Download PDF →

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
Toloxatone

Plain-language summaryIntrigue 38 / 100

Toloxatone (Humoryl) is a French reversible MAO-A inhibitor from Delalande, approved in France in 1984. Like moclobemide and pirlindole it can be displaced from the enzyme by dietary tyramine, which means patients can eat aged cheese without triggering a hypertensive crisis. The drug had a brief moment of relevance in French psychiatry but never spread to other markets, was not pursued for FDA approval, and was eventually discontinued in France in the 2000s as newer antidepressants displaced it. It is mostly of historical interest now, although it remains a useful research probe for MAO-A pharmacology because of its clean mechanism. 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

25/100

A 1984 French RIMA overtaken by moclobemide; minimal novelty, thin evidence base, shrinking research relevance

Look, toloxatone is a compound that made sense in 1984. Delalande was doing real chemistry, the RIMA concept was genuinely interesting at the time, and getting a reversible MAO-A inhibitor that didn’t require tyramine restriction was a meaningful step away from the irreversible MAOI era. We get that. But we’re not rating it for 1984.

The mechanism is single-enzyme competitive inhibition of MAO-A. That’s it. There’s no dual target story, no allosteric angle, no novel downstream pathway. MAO-A biology is about as well-mapped as neurochemistry gets at this point, and the RIMA concept was fully articulated and validated long before this compound hit its peak. Moclobemide became the reference RIMA because it has broader international approval, more trial data, and a cleaner pharmacological record. Toloxatone sits behind it on every dimension that matters to a working investigator.

The evidence situation is genuinely thin by current standards. French MDD trials from the 1980s were sufficient for a French approval in a different regulatory climate, but that literature hasn’t grown in any meaningful way. The compound never cleared regulatory review outside France. Clinical use has substantially declined, which is the field voting with its feet. There’s no live clinical program, no recent phase 2 data, nothing in ClinicalTrials.gov worth flagging. What you have is historical evidence that it works roughly as expected for a RIMA, which isn’t the same as having evidence that it does anything moclobemide doesn’t.

The only honest positive we can offer is the bench probe angle. The abstract notes it’s used as a reference oxazolidinone RIMA in mechanism studies, and thats real, if narrow. If you’re specifically studying the oxazolidinone scaffold or doing comparative binding work across RIMA chemotypes, toloxatone gives you a specific structural reference that moclobemide doesn’t. That’s a genuine, if limited, use case. But it doesn’t move the needle much for most programs.

Honestly, the compound reads like a chapter in the history of antidepressant pharmacology rather than an active research target. Investigators working on MAO biology will reach for moclobemide, harmaline derivatives, or clorgyline depending on selectivity needs. There’s no scenario where toloxatone is the first or second choice. The score reflects a real compound with real historical evidence that has been quietly made irrelevant by better alternatives and a mechanism that no longer surprises anyone.

Novelty

18

Mechanism promise

22

In-category differentiation

18

Evidence quality

32

Translational signal

38

Research bench value

28

Rationale Toloxatone scores low across the board because it’s a four-decade-old regional approval with no international uptake, a well-understood single-enzyme mechanism that moclobemide executes better, and an evidence base that never cleared the bar for approval outside France. The oxazolidinone scaffold gives it marginal probe identity but not enough to rescue the score.

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

Reversible MAO-A inhibitor

A 5-(hydroxymethyl)oxazolidinone RIMA approved in France in 1984; an early-generation reversible inhibitor of MAO-A.

Abstract

Toloxatone (5-(hydroxymethyl)-3-(3-methylphenyl)oxazolidin-2-one; CAS 29218-27-7; molecular formula C11H13NO3; molecular weight 207.23) is an oxazolidinone RIMA developed at Delalande in France and approved there in 1984 under the trade name Humoryl. The compound is a reversible competitive MAO-A inhibitor with a clinical profile broadly comparable to moclobemide; selectivity for MAO-A over MAO-B is approximately 50-fold at therapeutic concentrations. Plasma half-life is approximately 2 hours; hepatic metabolism is the primary clearance pathway. Tyramine restriction is not required at clinical doses. Clinical efficacy in major depressive disorder was demonstrated in French trials but the drug never received approval outside France and clinical use has substantially declined. Used historically and as a reference oxazolidinone RIMA in mechanism studies.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-230Open in new tab →

Download PDF →

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
Topiramate

Plain-language summaryIntrigue 68 / 100

Topiramate (Topamax) is a sugar-derived anticonvulsant from Johnson and Johnson, approved by the FDA in 1996. It hits multiple targets at once: blocks sodium channels, potentiates GABA-A receptors, blocks AMPA glutamate receptors, and inhibits carbonic anhydrase. The mechanistic breadth makes it useful well beyond epilepsy. It is approved for migraine prevention, where it is one of the more effective options. It has substantial off-label use for weight loss because the carbonic anhydrase inhibition produces a metallic taste that suppresses appetite, and for alcohol use disorder where it appears to reduce craving. The side effect signature includes word-finding difficulty (the patient slang is dopamax), tingling in hands and feet, and kidney stone risk. Co-formulated with phentermine as Qsymia for obesity. 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

50/100

Mature multifactorial anticonvulsant with real but narrowly concentrated bench utility in AMPA and glutamate programs

Look, topiramate is a compound that’s been around long enough to earn a nickname. “Dopamax” is what clinicians call it, a reference to the cognitive blunting that causes roughly 40 percent of patients to report word-finding difficulty and slowed mentation. That reputation didnt develop in a vacuum, and it tells you something real about what you’re working with when you put this molecule into a CNS research program.

What we actually find interesting isnt what a prescriber finds interesting. The five-target mechanism, state-dependent sodium channel inhibition, GABA-A potentiation at a non-benzodiazepine site, AMPA/kainate glutamate receptor antagonism, carbonic anhydrase inhibition across isozymes II and IV, and high-voltage calcium channel block, is genuinely unusual for a small molecule. You can source sodium channel blockers easily. GABA-A modulators are everywhere. The AMPA/kainate piece is the angle worth paying attention to, because topiramate remains one of the more pharmacologically accessible probes for AMPA receptor biology available to bench investigators. That has kept it relevant in CNS research programs even as its clinical novelty evaporated.

The evidence quality is not in question. Multiple phase 3 programs, FDA approval across four distinct indications, and decades of multi-site clinical data from populations in the tens of thousands. You dont have to speculate about whether topiramate produces a human signal. The question is whether the signal is interesting, and in most indications the answer is now mostly historical. The weight loss angle was differentiated in the Qsymia era, but GLP-1s have reframed that entire conversation and topiramate isnt competing there anymore.

The one area where current research still generates real signal is alcohol use disorder. Several controlled trials have shown suppression of craving and reduction in heavy drinking days, and the proposed mechanism, glutamatergic dampening of cue-induced salience, is both plausible and relatively underexplored compared to the naltrexone/acamprosate playbook. If your program touches AUD neuroscience or glutamate-driven compulsive behavior, topiramate is worth taking seriously as a reference compound with replicated human data.

We think the bench value is genuine but specific. If the program involves AMPA receptor pharmacology, CNS carbonic anhydrase biology, or glutamatergic contributions to addictive behavior, topiramate earns its place. For anything outside those domains, the cognitive liability and the largely-harvested literature make it a low-priority entry. Score of 50 reflects that kind of concentrated, real-but-narrow research utility: not a frontier compound, not a throwaway.

Novelty

22

Mechanism promise

45

In-category differentiation

45

Evidence quality

75

Translational signal

70

Research bench value

55

Rationale Topiramate’s unusually broad five-target mechanism and robust FDA-backed evidence base are real, but 30 years of thorough characterization suppresses novelty to the floor; the score reflects a compound whose research value is genuine but domain-specific, not frontier.

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

Sulfamate-substituted monosaccharide / multifactorial anticonvulsant

A sulfamate-substituted monosaccharide anticonvulsant with broad mechanism (sodium channels, GABA-A potentiation, AMPA antagonism, carbonic anhydrase inhibition); used for migraine prophylaxis and weight loss.

Abstract

Topiramate (2,3:4,5-bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate; CAS 97240-79-4; molecular formula C12H21NO8S; molecular weight 339.36) is a sulfamate-substituted monosaccharide anticonvulsant developed at Johnson and Johnson and approved by the FDA in 1996 under the trade name Topamax. Mechanism is multifactorial: state-dependent sodium channel inhibition; GABA-A receptor potentiation at a non-benzodiazepine site; AMPA/kainate glutamate receptor antagonism; carbonic anhydrase inhibition (isozymes II and IV); high-voltage calcium channel inhibition. The carbonic anhydrase activity contributes to the characteristic adverse events: paresthesias (40 percent of patients), nephrolithiasis (1.5 percent), metabolic acidosis. Cognitive side effects are pronounced: word-finding difficulty, slowed mentation. Plasma half-life is 21 hours; metabolism is approximately 70 percent renal excretion unchanged. Approved for partial-onset and generalized tonic-clonic seizures, Lennox-Gastaut syndrome, migraine prophylaxis, and (with phentermine, as Qsymia) chronic weight management. Used as the canonical multifactorial anticonvulsant and as a reference carbonic anhydrase inhibitor in CNS pharmacology.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-245Open in new tab →

Download PDF →

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
Ligandrol (LGD-4033)

Our opinion on this compoundEstablished, active research

39/100

Canonical high-affinity SARM with real phase 1 data, but mechanistically mature and clinically stalled

Look, there’s a version of this compound that sounds exciting on paper: sub-nanomolar AR affinity, tissue selectivity, phase 1 lean-mass data, and a development history at two serious pharmaceutical shops. That version isn’t wrong. But we’re scoring research merit in 2026, and the honest picture of LGD-4033 is a mature SARM with a mostly settled mechanism in a class that has been chasing the same tissue-selectivity promise for twenty years without a single approved drug to show for it.

The mechanism itself, tissue-selective androgen receptor agonism via a non-steroidal ligand, is real and reasonably well understood. LGD-4033 binds AR at roughly 1 nM (Ki), several-fold tighter than ostarine, and that affinity advantage is why it became the canonical reference compound for high-affinity SARM work. If your research question is specifically about the pharmacology of high-affinity partial AR agonism, theres a legitimate reason to reach for this molecule. That single-axis differentiation is real and we credit it in the bench value and differentiation scores. But it doesn’t change the fact that the mechanism hasn’t evolved, its single-receptor agonism in a class that has been around long enough that Ligand Pharmaceuticals itself spun the asset out to Viking Therapeutics to pursue it further.

The clinical story is complicated. The Bhasin phase 1 data (0.1-1 mg, 21 days, healthy males) is genuinely clean: dose-dependent lean body mass gains, no significant prostate signal, reasonable tolerability. Thats a real signal. The problem is what came after. The VK5211 hip fracture program has had intermittent readouts and hasn’t generated the sort of decisive phase 2 data that would make this compound compelling to follow right now. HPG axis suppression at the higher dose tier is a liability the class has never fully escaped, and recreational use at 5-10 mg (supratherapeutic by clinical standards) has muddied the human data pool considerably.

What we like: the canonical status matters. LGD-4033 is the molecule you’d reach for if you need a high-affinity SARM probe to interrogate AR-dependent pathways in vitro or in a clean animal model. The pharmacokinetics (24-36 hour half-life) are researcher-friendly. The phase 1 dataset is honest and reproducible. What we don’t like: the class promise has underdelivered for two decades, the VK5211 program hasn’t produced a decisive signal, and there’s genuinely nothing novel happening mechanistically. If you’re not specifically studying SARMs, there’s little here that you can’t get from a better-characterized or more clinically advanced tool. Score it accordingly: useful in the right context, not a priority pick outside of it.

Novelty

28

Mechanism promise

30

In-category differentiation

45

Evidence quality

45

Translational signal

42

Research bench value

58

Rationale LGD-4033 scores modestly on novelty and mechanism because selective AR agonism is a mature, well-trodden strategy, but its canonical status as the reference high-affinity SARM and solid phase 1 lean-mass data keep it out of the workhorse or established-mature basement. The intermittent phase 2 (VK5211) trajectory and HPG suppression signal cap the translational score.

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

Selective androgen receptor modulator

A non-steroidal SARM developed for muscle wasting; one of the more potent SARMs at AR binding.

Abstract

Ligandrol (LGD-4033, VK5211; CAS 1165910-22-4; molecular formula C14H12F6N2O; molecular weight 338.25) is a non-steroidal SARM developed by Ligand Pharmaceuticals (later out-licensed to Viking Therapeutics as VK5211). The compound is a high-affinity AR ligand (Ki approximately 1 nM, several-fold higher affinity than ostarine) with tissue-selective agonism similar to other SARMs. Phase 1 trials in healthy male volunteers demonstrated dose-dependent increases in lean body mass at doses of 0.1 to 1 mg daily over 21 days, with no significant prostate effects but with HPG axis suppression at the higher dose tier. Subsequent phase 2 development (VK5211) targeted hip fracture recovery; results have been intermittent. Plasma half-life is approximately 24 to 36 hours. The compound is widely used recreationally at supratherapeutic doses (5 to 10 mg) and is banned by WADA. Used as the canonical high-affinity SARM in mechanism studies.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-262Open in new tab →

Download PDF →

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
Finasteride

Plain-language summaryIntrigue 65 / 100

Finasteride (Proscar at 5 mg, Propecia at 1 mg) is a 1990s drug that blocks the type II 5-alpha-reductase enzyme, which converts testosterone into the more potent dihydrotestosterone (DHT) in the prostate, scalp, and skin. It cuts plasma DHT by about 65 to 70 percent at the 5 mg dose. Approved for benign prostate enlargement and male-pattern hair loss, with both indications driven by reducing local DHT. The hair-loss application is the famous one. Side effects include sexual dysfunction in a minority of users, with persistent symptoms after discontinuation (post-finasteride syndrome) reported in case series, though the frequency and biological basis remain debated. 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

46/100

The reference Type II 5AR inhibitor, mature and well-characterized, with real probe value but limited novelty

Look, finasteride is a 30-year-old approved drug with a completely characterized mechanism. That’s not a knock on it, thats just what it is. FDA cleared in 1992 for BPH and 1997 for androgenetic alopecia, it became the reference standard Type II-selective 5-alpha-reductase inhibitor in androgen biology research, and that’s the best argument for including it in a research library at all.

The mechanism is specific: finasteride inhibits the Type II isozyme (Ki approximately 10 nM) without meaningfully touching Type I, which lives in liver, skin, and the brain. Dutasteride hits both, dropping plasma DHT by around 95 percent. Finasteride gets you 65 to 70 percent at the 5 mg dose. That gap is actually what makes finasteride interesting on the bench, not therapeutically, but as a probe. If you want to ask what Type I versus Type II 5AR contributes to a given phenotype, finasteride is your tool. That question comes up in androgen pathway work, in skin biology, and increasingly in neurosteroid research.

The neurosteroid angle is genuinely the most interesting current research use. Finasteride inhibits the conversion of progesterone to 5-alpha-dihydroprogesterone, which is upstream of allopregnanolone synthesis. Allopregnanolone is a positive GABA-A allosteric modulator, and its reduction is one proposed mechanism behind what is now called post-finasteride syndrome (PFS). We dont want to over-claim here, the literature is contested and the mechanistic case is still being built, but the neurosteroid deprivation hypothesis has generated serious laboratory work, including papers from the Melcangi group at the University of Milan examining central nervous system steroid profiles after finasteride exposure in rodent models. Thats real bench science with real questions still open.

What works against a high score is straightforward: the compound isn’t novel, the core mechanism is completely solved, and for pure androgen pathway intervention dutasteride offers a more complete picture. Finasteride is useful because it’s the Type II selective option, not because it’s doing anything pharmacologically surprising. Its evidence quality and translational signal are excellent precisely because it’s a mature approved drug with decades of large-scale human data. Those scores pull the overall up, but they shouldn’t, because well-characterized evidence on a boring old mechanism isn’t research excitement.

We think of finasteride as a mature tool with a specific probe niche. It earns a spot as the reference Type II 5AR inhibitor and as a gateway into the PFS neurosteroid literature, but it’s not a compound that any serious investigator has on their want-to-study-more list in 2025 unless the question is specifically about Type I versus Type II isozyme contributions or GABA-A neurosteroid circuitry.

Novelty

20

Mechanism promise

25

In-category differentiation

35

Evidence quality

85

Translational signal

75

Research bench value

60

Rationale FDA-approved since 1992 with fully characterized mechanism and massive clinical evidence base; earns a library spot as the selective Type II 5AR probe in androgen and neurosteroid research, but novelty and differentiation scores are low because the mechanism is completely understood and dutasteride covers the therapeutic space more completely for most applications.

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

5-alpha-reductase type II inhibitor

A 4-azasteroid 5-alpha-reductase type II inhibitor; approved for benign prostatic hyperplasia and androgenetic alopecia.

Abstract

Finasteride (N-(2-methyl-2-propanyl)-3-oxo-(5-alpha,17-beta)-4-azaandrost-1-ene-17-carboxamide; CAS 98319-26-7; molecular formula C23H36N2O2; molecular weight 372.55) is a 4-azasteroid 5-alpha-reductase inhibitor developed at Merck and approved by the FDA in 1992 (Proscar 5 mg for BPH) and 1997 (Propecia 1 mg for androgenetic alopecia). Mechanism: selective inhibition of 5-alpha-reductase type II isozyme (Ki approximately 10 nM), which converts testosterone to dihydrotestosterone (DHT) in prostate, hair follicle, and skin. Plasma DHT is reduced by approximately 65 to 70 percent at the 5 mg dose. Type I 5AR (in liver, skin, and brain) is largely unaffected. Plasma half-life is approximately 6 to 8 hours; metabolism is via CYP3A4. The compound has well-documented sexual side effects (reduced libido, erectile dysfunction in approximately 1 to 5 percent of users) and the controversial post-finasteride syndrome (persistent symptoms after discontinuation, debated as a clinical entity). Used as the reference 5AR-II selective inhibitor in mechanism studies and as a positive control in androgen pathway research.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-279Open in new tab →

Download PDF →

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
Mazdutide

Plain-language summaryIntrigue 72 / 100

Mazdutide is a long-acting dual GLP-1 and glucagon receptor agonist developed by Eli Lilly and out-licensed to Innovent Biologics for development in China. Mechanistically similar to cotadutide and the natural peptide oxyntomodulin, but with a fatty-acid extension supporting once-weekly rather than daily dosing. Phase 2 trials in Chinese type 2 diabetes and obesity populations showed dose-dependent weight loss and HbA1c reduction comparable to or exceeding semaglutide at higher dose tiers. Phase 3 trials are ongoing in China. It is shaping up to be the first dual GLP-1/glucagon agonist to reach a major market, beating its Western competitors. 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, active research

55/100

Solid dual GLP-1/glucagon agonist with real Phase 2 human signal, but a crowded class and triple-agonist competition cap its ceiling

Look, mazdutide is a genuinely interesting peptide in a genuinely crowded lane. It’s a dual GLP-1/glucagon receptor agonist — modified glucagon backbone, GLP-1 activity grafted in, C18 fatty acid extension for once-weekly dosing — developed by Lilly and out-licensed to Innovent Biologics for the Chinese market. The mechanism does something single GLP-1 agonists don’t: the glucagon arm drives measurable thermogenesis and energy expenditure on top of the GLP-1-mediated appetite suppression, which is at least theoretically a better handle on weight loss than appetite alone.

Here’s the thing though. The dual GLP-1/glucagon mechanism isn’t new. Oxyntomodulin is the natural endogenous template. Cotadutide (AstraZeneca/Pfizer) ran into this space years ago. Survodutide from Boehringer Ingelheim is also in late development on the same dual axis. So mazdutide isn’t defining its category — its competing for second or third position in a class that retatrutide (triple GIP/GLP-1/glucagon) is already threatening to supersede entirely. On differentiation, the compound’s phase 2 data is encouraging — dose-dependent HbA1c reduction and weight outcomes at higher tiers that track with or slightly exceed semaglutide — but thats not the same as being best-in-class when tirzepatide and retatrutide exist.

We think the evidence base is legitimately respectable for where mazdutide sits developmentally. Phase 2 data are real, multi-site, and the DREAMS Phase 3 program in China is ongoing. There’s a clear human signal for the mechanism, which is more than most peptides in the library can claim. What we dont get is the certainty of full Phase 3 readout or the regulatory history that would push evidence quality into the 70s.

From a research bench standpoint, mazdutide is useful primarily as a reference compound for the long-acting dual GLP-1/glucagon format. Investigators studying the glucagon thermogenesis contribution, the energy expenditure differential versus pure GLP-1, or the pharmacokinetic profile of C18-extended dual agonists have a reason to reach for it. It’s not irreplaceable — survodutide and cotadutide cover overlapping ground — but it’s a credible tool in that niche.

Honestly, the compound’s story is hard to tell without returning to the question of where it sits relative to retatrutide. If triple agonists prove out in Phase 3 with the weight loss magnitude early data suggests, dual GLP-1/glucagon becomes a historical stepping stone rather than a destination. Mazdutide is worth watching, worth understanding, and a solid addition to a research library focused on incretin pharmacology. It’s just not the lead compound in that conversation anymore.

Novelty

58

Mechanism promise

73

In-category differentiation

35

Evidence quality

54

Translational signal

62

Research bench value

48

Rationale Mazdutide scores well on mechanism and translational signal — the glucagon-driven energy expenditure layer on top of GLP-1 appetite suppression is real pharmacology with Phase 2 HbA1c and weight data to back it — but differentiation is the key drag: cotadutide, survodutide, and above all retatrutide make mazdutide a follower in a class it doesn’t define. The compound’s China-centric development trajectory also limits global bench relevance.

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

GLP-1 / glucagon dual receptor agonist

A long-acting dual GLP-1 and glucagon receptor agonist; under development for obesity and type 2 diabetes.

Abstract

Mazdutide (IBI362, LY3305677; modified peptide with glucagon backbone and GLP-1 modifications; molecular weight approximately 4500 Da) is a dual GLP-1/glucagon receptor agonist developed by Eli Lilly and out-licensed to Innovent Biologics for development in China. The compound is structurally and mechanistically similar to cotadutide and oxyntomodulin, with C18 fatty acid extension for once-weekly dosing. Phase 2 trials in type 2 diabetes and obesity demonstrated dose-dependent HbA1c reduction and weight loss comparable to or exceeding semaglutide at higher dose tiers. Phase 3 trials are ongoing in China (DREAMS program) and US. The dual mechanism produces increased energy expenditure (glucagon effect) on top of the GLP-1 appetite suppression. Used as a reference long-acting dual GLP-1/glucagon agonist.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-296Open in new tab →

Download PDF →

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
URB597

Plain-language summaryIntrigue 60 / 100

URB597 is the standard research tool for blocking the FAAH enzyme that breaks down anandamide. Developed by Daniele Piomelli’s group at UC Irvine, it permanently inactivates FAAH by latching onto the active site, which raises endogenous anandamide for hours without giving cannabinoids directly. In animal studies it produces anxiolytic and analgesic effects without the cognitive impairment or reward signal that comes with direct CB1 activation, suggesting that elevated endocannabinoid tone might be therapeutically useful. The compound itself never reached human trials, but it laid the conceptual groundwork for clinical FAAH inhibitors like PF-04457845. 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 compoundNiche research probe

55/100

Canonical FAAH probe with strong bench utility but murky translational story after Phase 2 MDD failure

Look, if you work in endocannabinoid biology, URB597 is probably already sitting on your shelf. Piomelli’s group at UC Irvine gave the field a genuinely clean probe: a covalent carbamate that carbamoylates the active-site serine of FAAH, producing irreversible inhibition with real selectivity over MAGL and other lipid hydrolases. That mechanism is what we like most about this compound. You’re not agonizing CB1 directly; you’re elevating endogenous anandamide and the other N-acylethanolamines and letting the system respond on its own terms. The pharmacological consequence is real and distinguishable from THC-like full agonism: anxiolytic and analgesic signal without the catalepsy, hypothermia, or intoxication that makes direct CB1 agonists so hard to work with in behavioral models.

The selectivity story holds up across labs. Multiple groups have used URB597 to dissect FAAH’s role in pain processing, fear extinction, and stress-induced analgesia, and the results have replicated reasonably well. The FAAH inhibition literature is one of the more coherent bodies of work to come out of the eCB field, and URB597 is at the center of it. If you’re running a FAAH knockout against a pharmacological model, URB597 is your positive control. There isnt a cleaner option for acute pharmacological FAAH inhibition in preclinical work right now.

Here’s the thing, though. The Phase 2 clinical trial in major depressive disorder didn’t pan out. No efficacy signal worth advancing to Phase 3. That failure doesnt invalidate the probe, and it doesn’t mean FAAH inhibition is biologically inert in humans, but it does mean the translational story is murky. The anxiolytic preclinical data hasn’t cleanly mapped to any approved indication. Pain is still an open question. The newer selective FAAH inhibitors like PF-04457845 showed early promise in pain work and also stalled. The BIA 10-2474 safety disaster in France in 2016 cast a shadow over the whole class even though URB597’s own selectivity profile looks meaningfully better. That shadow hasn’t fully lifted from the field’s reputation.

What does this mean for the research score? We think URB597 earns its place as a bench tool. It’s the reference probe for a still-active area of neuropharmacology. The endocannabinoid tone hypothesis isn’t dead; it’s waiting on better target engagement biomarkers and possibly a different indication space. The compound has enough replicated literature behind it that you know exactly what you’re getting. We don’t think it’s a priority new research direction, though. The novelty is gone, the clinical signal is weak, and the field has been trying to translate FAAH inhibition for over a decade with limited success. As a probe for answering specific mechanistic questions about eCB tone: yes, absolutely. As an exciting frontier research target in its own right: no. That’s a 55.

Novelty

38

Mechanism promise

60

In-category differentiation

65

Evidence quality

58

Translational signal

40

Research bench value

75

Rationale URB597 scores high on bench value as the definitive reference FAAH inhibitor in endocannabinoid research, but failed Phase 2 MDD trials and a decade of limited clinical translation drag the overall down hard. It earns its place in any serious eCB research program as a probe, not as a frontier therapeutic lead.

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

Selective FAAH inhibitor (research)

A carbamate inhibitor of fatty acid amide hydrolase (FAAH); the canonical research probe for elevating endogenous anandamide.

Abstract

URB597 (KDS-4103, cyclohexyl carbamic acid 3′-carbamoyl-biphenyl-3-yl ester; CAS 546141-08-6; molecular formula C20H22N2O3; molecular weight 338.40) is a covalent carbamate inhibitor of fatty acid amide hydrolase (FAAH) developed by Piomelli and colleagues at UC Irvine. The compound carbamoylates the active-site serine of FAAH, producing irreversible enzyme inactivation. Selective for FAAH over MAGL and other lipases. Pharmacological consequence: elevation of endogenous anandamide and other N-acylethanolamides without direct CB receptor agonism. The behavioral profile differs from direct CB1 agonists like THC: anxiolytic and analgesic effects without the catalepsy, hypothermia, and intoxication characteristic of CB1 full agonism. Phase 2 clinical trials in major depressive disorder did not demonstrate efficacy; the compound did not advance to phase 3. Plasma half-life is approximately 6 hours; the irreversible mechanism produces effective FAAH inhibition for 24-48 hours after a single dose. Used as the canonical FAAH inhibitor in academic neuroscience.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-328Open in new tab →

Download PDF →

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
Dexmedetomidine

Plain-language summaryIntrigue 68 / 100

Dexmedetomidine, sold as Precedex, is an intravenous sedative that works through alpha-2A adrenergic receptors in the brainstem rather than through the GABA system used by virtually every other sedative. The unusual mechanism has a clinically remarkable consequence: it produces sedation that resembles natural sleep, from which patients can be awakened to follow commands, without depressing respiration. It is heavily used in intensive care units for ventilated patients and procedural sedation. The main side effects are bradycardia and hypotension from systemic alpha-2 activation. 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 compoundNiche research probe

55/100

Best-in-class alpha-2A probe with deep clinical evidence but low novelty and a narrow research niche

Look, dexmedetomidine is genuinely useful, and we want to be precise about why that doesnt translate into a high score here. The compound has been approved since 1999 under Precedex, the mechanism is textbook-level understood, and the clinical story is already told. ICU sedation, procedural sedation, arousable sleep-mimicking pharmacology via locus coeruleus alpha-2A activation. None of that is surprising to anyone who’s opened an anesthesia pharmacology chapter in the last two decades.

What dexmedetomidine does have going for it is probe selectivity. The 1620-fold preference for alpha-2 over alpha-1 receptors is substantially cleaner than clonidine, which sits closer to 200-fold. If you’re running experiments that require isolating alpha-2A-mediated effects without alpha-1 contamination, dexmedetomidine is the tool. Thats the bench value case, and it’s real. Its why the compound ends up in papers on adrenergic receptor subtype biology, sympatholytic pharmacology, delirium prevention mechanisms, and the neurochemistry of natural sleep versus drug-induced sedation. As a pharmacological probe, it earns its place on the shelf.

But the research conversation around dexmedetomidine isnt particularly live or frontier-facing. The mechanism of action at the locus coeruleus and spinal cord is fully characterized. The clinical evidence base is robust by any measure, which is exactly the problem from a novelty perspective. When a drug has undergone decades of multicenter trials and sits in anesthesiology formularies worldwide, the interesting questions have mostly been answered. What’s left is refinement: pediatric dosing optimization, opioid-sparing protocols, delirium incidence in specific ICU subpopulations. Legitimate work, but not the kind that demands a dedicated research program for a bench scientist who isn’t already in that clinical orbit.

We think the differentiation score is the honest bright spot. Among alpha-2 agonists available as research tools, dexmedetomidine is clearly the reference standard. Clonidine is cheaper and more accessible but pharmacologically messier. Guanfacine has the alpha-2A selectivity story but in a different pharmacokinetic and CNS-distribution context. For receptor-level mechanistic work, dex is the right choice. That matters for labs doing adrenergic subtype work or investigating the molecular basis of norepinephrine-mediated sedation.

Honestly, the 55 reflects a compound that is precisely as useful as it looks and not one point more. It’s not overlooked, not underrated, not sitting on a hidden research signal. The literature is mature, the mechanism is settled, and the novelty clock stopped running a long time ago. Serious researchers in alpha-2A biology or ICU neuroscience will already know it. Everyone else can deprioritize it without missing anything.

Novelty

20

Mechanism promise

40

In-category differentiation

65

Evidence quality

78

Translational signal

72

Research bench value

75

Rationale Dexmedetomidine scores high on differentiation and bench value because its 1620:1 alpha-2:alpha-1 selectivity makes it the canonical tool for isolating alpha-2A-specific effects, but the compound is 25 years old, the mechanism is fully characterized, and the translational story is already written by the FDA approval. Score reflects a useful but unexciting research probe, not a frontier target.

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

Selective alpha-2A adrenergic agonist (anesthetic)

A potent selective alpha-2A adrenergic agonist; an intravenous sedative producing arousable sedation without respiratory depression.

Abstract

Dexmedetomidine ((S)-4-[1-(2,3-dimethylphenyl)ethyl]-1H-imidazole; CAS 113775-47-6; molecular formula C13H16N2; molecular weight 200.28) is a highly selective alpha-2A adrenergic agonist developed at Farmos and approved by the FDA in 1999 (Precedex). The compound is the active S-enantiomer of medetomidine (used in veterinary anesthesia). Alpha-2A selectivity over alpha-2B and alpha-2C is approximately 8-fold; selectivity over alpha-1 is approximately 1620-fold, much higher than clonidine. The clinical profile is unique: the alpha-2A activation in the locus coeruleus produces sedation that mimics natural sleep architecture, with patients arousable on stimulation; respiratory drive is preserved. Approved indications: ICU sedation, procedural sedation, conscious sedation. Plasma half-life is approximately 2 hours; metabolism is hepatic. Used as the canonical highly selective alpha-2A agonist in anesthesia research.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-343Open in new tab →

Download PDF →

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
Stamulumab (MYO-029)

Our opinion on this compoundNiche research probe

37/100

First-in-class anti-myostatin antibody with clinical failure and residual selective probe value

Here’s the thing about stamulumab: it earns its place in the historical record as the first IgG1 antibody to selectively neutralize circulating myostatin (GDF-8), and the Wyeth program that produced it genuinely opened up an entire research program in muscle biology. But history and utility aren’t the same thing, and by now the compound has largely been superseded by what came after it.

The Phase 1/2 trial data is what it is. Across becker muscular dystrophy, facioscapulohumeral dystrophy, and limb-girdle dystrophy cohorts, stamulumab showed acceptable tolerability but produced muscle mass gains in the range of 0.5 to 1 percent. That’s not a rounding error on a real signal. That’s essentially not working. Wyeth (later Pfizer) chose not to advance it, which was the rational call. The compound’s mechanism is real, myostatin is a real negative regulator of skeletal muscle, but stamulumab itself didn’t translate the biology into a meaningful clinical effect.

What we find genuinely interesting is how the stamulumab failure shaped the next generation. Bimagrumab took a smarter angle, blocking ActRIIA/B at the receptor level rather than neutralizing circulating myostatin directly, and has achieved substantially larger lean mass effects in sarcopenia and metabolic disease trials. Domagrozumab and landogrozumab came later with refined anti-myostatin approaches. All of them owe something to stamulumab’s proof-of-concept work and failure map. That’s a real contribution to the field, even if it doesn’t push the compound’s score higher.

For a bench investigator, stamulumab still has some value as a selective myostatin neutralizer. If the research question is specifically about circulating GDF-8 and you want a well-characterized antibody with documented pharmacokinetics across multiple dose levels in actual humans, it’s a legitimate probe. Most research antibodies don’t have that. But we’d be honest: for most muscle biology programs, bimagrumab or more recent tools are going to be the better choice on nearly every dimension, including efficacy signal and mechanism breadth.

Thats the core issue here. The compound isn’t retracted, it isn’t disproven, the target is real. But it’s been outperformed on efficacy and superseded on mechanism design. It scores where it scores because it’s historically significant but no longer the leading edge of the question it helped define. For narrow, GDF-8-specific probe work, fine. For a general muscle biology or sarcopenia program, we’d look at the compounds stamulumab inspired before we’d reach for stamulumab itself.

Novelty

35

Mechanism promise

48

In-category differentiation

22

Evidence quality

50

Translational signal

25

Research bench value

45

Rationale Stamulumab was genuinely first-in-class for myostatin neutralization but Phase 1/2 data returned only 0.5-1% muscle mass gains across three dystrophy populations, deemed insufficient for advancement; it retains narrow probe utility for selective GDF-8 research but has been superseded by bimagrumab and later-generation agents on both mechanism design and clinical signal.

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

Anti-myostatin monoclonal antibody (research)

A humanized monoclonal antibody selective for myostatin (GDF-8); the first-in-class anti-myostatin antibody investigated for muscular dystrophy.

Abstract

Stamulumab (MYO-029; humanized IgG1 monoclonal antibody; molecular weight approximately 145 kDa) is a humanized monoclonal antibody selective for myostatin (GDF-8), developed at Wyeth (now Pfizer). The compound binds circulating myostatin in plasma, neutralizing the negative regulator of muscle growth. Phase 1/2 trials in adults with becker muscular dystrophy, facioscapulohumeral muscular dystrophy, and limb-girdle muscular dystrophy demonstrated tolerability but limited muscle mass increases (approximately 0.5 to 1 percent), which were considered insufficient to justify advancement. The compound is the first-in-class anti-myostatin antibody and informed subsequent development of bimagrumab (broader receptor target), domagrozumab, and landogrozumab. Used as a research compound for selective myostatin neutralization.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-360Open in new tab →

Download PDF →

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
D-Cycloserine

Plain-language summaryIntrigue 70 / 100

D-cycloserine is an old tuberculosis antibiotic isolated from a Streptomyces bacterium and approved in 1956. Decades later researchers noticed it also acts as a partial agonist at the NMDA glycine site, meaning it activates the receptor but only about halfway. That partial behavior makes its effect dose-dependent: at low doses it boosts NMDA function (because endogenous co-agonists are not saturating the site), at high doses it actually competes with the full natural agonists and dampens NMDA signaling. The low-dose facilitating effect inspired its use as an extinction-learning enhancer paired with exposure therapy for phobia, PTSD, OCD, and social anxiety. Trials show modest effects with strict timing requirements (give it shortly before therapy or it does not work). Canonical NMDA glycine-site partial 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 compoundNiche research probe

49/100

The canonical NMDA glycine-site probe, clinically useful but past peak novelty in extinction-learning research

Look, D-cycloserine is one of those compounds that lives two separate lives, and you have to score both honestly. As an antibiotic it’s been FDA-approved since 1956 and is thoroughly, almost painfully, understood. As an NMDA glycine-site partial agonist it became one of the more interesting pharmacological tools of the 1990s and 2000s, and that second life is why it belongs in this library at all.

The mechanism is genuinely worth understanding. D-cycloserine sits at the NMDA receptor glycine co-agonist site and behaves as a partial agonist with roughly 40-60 percent intrinsic activity. That creates a bidirectional dose-response profile that most researchers find counterintuitive at first: at concentrations below the endogenous glycine/D-serine tone, it potentiates NMDA function; at higher concentrations it competes with the full co-agonists and acts as a functional antagonist. The extinction-learning hypothesis follows directly from that lower-dose facilitating effect. NMDA receptor activation during extinction memory consolidation is necessary for durable fear reduction, and pre-session dosing with D-cycloserine was supposed to amplify exactly that window. It’s elegant pharmacology on paper.

What we dont love is what the clinical literature actually delivered. The extinction-learning trials in PTSD, OCD, phobia, and social anxiety disorder span two decades and multiple serious groups, including Michael Davis’s lab at Emory, Edna Foa’s group, and several independent European programs. The results are real but modest and frustratingly timing-dependent. Get the dosing window wrong and you may consolidate a worse extinction session rather than a better one. Meta-analyses have consistently struggled to show a clean, reproducible effect across disorders. The signal isn’t gone, but it’s smaller and less reliable than the early data suggested. Translational enthusiasm has cooled appropriately.

Here’s the thing, though: as a bench tool this compound is essentially irreplaceable. If you’re running any research program that touches NMDA receptor glycine-site pharmacology, fear extinction circuits, or the interface between NMDA modulation and behavioral plasticity, D-cycloserine is the reference standard. Nothing else occupies this exact pharmacological niche with its combination of FDA approval, known PK, and decades of protocol literature. For investigators in those areas it’s not optional; it’s the probe you reach for first when you need to ask whether glycine-site occupancy is doing the work you think it is.

We’d call it a niche probe with a legitimate but fully mature research story. The interesting questions it can still answer are mechanistic and tool-level questions, not frontier indication questions. Score reflects that honestly: high bench value, genuine differentiation within its niche, but novelty and translational excitement that belong to the 2000s rather than right now.

Novelty

20

Mechanism promise

50

In-category differentiation

62

Evidence quality

60

Translational signal

42

Research bench value

75

Rationale D-cycloserine scores well on bench value as the reference glycine-site partial agonist and holds a differentiated position as the defining compound in that niche, but its 1956 vintage, well-characterized mechanism, and a clinical literature that has delivered mixed results over three decades drag novelty and translational signal into the basement. No structural cap applies; the score reflects genuine probe utility without the novelty premium.

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

NMDA receptor glycine-site partial agonist

An antibiotic with NMDA receptor partial agonist activity; investigated as an extinction-learning enhancer in exposure therapy for anxiety disorders.

Abstract

D-cycloserine ((4R)-4-amino-1,2-oxazolidin-3-one; CAS 68-41-7; molecular formula C3H6N2O2; molecular weight 102.09) is a cyclic amino acid antibiotic isolated from Streptomyces orchidaceus and approved by the FDA in 1956 for second-line tuberculosis treatment. The compound is a partial agonist at the NMDA receptor glycine site (intrinsic activity approximately 40 to 60 percent), and the partial agonism produces dose-dependent NMDA receptor modulation: at low concentrations relative to endogenous glycine/D-serine, D-cycloserine functions as a positive modulator (enhancing NMDA function); at higher concentrations it competes with the full-agonist endogenous co-agonists and behaves as a functional antagonist. The lower-dose facilitating effect underlies use as an extinction-learning enhancer in exposure therapy for phobia, PTSD, OCD, and social anxiety; clinical trials have shown modest effects with timing-dependent results (administration shortly before therapy session is critical). Plasma half-life is approximately 10 hours. Used as the canonical NMDA glycine-site partial agonist in research.

Read the full monograph

The full reference document covers compound identification, discovery and developmental history, mechanism of action, pharmacokinetics, sourcing and quality verification, and a curated reference list. Embedded inline below; download for offline reading.

KDC-MN-377Open in new tab →

Download PDF →

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

←Previous Page

1 … 39 40 41 42 43 … 69

Bench-grade research compounds. Cited research. Verified COAs.

kodiac.bio

Explore

Shop
Monographs
Lab Results
About
Affiliate program
Affiliate handbook

Account

Cart
My account

Help

Compliance
Contact

Quarterly dispatch

New batches and new monographs only. Unsubscribe in one click.

Write to us from the contact page to join the list.

Kodiac biolabs sells research compounds for in vitro and in vivo investigative purposes only. Products are not for human or veterinary consumption. Not for medical, diagnostic, or therapeutic use. By using this site you confirm you are acquiring research compounds for research purposes only.

Kodiac biolabs is not affiliated with the U.S. Food and Drug Administration. Products are research reagents, have not been evaluated by the FDA, and are not intended to diagnose, treat, cure, or prevent any disease.

© 2026 Kodiac biolabs LLC. All rights reserved.