Skip to content

Shop
Scholar
Lab Results
Learn
Vote
Forum
About

Search Kodiac

Sign in Sign up Account

Tag: MONOGRAPH

Romosozumab

Plain-language summaryIntrigue 72 / 100

Romosozumab, sold as Evenity, is a humanized antibody against sclerostin, a protein that osteocytes (bone cells embedded in mature bone) secrete to put a brake on the Wnt signaling pathway that promotes osteoblast bone formation. By neutralizing sclerostin, romosozumab simultaneously increases bone formation and decreases bone resorption, a dual-action mechanism unique among osteoporosis drugs. FDA-approved in 2019 for postmenopausal osteoporosis, it produces large bone density gains in twelve months. The label carries a black box warning for cardiovascular events based on a signal in the comparison-to-alendronate ARCH trial. 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 Kodiac editorial, not peer-reviewed.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

69/100

Dual-action bone anabolic with solid phase 3 data; canonical anti-sclerostin research probe

Look, the sclerostin story is one of the more genuinely interesting pieces of bone biology to emerge in the last twenty years. Sclerostin, encoded by the SOST gene and secreted primarily by osteocytes, suppresses Wnt/beta-catenin signaling in osteoblasts. When you knock out SOST in mice you get dramatically increased bone density. Romosozumab is the pharmacological expression of that finding: a humanized IgG2 antibody that neutralizes sclerostin and, as a result, simultaneously de-inhibits bone formation and reduces osteoclast activity. That dual-action profile is genuinely unusual. Most osteoporosis pharmacology is either anabolic (teriparatide, abaloparatide) or anti-resorptive (bisphosphonates, denosumab). Romosozumab does both through a single molecular target, which is mechanistically elegant in a way the field hadn’t seen before this compound.

The evidence base is solid. The FRAME trial established safety and early efficacy against placebo; the ARCH trial went further, comparing romosozumab head-to-head against alendronate over a sequential 24-month period. ARCH showed superior vertebral, hip, and nonvertebral fracture reduction. That’s a meaningful clinical result, not a biomarker endpoint. FDA approved in 2019, black-box warning included for cardiovascular risk: in ARCH, there were more serious cardiovascular adverse events in the romosozumab arm versus alendronate. The CV signal is real and shapes research design as much as clinical practice, particularly if you’re running longer-duration bone turnover studies in cardiovascular-risk populations.

For bench-scale investigators, romosozumab is most useful as the canonical reference tool for the anti-sclerostin axis. If you’re studying Wnt pathway regulation in bone, osteocyte-osteoblast crosstalk, or sequential anabolic-to-antiresorptive strategies, this is the probe you reach for to isolate what sclerostin inhibition specifically contributes. There’s genuine ongoing mechanistic work around P1NP and CTX kinetics during the anabolic window before formation signal attenuates, and romosozumab is the defining tool for that question. No other approved compound occupies this niche.

What we dont love: the 12-month treatment ceiling (loss of efficacy with continued dosing) is a biological puzzle thats not fully resolved, and the CV safety signal creates uncertainty that constrains some long-term experimental designs. It’s also a large biological at approximately 145 kDa; sourcing research-grade material at a price that makes routine mechanistic bench work practical isn’t trivial compared to small-molecule alternatives in adjacent research areas. The overall picture is a well-validated approved biologic with genuinely interesting dual-action biology and a clear role as the defining anti-sclerostin tool. The mechanism was novel when it emerged; the biology it probes remains active. Not frontier anymore, but far from boring.

Novelty

50

Mechanism promise

75

In-category differentiation

72

Evidence quality

80

Translational signal

75

Research bench value

62

Rationale Romosozumab scores well on mechanism (dual anabolic/anti-resorptive via Wnt de-inhibition), differentiation (sole approved anti-sclerostin agent, defines its class), and evidence (FDA-approved 2019, ARCH and FRAME trials), but novelty is tempered by six years of post-approval literature and a now well-characterized Wnt/sclerostin axis. No hard cap applies; the overall lands in established-active territory where strong clinical validation meets a mechanistically interesting but no longer frontier biology.

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

Anti-sclerostin monoclonal antibody

A humanized monoclonal antibody against sclerostin; a dual-action bone agent that increases formation and decreases resorption.

Abstract

Romosozumab (CAS 909395-70-6; humanized IgG2 monoclonal antibody against sclerostin; molecular weight approximately 145 kDa) is a humanized monoclonal antibody developed by Amgen and UCB and approved by the FDA in 2019 (Evenity). The compound binds sclerostin (a glycoprotein produced by osteocytes that inhibits Wnt signaling on osteoblasts), neutralizing its inhibitory effect on bone formation. Mechanism is dual-action: increased bone formation (Wnt pathway de-inhibition on osteoblasts) plus decreased bone resorption (reduced osteoclast differentiation), an unusual combination producing more rapid BMD gains than any other osteoporosis agent. Approved for postmenopausal osteoporosis at high fracture risk. The ARCH trial demonstrated superior fracture reduction versus alendronate. Cardiovascular safety signal (increased cardiovascular events versus alendronate in ARCH) led to a black-box warning; the compound is contraindicated in patients with recent myocardial infarction or stroke. Treatment duration is 12 months (loss of effect with longer treatment). Used as the canonical anti-sclerostin agent.

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-368Open 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
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.

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-384Open 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
Beta-Hydroxybutyrate (BHB)

Our opinion on this compoundEstablished, active research

49/100

Endogenous ketone with a real HDAC story, but novelty ceiling is low for a metabolite your liver makes daily

Look, BHB is one of those compounds where the question isn’t whether it does something interesting, it’s whether you’re actually learning anything new by studying it. Your liver produces it whenever you fast past 12 hours. That basic fact puts a ceiling on how exciting the molecule can be as a research object, no matter how elegant the downstream biology turns out to be.

And the downstream biology is genuinely more interesting than the fuel-substrate story suggests. The Shimazu group’s 2013 Cell paper showing BHB inhibits class I HDACs (specifically HDAC1, 2, and 3) at low millimolar concentrations changed how serious metabolic researchers think about fasting. That’s not a trivial mechanism. HDAC inhibition drives FOXO3a activation and upregulates oxidative stress resistance genes, which connects the ketogenic state to longevity biology in a way thats not just hand-waving. The GPR109A agonism adds another layer: this receptor mediates anti-lipolytic and anti-inflammatory effects in adipose and immune tissue, and it’s the same target that makes niacin interesting at the vascular level. Multi-target, real signal.

The problem is the evidence base is scattered across too many indications to cohere into a single compelling research story. Exercise performance data from the Clarke and Holdsworth labs using ketone esters is among the cleanest human data we have on exogenous ketones, but effect sizes in trained athletes are modest and context-dependent. The Alzheimer and cognitive work is built mostly on the AC-1202/Axona medium-chain triglyceride history and more recent ketone ester pilot studies: directionally interesting, replication incomplete. The longevity angle via mTOR modulation and autophagy induction is predominantly preclinical, and isolating BHB’s contribution from the broader fasting context is methodologically hard.

What we actually like about BHB for bench work is the HDAC angle used as an epigenetic tool. If you want to model class I HDAC inhibition in a physiologically relevant way, exogenous BHB gives you a probe that your cell already recognizes. That has real value in metabolic and neuroepigenetics research that synthetic HDAC inhibitors with off-target profiles don’t fully replicate. The ketone monoester formulation (Delta G, formerly HVMN Ketone) is the format serious exercise physiology labs have standardized on for controlled BHB elevation; BHB salts are cheaper but raise plasma osmolality in ways that confound interpretation.

The overall picture: a compound worth having in a metabolic or longevity research program, with a mechanism story that holds up, but not something that would make a serious investigator rearrange their priorities. The HDAC and GPR109A angles keep it above the metabolite baseline; the endogenous ceiling keeps it from competing with genuinely novel research compounds.

Novelty

30

Mechanism promise

55

In-category differentiation

45

Evidence quality

58

Translational signal

50

Research bench value

65

Rationale BHB escapes the foundational-metabolite cap because the HDAC class I inhibitor discovery (Shimazu et al., 2013) and GPR109A signaling angle constitute a genuinely mechanistically interesting layer beyond simple fuel supplementation, analogous to how Mg-threonate escapes the basic-mineral cap. Scored as established-active: solid multi-mechanism biology, decent clinical evidence in exercise and some cognitive work, but novelty is inherently constrained because this is an endogenous molecule produced by normal hepatic metabolism.

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

Endogenous ketone body / signaling metabolite

Beta-hydroxybutyric acid; the principal endogenous ketone body; a metabolic fuel and HDAC inhibitor with cognitive and longevity research interest.

Abstract

Beta-hydroxybutyrate (BHB, (R)-3-hydroxybutyric acid; CAS 625-72-9; molecular formula C4H8O3; molecular weight 104.10) is the principal endogenous ketone body, produced by hepatic mitochondrial beta-oxidation of fatty acids during fasting, ketogenic dieting, prolonged exercise, or insulin deficiency. The compound serves multiple roles: as a metabolic fuel substrate for brain, heart, and skeletal muscle (oxidized via beta-hydroxybutyrate dehydrogenase to acetoacetate, then to acetyl-CoA for TCA cycle entry); as an endogenous HDAC inhibitor (specifically class I HDACs at low millimolar concentrations); and as a ligand at hydroxycarboxylic acid receptor 2 (HCA2/GPR109A). Approved clinical use is the historical ketogenic diet for refractory pediatric epilepsy. Research interest spans neurodegenerative disease (Alzheimer, Parkinson), cognition, longevity (mTOR/autophagy modulation), and exercise performance (ketone supplementation in endurance sport). BHB salts (Ca, Na, Mg, K salts) and esters (1,3-butanediol esters of BHB) are sold as ergogenic supplements; the ketone monoester (HVMN Ketone, Delta G) is the most thoroughly studied. Plasma half-life of exogenous BHB is approximately 1 to 3 hours depending on formulation. Used as the canonical ketone body in metabolic and longevity 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-400Open 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
CDP-Choline (Citicoline)

Plain-language summaryIntrigue 66 / 100

CDP-Choline (citicoline) is a nucleotide form of choline used in stroke recovery research and as a cognitive supplement. It supports acetylcholine and phospholipid synthesis. 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

43/100

Mature multi-target cholinergic nucleotide with real mechanism depth, undercut by two decisive null pivotal trials

Look, CDP-choline is one of those compounds where the mechanism story is genuinely more interesting than the clinical track record deserves. The compound has been characterized since Kennedy and Weiss worked out the phosphatidylcholine biosynthesis pathway in 1956, which already tells you something about where we are on the novelty curve. What makes it more than a simple choline donor is the dual-delivery design: oral CDP-choline is rapidly hydrolyzed at the intestinal wall and liver into cytidine and choline, and it’s the cytidine that adds real pharmacological texture. Cytidine converts in human plasma to uridine, which gets into pyrimidine signaling, nerve growth factor potentiation, and synaptic glycoprotein synthesis in a way that plain alpha-GPC or choline bitartrate simply cant replicate. Thats the mechanism angle that keeps this compound interesting even after six decades of use.

Here’s the thing though: the flagship human trials are a real problem. ICTUS was a large, well-powered multicenter RCT in acute ischemic stroke across Spain, and it came back negative on its primary functional endpoint at 90 days. COBRIT was the NIH-sponsored TBI trial, and it too showed no benefit over placebo on the neurological function composite. These weren’t small or poorly designed trials. If CDP-choline’s membrane-stabilizing and phospholipid-restorative mechanisms were going to show up clinically, stroke and TBI are exactly where you’d expect it. They didn’t. That’s not fatal to the compound, but it does define where you should and shouldn’t be investing research effort in 2026.

The areas where the human signal is more credible are also more modest: age-related cognitive impairment, where multiple smaller RCTs have shown consistent if unremarkable improvements on memory and attention composites, and the glaucoma and optic neuropathy literature, where there’s a plausible mechanism (retinal ganglion cell phospholipid support) and some early multi-center replication. The substance dependence signal (cocaine cravings, heavy smoking) is also genuinely interesting and worth tracking, though the effect sizes are modest and the mechanism isnt fully articulated.

For bench use, CDP-choline is a real and useful compound for investigators studying the Kennedy pathway, cholinergic modulation in cortical circuits, or uridine signaling in neurotrophic contexts. It’s not an indispensable probe in the way rapamycin is for mTOR work, but it’s not bench-inert either. We think the most underexplored legitimate angle right now is the cytidine-to-uridine conversion and what that does upstream of NGF signaling in aging neural tissue. That question hasn’t been adequately answered. Everything else about CDP-choline has been reasonably well characterized, which is also why a serious researcher looking for their next project probably doesn’t start here. Solid compound, mature story, ceiling is visible from where you’re standing.

Novelty

22

Mechanism promise

45

In-category differentiation

45

Evidence quality

60

Translational signal

48

Research bench value

42

Rationale CDP-choline scores in the established-active tier because it has genuine mechanism complexity (Kennedy pathway dual delivery plus uridine signaling) and a substantial multi-RCT evidence base, but the ICTUS stroke trial and COBRIT TBI trial both returned null primary endpoints, which compresses translational signal and novelty scores significantly. The compound retains differentiated bench utility relative to plain cholinergic donors but is not a frontier research target.

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

Cholinergic precursor / nucleotide

Cytidine 5′-diphosphocholine, an endogenous nucleotide intermediate in phosphatidylcholine synthesis with neuroprotective and cognitive enhancement applications.

Abstract

Citicoline (cytidine 5′-diphosphocholine, CDP-Choline; CAS 987-78-0; molecular formula C14H26N4O11P2; molecular weight 488.32) is an endogenous nucleotide intermediate in the Kennedy pathway for phosphatidylcholine biosynthesis. Exogenous citicoline is hydrolyzed in the gut to cytidine and choline, which are absorbed independently and reassembled centrally as needed. The bioavailability profile differs from alpha-GPC: citicoline does not cross the blood-brain barrier intact at therapeutic concentrations; the elevation in central choline derives from increased availability of the precursor pools. The compound is approved as a medicine in many countries (Italy, Spain, Japan, Mexico, much of Latin America) for ischemic stroke, traumatic brain injury, and chronic cerebrovascular disease. Large randomized trials (ICTUS, COBRIT) have produced mixed results; meta-analysis suggests modest benefit in acute stroke recovery and chronic cognitive impairment with effect sizes in the 0.2 to 0.4 range. The compound is sold as a dietary supplement in the United States. Pharmacokinetics: plasma half-life of cytidine and choline components is several hours after dissociation; the CDP-Choline structure itself is not detectable in serum after oral administration. Doses are typically 500 to 2000 mg per day. Excellent safety profile with rare serious adverse events.

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-042Open 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
PEPA

Plain-language summaryIntrigue 32 / 100

PEPA is a sulfonamide AMPA potentiator developed in Japan. Used as a research probe for AMPA receptor 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 compoundNiche research probe

42/100

Potent AMPA PAM with sharp in vitro probe value but fatal PK and no translational signal

Look, PEPA occupies a very specific niche in the AMPA receptor pharmacology toolkit, and understanding that niche is the whole story. The compound’s core value is as a high-potency positive allosteric modulator of AMPA-type glutamate receptors, and its sulfonamide scaffold gives it a mechanistic fingerprint distinct from the benzamide ampakines like CX-614 or the aniracetam derivatives that most investigators reach for first. AMPA receptor potentiation is genuinely interesting biology. Positive allosteric modulation slows receptor desensitization and deactivation, amplifies AMPA-mediated currents, and downstream recruits BDNF signaling cascades implicated in LTP and synaptic consolidation. That’s a real mechanism with real relevance to cognitive neuroscience.

Here’s the thing though: PEPA’s potency advantage over marketed ampakines is real in vitro and essentially academic in vivo. The compound has poor oral bioavailability and a short plasma half-life that have kept it firmly in the cell culture and slice prep world. Investigators trying to use it for in vivo behavioral work face serious delivery challenges that newer AMPA PAMs in the research literature dont have. That PK profile isn’t a minor inconvenience, it’s a structural limitation that caps how much you can ask of this compound as a research tool.

What we like: the potency-per-molecule is legitimately high, and for receptor binding studies, selectivity profiling, and electrophysiology in brain slices, PEPA gives you sharp, clean AMPA potentiation that’s useful for dissecting receptor subtype contributions. The sulfonamide scaffold also offers SAR diversity that benzamide-class AMPA PAMs dont, which gives it genuine value for chemists doing scaffold comparisons or exploring allosteric site geometry. For a program centered squarely on AMPA receptor biology, this compound earns a spot on the shelf.

What we dont like: availability is a real constraint. PEPA hasn’t crossed into research-chemical-grade commercial supply in any meaningful way, which means sourcing is limited to academic supply chains and adds friction to any program trying to use it at scale. And without human data of any kind, its translational story is essentially zero. The broader ampakine class has had a rough decade in Phase 2 trials, and PEPA’s poor PK means it was never even a candidate to generate the kind of clinical signal that would make it more interesting from an investment standpoint.

Honestly, this is a probe compound doing exactly what probe compounds are supposed to do: give you mechanistic resolution in controlled in vitro settings. For AMPA receptor pharmacologists specifically, its genuinely useful. For anyone outside that niche, theres little reason to engage with it over compounds that offer better translational geometry. A score of 42 reflects that accurately. High bench value in a narrow context, with almost nothing pointing toward broader relevance.

Novelty

38

Mechanism promise

58

In-category differentiation

42

Evidence quality

38

Translational signal

18

Research bench value

60

Rationale PEPA’s primary scoring axis is bench value as a high-potency sulfonamide AMPA PAM with a distinct mechanistic fingerprint from the benzamide ampakines, but poor oral bioavailability and a short plasma half-life confine it to cell culture and slice prep applications, producing essentially zero translational signal and dragging the overall down to niche-probe territory; novelty is modest because AMPA PAMs as a class date to the 1990s.

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

Sulfonamide AMPA potentiator

A potent benzothiazide AMPA potentiator used principally as a research probe for AMPA receptor pharmacology.

Abstract

PEPA (4-[2-(phenylsulfonylamino)ethylthio]-2,6-difluoro-phenoxyacetamide; CAS 158235-23-7) is a potent sulfonamide-class AMPA receptor positive allosteric modulator developed as a research tool compound. The compound shows substantially greater AMPA potentiation per molecule than the marketed and Phase 2 ampakines, but with poor pharmacokinetic properties (low oral bioavailability, short plasma half-life) that limit clinical translation. PEPA is used principally as a research probe for AMPA receptor pharmacology in vitro and ex vivo. The compound has not been advanced to human clinical trials and has no significant research-chemical-grade availability outside academic research supply chains.

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-059Open 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
GHRP-2

Plain-language summaryIntrigue 60 / 100

GHRP-2 is a synthetic peptide that activates the ghrelin receptor and triggers growth hormone release. It is a stronger growth hormone releaser than ipamorelin but also raises cortisol and prolactin slightly. 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

Solid second-generation GHRP with clinical validation but largely outpaced by cleaner, more selective successors

Look, GHRP-2 is a legitimate compound with a real mechanism and honest clinical use. It’s approved in Japan as a GH stimulation test agent, which is more than most peptides in this library can claim. GHS-R1a agonism is well-characterized, the synergy with GHRH analogs is reproducible across labs, and the pharmacokinetics are understood well enough to design clean experiments around it. For basic GH-axis work, it does exactly what it says.

But here’s the thing: GHRP-2 occupies an awkward middle position in its own class. It came after GHRP-6 and before ipamorelin, and that timeline shows. GHRP-6 still has a niche because its off-target ghrelin receptor effects drive appetite stimulation, which some investigators actually want to study. Ipamorelin has the opposite advantage: far cleaner selectivity, minimal cortisol and prolactin bleed, and a sharper tool for anyone trying to isolate GH-axis pharmacology from the noise. GHRP-2 sits between those two, offering stronger GH output than GHRP-6 but less receptor fidelity than ipamorelin. In practice, most researchers who care about clean GH secretagogue biology reach for ipamorelin. Those who want ghrelin receptor pleiotropy study GHRP-6 or ghrelin itself. GHRP-2 doesnt own either lane.

On the evidence side, theres real multi-lab data, replicated GH stimulation studies, and the diagnostic clinical use that most peptides lack. We’re not calling this single-lab-only territory. The problem is that the evidence base is mature in the wrong direction: most of it is decades old, and recent literature on GHRP-2 specifically is thin. When researchers publish GH secretagogue work now, theyre comparing newer molecules, and GHRP-2 mostly appears as a historical comparator or a positive control.

We think bench value is real but unexceptional. GHRP-2 is a serviceable probe for GHS-R1a biology, and it has the advantage of being widely sourced with decent quality consistency. But its not the tool you pick when you want to ask a sharp, specific question about ghrelin receptor pharmacology. Ipamorelin gives you better receptor selectivity for those experiments. GHRP-2 gives you more raw GH output, which matters if GH pulse amplitude is itself the variable of interest rather than a confound.

Honestly, if you’re building a GHRP-focused program from scratch today, GHRP-2 is probably not your first choice. It earns its place in reference panels and in labs that already have it on the shelf, but its not where the interesting new biology in this space is happening. The overall score reflects a compound with genuine historical significance and solid evidence, that is nonetheless unlikely to surprise a serious investigator or open a research question they couldn’t otherwise pursue.

Novelty

28

Mechanism promise

42

In-category differentiation

28

Evidence quality

52

Translational signal

48

Research bench value

48

Rationale GHRP-2 sits in the middle of the GHRP class: more efficacious than GHRP-6 on GH output, less selective than ipamorelin, and carrying 1990s-era origins that put it squarely in the established-mature bracket. Its clinical diagnostic use in Japan gives it real translational standing, but that distinction does little to differentiate it from ipamorelin, which is the GHRP most serious GH-axis investigators now reach for first.

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

Growth hormone releasing peptide / ghrelin receptor agonist

A second-generation hexapeptide ghrelin receptor agonist for growth hormone release, characterized by stronger GH stimulation than GHRP-6 with reduced cortisol/prolactin elevation.

Abstract

GHRP-2 (Pralmorelin; D-Ala-D-2-Naphthyl-Ala-Ala-Trp-D-Phe-Lys-NH2; CAS 158861-67-7; molecular formula C45H55N9O6; molecular weight 817.97) is a second-generation growth hormone releasing peptide developed in the 1990s as a synthetic ghrelin receptor (GHS-R1a) agonist. The compound stimulates pituitary GH release through a mechanism distinct from GHRH (different receptor; synergistic when combined with GHRH or GHRH analogs). GHRP-2 produces robust GH pulses approximately 2 to 5 times baseline with parenteral administration. Pharmacokinetics: plasma half-life 15 to 60 minutes; subcutaneous and intravenous routes; oral bioavailability poor due to peptidase degradation. The compound is used clinically in Japan as a GH stimulation test. Compared with GHRP-6, GHRP-2 produces stronger GH release with reduced cortisol and prolactin elevation. Compared with ipamorelin, GHRP-2 has higher GH efficacy but less receptor selectivity. Research-grade doses are typically 100 to 300 micrograms subcutaneously per administration, often combined with a GHRH analog.

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-076Open 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
Melanotan II

Plain-language summaryIntrigue 65 / 100

Melanotan II is a cyclic version of melanotan I, more potent and shorter-acting. It produces tanning, libido enhancement, and appetite suppression through different melanocortin receptor subtypes. Used in research and unsanctioned tanning communities. 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 compoundOverhyped vs evidence

29/100

Superseded by selective analogs on every front, with safety signals that compound the case against it as a research tool

Look, MT-II had its moment. The University of Arizona melanocortin program in the early 1990s was genuinely interesting science: a cyclic heptapeptide that simultaneously drives pigmentation and sexual response by hitting MC1 and MC4 with real affinity, plus meaningful activity at MC3 and MC5. That non-selective receptor hit profile taught us a lot about melanocortin biology. The problem is that what we learned from it was essentially: we need selective analogs. And we got them.

Every application MT-II was being studied for now has a better tool. For pigmentation and erythropoietic protoporphyria applications, afamelanotide (Scenesse) is MC1-selective, approved in both Europe and the US, backed by legitimate phase 3 data. For sexual dysfunction research, bremelanotide (PT-141, Vyleesi) hit FDA approval in 2019 as the MC4/MC3-selective successor. MT-II is the crude substrate that both of those compounds were explicitly designed to replace. Thats not a minor historical footnote; it’s the primary frame for evaluating what MT-II is good for now.

The non-selectivity is the core bench problem. If you’re studying MC4 signaling, you don’t want MC1, MC3, and MC5 activation muddying the readout. If you’re studying melanocyte biology, simultaneous cardiovascular and autonomic effects from MC3/MC4 hit complicate every endpoint. Selective tools now exist for every sub-problem MT-II was applied to, and serious mechanistic work has largely moved to them. MT-II is a blunt instrument in a field that has scalpels.

The safety signals are real and not dismissible. Case reports of melanocyte dysplasia and atypical mole development following MT-II use are in the literature. Blood pressure elevation and nausea are reliable enough adverse effects that no honest monograph omits them. None of this makes bench research impossible, but it raises the cost and the risk-management overhead of every experiment without providing a corresponding mechanistic advantage.

The evidence base itself is lopsided. The Arizona trials generated real early human data, but once afamelanotide and bremelanotide entered clinical development, the research community followed the selective analogs. What remains for MT-II is a scattered mix of older preclinical work, small uncontrolled human observations, and a large volume of gray-market anecdote that doesn’t belong in a research context. We don’t see a compelling case for prioritizing MT-II. The melanocortin system is legitimately interesting biology; if thats your program, the selective tools give you cleaner signal, better safety profiles, and actual regulatory precedent to anchor your study design.

Novelty

22

Mechanism promise

35

In-category differentiation

18

Evidence quality

35

Translational signal

40

Research bench value

28

Rationale MT-II’s non-selective MC1/MC3/MC4/MC5 profile was historically instructive but has since been deliberately engineered away in every downstream clinical application; afamelanotide owns the pigmentation space and bremelanotide owns the sexual function space, both with actual regulatory backing. Melanocyte dysplasia case reports and cardiovascular adverse events raise the cost of experimental use without providing any compensating mechanistic advantage over the selective tools now available.

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

Cyclic alpha-MSH analog

A cyclic alpha-MSH analog with both skin pigmentation and sexual response effects, sold as a research chemical with significant safety concerns.

Abstract

Melanotan II (MT-II; CAS 121062-08-6; molecular formula C50H69N15O9; molecular weight 1024.18) is a cyclic heptapeptide alpha-MSH analog developed at the University of Arizona in parallel with Melanotan I. The compound shows higher receptor affinity than the linear Melanotan I but with non-selective melanocortin receptor activity (MC1, MC3, MC4, MC5). The clinical effect profile combines the skin pigmentation of MC1 activation with the sexual response effects of MC4 activation; this dual activity led to development of the more selective bremelanotide for sexual function applications and sustained pigmentation via Melanotan I. Melanotan II is not approved by any regulatory authority and is sold as a research chemical with significant safety concerns: the non-selective receptor activity produces reliable adverse events including nausea, flushing, blood pressure elevation, and concerning case reports of melanocyte dysplasia and atypical mole development. The compound should be regarded as substantially more hazardous than the more selective marketed melanocortin agonists.

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-093Open 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
Ashwagandha (Withania somnifera)

Plain-language summaryIntrigue 62 / 100

Ashwagandha (Withania somnifera) is an Ayurvedic adaptogenic root used for thousands of years. The withanolides class drives the cortisol-lowering and anxiolytic effects. Studies show modest cortisol reduction and stress benefit. 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 compoundGeneric nutrient

35/100

Well-characterized OTC adaptogen with real but modest clinical signal, now largely settled science

Cap applied Common OTC food/herb (max 35)

Look, ashwagandha is about as well-characterized as a botanical gets in 2026. KSM-66 (Ixoreal Biomed) and Sensoril (Natreon) have accumulated a genuine RCT base that most herbs can only dream about. The cortisol reduction is real. The anxiety signal on DASS-21 and Hamilton Anxiety scales is real. The modest testosterone bump in men with suppressed baseline is real. We’re not dismissing those findings. The problem is that all of those findings are also now settled, replicated, and frankly unremarkable for a serious bench scientist looking for frontier work.

The mechanism story is the central weakness here. “Multimodal” sounds like a feature but in this case its a liability. GABA-A allosteric modulation, diffuse HPA axis effects, modest serotonergic activity, and withanolide-driven heat shock protein modulation — these are not cleanly separable in any extract you can actually run an experiment with. Withaferin A has its own cancer biology angle that gets published separately and is more interesting than the anxiolytic story, but that’s a different compound question entirely. When you want to probe a receptor system, you reach for a compound that binds it with specificity. Ashwagandha doesn’t give you that.

What we don’t like: the standardized extract space is saturated with commercial interests. KSM-66 has funded a significant portion of its own trial literature, and while the data aren’t fabricated, the independence question is real. The effect sizes in cortisol trials (typically 15 to 25 percent reduction) and muscle strength studies are modest. These are clinically soft endpoints, not mechanistic windows into biology. And the compound has been in continuous human use for several thousand years — theres no indication space left that’s genuinely unexplored.

For a researcher whose program touches HPA axis biology, there are more useful and selective tools: metyrapone for cortisol synthesis blockade, CRH antagonists, ACTH analogs. For GABA-A work, you have a century of defined pharmacology to pull from. Ashwagandha sits in neither of those lanes cleanly. It’s a genuinely well-evidenced OTC supplement, which is almost the definition of a low research-priority compound for investigators who can work with defined chemistry. The withanolide chemistry itself is undercharacterized at the single-molecule level, and thats probably where the actual frontier is if there is one — but thats not what standardized root extract gives you.

Honest bottom line: this belongs in a clinical nutrition context, not a serious research program. The literature is mature, the effects are modest, the probe value is low, and the mechanism is too diffuse to build a serious investigative program around.

Novelty

22

Mechanism promise

30

In-category differentiation

38

Evidence quality

50

Translational signal

50

Research bench value

30

Rationale Ashwagandha clears the bar for real clinical evidence in its class, with KSM-66 and Sensoril RCT data producing genuine cortisol and anxiety signals, but novelty is essentially zero and its messy withanolide mixture makes it a poor pharmacological probe. The OTC herb cap binds at 35, and the raw weighted score (36) lands just above it, confirming placement.

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

Ayurvedic adaptogenic root extract

A root extract from Withania somnifera standardized to withanolides, with documented anxiolytic, cortisol-lowering, and testosterone-supporting effects.

Abstract

Ashwagandha (Withania somnifera) is a small evergreen shrub root used in Ayurvedic medicine for stress, anxiety, fatigue, and physical performance. The active constituents are withanolides (notably withaferin A, withanolide A, and others), with commercial extracts standardized to total withanolide content (typically 5 percent or higher). The KSM-66 (Ixoreal Biomed) and Sensoril (Natreon) extracts are the most extensively studied in clinical trials. Multiple randomized trials demonstrate cortisol reduction, anxiety reduction (DASS-21, Hamilton Anxiety), modest testosterone elevation in men with low baseline, and improvements in muscle strength and endurance. Mechanism is multimodal including GABA-A receptor allosteric modulation, modest serotonergic effects, and HPA axis modulation. Doses are typically 300 to 600 mg of standardized extract per day.

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-108Open 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
ARA-290 (Cibinetide)

Plain-language summaryIntrigue 78 / 100

ARA-290 (cibinetide) is an 11-amino-acid peptide derived from the helix B portion of erythropoietin. It activates a tissue-protective receptor without raising hematocrit. Investigated for neuropathic pain. 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 compoundNovel, promising

62/100

Cleanly dissects EPO’s tissue-protective arm from erythropoiesis; novel IRR mechanism with real Phase 2 neuropathy data

Here’s the thing about ARA-290: its core insight is genuinely elegant. Erythropoietin does two very different jobs through two very different receptor complexes, and Araim’s group figured out you can have one without the other. The erythropoietic activity runs through the classical EPO homodimer. The tissue-protective, anti-inflammatory side runs through the heteromeric innate repair receptor (IRR), assembled around the CD131 beta chain it shares with IL-3 and IL-5 receptors. Brines, Cerami, and colleagues rationally designed ARA-290’s 11-residue helix B sequence to engage the IRR selectively while leaving the homodimer untouched. That isn’t lucky fragment screening; that’s real structure-guided design, and it shows.

What we like about the evidence here is the indication specificity. Small fiber neuropathy in sarcoidosis is a genuinely underserved corner of neurology. The autonomic and sensory small fibers that SFN destroys are exactly what IRR signaling appears to defend. The Phase 2 RCT in sarcoid-associated SFN showed statistically significant reductions in neuropathic pain scores alongside improvements in autonomic measures. Thats a human signal in real patients with a real unmet need, not a hopeful extrapolation from rodent nerve ligation. The bench-to-clinic translation has, at minimum, partially happened.

The limits are worth being clear about. Araim is essentially the sole development vehicle for this compound, and the trial base is still Phase 2. The mechanism literature from Brines and Cerami is solid and these are credible people with serious EPO biology credentials going back two decades, but independent multi-lab replication of the IRR pharmacology in ARA-290-specific contexts is thin. That’s not a fatal problem; it’s a real constraint on how confident you can be in the evidence package relative to compounds with broader investigator adoption.

For bench investigators, the probe value here is non-trivial. Historically, any EPO-related biology experiment had to account for the erythropoietic confound: change EPO signaling and youre also changing red cell mass, oxygen delivery, and a cascade of secondary effects. ARA-290 removes that variable cleanly. If you’re studying neuroprotection, neuroinflammation, or IRR-mediated tissue repair, this is one of the only tools that lets you probe that biology without the hematological noise. That specificity has real utility across a broader range of research contexts than the SFN indication alone implies.

We think this is a compound worth tracking for anyone working in EPO signaling, innate repair biology, or neuroprotective peptides generally. Its not top-priority for most programs, but the mechanism is genuinely novel, the clinical backing is better than most peptides in this space ever achieve, and the IRR axis may turn out to be relevant to a much wider range of tissue-injury and neuroinflammatory contexts. The score reflects real promise constrained by early-stage single-sponsor evidence, not a knock on the biology.

Novelty

62

Mechanism promise

70

In-category differentiation

68

Evidence quality

50

Translational signal

52

Research bench value

62

Rationale ARA-290 earns its score primarily on the elegance of its receptor selectivity design and genuine Phase 2 RCT backing in sarcoidosis-associated SFN; evidence quality is constrained by single-sponsor development and no Phase 3 replication yet, which keeps the overall in the low 60s rather than pushing toward the established-active tier.

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

EPO-derived helix B peptide

An 11-amino-acid fragment of erythropoietin’s helix B with tissue-protective activity but without erythropoietic activity.

Abstract

ARA-290 (Cibinetide; Gln-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser; CAS 1208243-50-8) is an 11-residue peptide derived from the alpha-helix B region of erythropoietin (EPO). The peptide retains the tissue-protective and anti-inflammatory activity of EPO (mediated through the heteromeric EPO/CD131 innate repair receptor) without the erythropoietic activity (mediated through the EPO receptor homodimer). The compound was developed by Araim Pharmaceuticals for diabetic neuropathy, sarcoidosis-associated small fiber neuropathy, and other neuropathic pain indications. Phase 2 trials in sarcoidosis-associated SFN showed reductions in neuropathic pain and improvements in autonomic measures. Doses are 4 mg subcutaneously per day in clinical trials.

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-126Open 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
Atomoxetine

Plain-language summaryIntrigue 70 / 100

Atomoxetine, sold as Strattera, is a non-stimulant ADHD medication that selectively inhibits norepinephrine reuptake. It is the standard non-stimulant choice for patients who cannot tolerate or should not take stimulants. 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

43/100

Mature unscheduled NRI with solid clinical evidence but little remaining research excitement

Look, atomoxetine is genuinely useful, and we dont want to be unfair to it. The FDA approval in 2002, the extensive clinical trial record, the well-characterized CYP2D6 pharmacogenomics, the fact that it isnt scheduled when methylphenidate and amphetamine are — all of that is real and matters. If youre building an in vitro selectivity panel for NET vs DAT vs SERT, atomoxetine is a legitimate reference compound. Its hard to argue with that.

The problem is that none of it is interesting anymore. Pure selective NET inhibition was a clinically clever idea in 2001 when the goal was avoiding stimulant scheduling issues. As a mechanism for bench-scale research in 2025, its honestly just… not compelling. Single-target, single receptor class, mechanism completely understood, pharmacology fully characterized decades ago. The CYP2D6 angle — where poor metabolizers hit a half-life of 21.6 hours versus 5.2 hours in extensive metabolizers — is one of the more underappreciated aspects, and we think theres probably still some pharmacogenomic probe value there, but that doesnt rescue the compound as a primary research target.

Differentiation has also eroded over time. Atomoxetine was first-in-class as a non-stimulant ADHD approval, and that mattered a lot in 2002. But viloxazine (Qelbree) has since entered the space with an additional serotonin modulatory component that makes it mechanistically more interesting as a research object, and guanfacine remains the go-to for the alpha-2 adrenergic story. Atomoxetine is now one of several options, not the defining compound in its category.

The translational signal is solid — multiple replicated RCTs, real effect in target populations, FDA-approved labeling that covers pediatric through adult populations. But the effect sizes versus stimulants are consistently modest, and the clinical literature is mature enough that theres limited room for a novel finding to emerge from a new atomoxetine study unless youre doing something very specific (pharmacogenomic subgroup work, cognitive subtypes, some off-label signal). We’re not seeing that kind of research momentum in the current literature.

What we like: unscheduled status, clean selectivity profile, solid sourcing and QA pipeline for a pharma compound, and genuine utility as a NET-selectivity tool in mechanistic panels. What we dont like: the mechanism is fully explored, the clinical space is mature, and if youre spending bench hours on norepinephrine biology there are more interesting entry points right now. Score of 43 reflects a compound that earns its place in a reference library but wouldnt be on our shortlist for a new research program.

Novelty

22

Mechanism promise

28

In-category differentiation

38

Evidence quality

75

Translational signal

65

Research bench value

42

Rationale Atomoxetine scores well on evidence and translational signal by virtue of its FDA approval and extensive RCT base, but novelty and mechanism promise are both low: pure NET inhibition approved in 2002, no dual-target angle, and a growing field of competitors. The overall of 43 reflects a useful-but-boring profile that a bench scientist would deprioritize against more mechanistically interesting NE-adjacent targets.

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

Selective norepinephrine reuptake inhibitor

A selective NRI FDA-approved as Strattera for ADHD, the first non-stimulant FDA-approved for the indication.

Abstract

Atomoxetine (Strattera; CAS 83015-26-3; molecular formula C17H21NO; molecular weight 255.36) is a selective norepinephrine reuptake inhibitor (NRI) developed by Eli Lilly and approved by the FDA in 2002 for ADHD in children, adolescents, and adults. The compound is the first non-stimulant FDA-approved for ADHD. Mechanism is NET inhibition; the compound is essentially inactive at DAT and SERT. Pharmacokinetics: plasma half-life 5.2 hours in extensive metabolizers via CYP2D6, 21.6 hours in poor metabolizers; doses are titrated based on response and tolerability. Approved doses are 40 to 100 mg per day. Schedule status: not scheduled (distinguishing it from amphetamine and methylphenidate ADHD therapies).

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-142Open 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 … 52 53 54 55 56 … 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.