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Author: kodiac

L-Glutamine

Plain-language summaryIntrigue 38 / 100

L-glutamine is the most abundant free amino acid in human plasma, serving as a fuel substrate for gut lining cells and immune cells and as an ammonia transport carrier. Clinical evidence is solid in critical illness contexts (severe burns, sepsis, post-surgical recovery), where parenteral or enteral glutamine improves nitrogen balance and may reduce infection rates. The popular supplement use in healthy athletes for recovery and immune support, however, has very thin supporting evidence: most oral glutamine is extracted by the gut on first pass and never reaches systemic circulation. Reference amino acid in immunometabolism and clinical nutrition research, but generally overhyped in the supplement context. 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 Kodiac editorial, not peer-reviewed.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 compoundBasic amino acid

28/100

Conditionally essential amino acid with solid critical-care history but minimal frontier research value

Look, glutamine is the most abundant free amino acid in human plasma, and that abundance tells you something important: this is basic cellular infrastructure, not frontier pharmacology. The compound has been characterized for decades. The biology is mature. The interesting questions about glutamine have largely been answered, and the field has moved on to more specific modulators of the pathways glutamine feeds into.

The mechanism is real and worth understanding. Enterocytes and immune cells run on glutamine during catabolic stress states, and in the ICU context, burns, sepsis, post-surgical recovery, parenteral and enteral glutamine supplementation has demonstrated genuine benefit. Nitrogen balance improvements and reduced infection rates have been replicated across multiple centers. Thats legitimate evidence, and we give it credit here. The problem is what happens when you move outside the critical care ward.

Oral supplementation in healthy or recreationally active individuals is a fundamentally different situation. The gut extracts the vast majority before it reaches systemic circulation. Plasma half-life is about an hour. Claims around athlete recovery, gut permeability, and immune support in healthy populations have not held up well under controlled conditions. The supplement market ran well ahead of the evidence and stayed there. We dont find this surprising given the pharmacokinetics.

As a research tool, glutamine has a narrow supporting role. It functions as a reference amino acid in immunometabolism work, useful for establishing nitrogen flux baselines, tracking amino acid transfer via metabolic tracers, and studying enterocyte energy dependence. But thats a background role in someone else’s experiment. The more interesting action in amino acid signaling right now sits with SLC1A5/ASCT2 modulators, glutaminase inhibitors in oncology (CB-839 and related compounds), and the intersection of glutamine sensing and mTOR complex activation. Those are the derivative questions worth pursuing; glutamine itself is the substrate, not the lever.

The one area we’d monitor is the critical-illness subpopulation question. There’s ongoing effort to define which patients actually benefit and at what illness stage, including revisiting the mixed results from the REDOX and SUGARMILL trials. That’s clinical nutrition work with real stakes. But it’s not exploratory pharmacology and it doesn’t change what glutamine is as a research object.

For the library, glutamine earns its place as reference context. It’s part of the vocabulary. It’s not an investigation target for a serious bench program right now.

Novelty

10

Mechanism promise

18

In-category differentiation

18

Evidence quality

52

Translational signal

48

Research bench value

38

Rationale Raw calculation lands at 28, already below the 32 basic-aa cap, so the cap does not further limit the score. Novelty and differentiation drag the total down hard; evidence gets partial credit for replicated critical-care trials, but bench value is narrow and translational signal evaporates outside the ICU context.

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

Conditionally essential amino acid (immunometabolic substrate)

L-glutamine; the most abundant free amino acid in plasma; a substrate for enterocyte and immune cell metabolism and a popular but evidence-limited supplement.

Abstract

L-glutamine ((S)-2,5-diamino-5-oxopentanoic acid; CAS 56-85-9; molecular formula C5H10N2O3; molecular weight 146.14) is a conditionally essential alpha-amino acid that is the most abundant free amino acid in human plasma (approximately 500 to 800 micromolar). Glutamine is biosynthesized from glutamate and ammonia by glutamine synthetase, with skeletal muscle and lung as principal source tissues. The compound serves as a substrate for enterocyte and immune cell metabolism (the principal biological role outside protein synthesis) and as an ammonia transport carrier. Clinical use is well-established in critical illness (burn injury, sepsis, post-surgery) where parenteral or enteral glutamine improves nitrogen balance and may reduce infection rates; the supplement use in healthy athletes for recovery and immune support has limited supporting evidence. Plasma half-life is approximately 1 hour; the gut largely extracts oral glutamine, with minimal systemic delivery. Used as a reference amino acid in immunometabolism and clinical nutrition research.

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

May 9, 2026
Gabapentin

Plain-language summaryIntrigue 65 / 100

Gabapentin (Neurontin) is the older sibling of pregabalin from Parke-Davis, FDA-approved in 1993, and it works by the same mechanism: binding the alpha-2-delta subunit of voltage-gated calcium channels, with no actual effect on GABA receptors despite the misleading name. The big practical difference from pregabalin is dose-response: gabapentin’s intestinal absorption saturates, so doubling the dose does not double the blood level, which makes high doses inefficient. Approved for postherpetic neuralgia and partial seizures, with massive off-label use for anxiety, sleep, alcohol withdrawal, restless legs, and chronic pain. The Pfizer off-label marketing campaign that drove its sales in the 1990s was the subject of a landmark fraud settlement. Abuse potential is real but lower than pregabalin’s. 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

41/100

Mature alpha-2-delta ligand superseded by pregabalin clinically; still a clean reference probe for VGCC subunit biology

Look, gabapentin has been in the literature since 1993 and the research community has had more than three decades to extract novelty from it. For a bench scientist asking what deserves time right now, this isn’t the answer. But thats not the same as saying it has no place in the library.

The mechanism is genuinely specific: gabapentin binds the alpha-2-delta-1 subunit of voltage-gated calcium channels with a Ki of roughly 80 nM. Despite the name, it has no meaningful activity at GABA-A or GABA-B receptors. What it does is reduce presynaptic calcium influx and downstream neurotransmitter release at sensitized synapses. That mechanism is clean and validated across hundreds of independent studies. The problem is that everyone already knows this. The pharmacology has been squeezed for novelty and the returns have diminished sharply.

What really sinks it as a frontier research target is the pharmacokinetics combined with the availability of better tools. Gabapentin relies on a saturable intestinal transporter for absorption. Bioavailability can hit 80 percent at low doses and collapse to around 27 percent at 1600 mg, producing nonlinear dose-response and frustrating individual variability in clinical work. Pregabalin solved that transporter saturation problem and achieved linear absorption, which is a large part of why it has displaced gabapentin in most new pharmacological programs. If you need a selective alpha-2-delta-1 ligand for a clean assay, you have options and some are meaningfully better.

The clinical evidence base is real and substantial. Multiple large phase 3 trials, FDA approval for postherpetic neuralgia and partial-onset seizures, and an extensive off-label literature covering neuropathic pain broadly, anxiety, alcohol withdrawal, and restless legs syndrome. We don’t find the off-label literature particularly compelling as a research signal. Much of it is small-N, inconsistent in methodology, and complicated by the well-documented history of off-label promotion litigation against Pfizer. The clean translational signal sits in the original approved indications.

As a probe, gabapentin still earns its keep in a narrow context. If you’re studying alpha-2-delta-1 subunit trafficking, presynaptic calcium dynamics in dorsal root ganglia, or the molecular basis of central sensitization, gabapentin is the reference ligand. The literature density means any result you generate is immediately contextualizable. For that specific utility, we actually think it belongs in the library.

What we don’t think is that it qualifies as interesting research territory. The real mechanistic questions in this space are being asked with more selective or structurally novel tools. Gabapentin functions like a positive control: necessary to have, not exciting to use. A score of 41 reflects exactly that balance, strong evidence and clinical history dragging up a compound with very little research novelty left in the tank.

Novelty

20

Mechanism promise

28

In-category differentiation

22

Evidence quality

72

Translational signal

68

Research bench value

55

Rationale Gabapentin scores low on novelty and differentiation because it is a 1993 approval with a well-understood mechanism and a clearly superior successor in most contexts; evidence and translational scores are pulled up by its approved-drug pedigree and large clinical dataset, while bench value is rescued by its canonical role as the alpha-2-delta-1 probe in seizure and pain pharmacology programs.

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

GABA analog calcium channel ligand

A GABA analog binding the alpha-2-delta subunit of voltage-gated calcium channels; the structural and clinical predecessor to pregabalin.

Abstract

Gabapentin (1-(aminomethyl)cyclohexaneacetic acid; CAS 60142-96-3; molecular formula C9H17NO2; molecular weight 171.24) is a GABA analog developed at Parke-Davis (Pfizer) in the 1980s and approved by the FDA in 1993 under the trade name Neurontin. Mechanism mirrors pregabalin: binding to the alpha-2-delta-1 subunit of voltage-gated calcium channels (Ki approximately 80 nM, weaker than pregabalin), reducing presynaptic neurotransmitter release. No direct GABA receptor activity. Plasma half-life is 5 to 7 hours. Distinguished from pregabalin by saturable absorption: oral bioavailability ranges from 80 percent at 100 mg to 27 percent at 1600 mg, producing nonlinear dose-response and unpredictable individual responses at higher doses. Approved for postherpetic neuralgia and partial-onset seizures (adjunctive); off-label use is extensive (anxiety, alcohol withdrawal, restless legs syndrome, hot flashes, hiccups, neuropathic pain of all causes, migraine prophylaxis). The compound has been the subject of extensive off-label promotion litigation and is now scheduled in some US states reflecting abuse potential. Used as the canonical alpha-2-delta-1 calcium channel ligand and a reference compound in seizure pharmacology.

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

May 9, 2026
Hydroxyzine

Plain-language summaryIntrigue 56 / 100

Hydroxyzine (Atarax, Vistaril) is a first-generation antihistamine from UCB, approved in 1956, that crosses the blood-brain barrier readily and produces sedation and anxiolysis as a result. It is FDA-approved for anxiety and pruritus (itching), and unlike benzodiazepines it has no dependence or withdrawal potential, which makes it a useful first-line option for situational anxiety in patients with substance use histories. The trade-off is that the same antihistamine and anticholinergic effects produce dry mouth, constipation, urinary retention, and next-day grogginess. The active leftover after liver metabolism is cetirizine (Zyrtec), the over-the-counter allergy drug, which does not cross into the brain at clinical doses. 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

38/100

A 1956-approved FDA drug with solid clinical evidence and essentially no research frontier left to explore

Look, hydroxyzine is a real drug. FDA approved in 1956, over a billion patient-exposures, solid randomized data for generalized anxiety and pruritus, a clean non-scheduled status that made it clinically useful before buspirone or the SSRIs arrived. We’re not dismissing it clinically. We’re saying there’s almost nothing here for a bench investigator in 2026 that hasn’t been settled for decades.

The mechanism is H1 antagonism at roughly 2 nM affinity, secondary 5-HT2A blockade around 10 nM, and a weak D2 component. That multi-receptor fingerprint is interesting in the abstract, but it’s fully mapped, well-understood, and not pointing at anything new. The 5-HT2A angle doesn’t give you psychoplastogen biology; the D2 component isn’t the basis for a new antipsychotic story. You’re reading 1980s receptor binding papers when you go looking for mechanism literature here.

What’s genuinely useful about hydroxyzine as a research tool is the metabolite relationship. Hydroxyzine produces cetirizine in vivo, and cetirizine loses CNS penetration because of the carboxylic acid group. That pairing has been used as a probe model to interrogate what H1-mediated CNS penetration actually contributes versus peripheral H1 blockade. Thats a narrow but real utility. If you’re building a pharmacokinetic or CNS-penetration model around first-generation antihistamines, hydroxyzine earns a seat at the table. For anything else, it doesn’t.

The evidence base is strong by the standards of research compounds. Multiple replicated RCTs across anxiety and pruritus indications, decent Hamilton Anxiety Rating Scale data, perioperative sedation trials. The HAMA studies from the 1970s through the 1990s were reasonably well-designed for their era. You’re not dealing with single-lab preclinical data and Croatian rodent models here. But strong evidence for a fully-characterized approved drug is actually the least interesting kind of strong evidence when you’re trying to identify what to study next.

We don’t see a compelling frontier angle. The anxiolysis mechanism isn’t being revisited in a new light. The H1 space isn’t generating exciting new biology. The drug’s non-controlled status is a clinical feature, not a research opportunity. If your program touches first-gen antihistamines as comparators or pharmacokinetic probes, hydroxyzine is a reasonable tool to have documented. As a primary research target in its own right, honestly, you’re working from a 1956 foundation with nowhere obvious to go.

Novelty

12

Mechanism promise

22

In-category differentiation

32

Evidence quality

68

Translational signal

65

Research bench value

45

Rationale Hydroxyzine scores low on novelty and mechanism because it’s a 70-year-old approved drug with a fully characterized H1/5-HT2A/D2 profile; the high evidence and translational scores reflect its genuine approved-drug trial base, but those can’t rescue the overall when the compound offers nothing a serious investigator hasn’t seen. Bench value gets a modest credit for its canonical probe role comparing CNS-penetrant vs. non-penetrant antihistamine effects via its cetirizine metabolite relationship.

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

First-generation H1 antihistamine anxiolytic

A first-generation piperazine H1 antihistamine with anxiolytic activity; the first non-controlled anxiolytic widely used in psychiatry.

Abstract

Hydroxyzine (2-(2-{4-[(4-chlorophenyl)(phenyl)methyl]piperazin-1-yl}ethoxy)ethanol; CAS 68-88-2; molecular formula C21H27ClN2O2; molecular weight 374.91) is a first-generation piperazine H1 antihistamine developed at UCB and approved by the FDA in 1956 under the trade names Atarax and Vistaril. Distinct from later antihistamines by clinically significant CNS penetration, producing the sedation and anxiolytic effects characteristic of first-generation H1 blockers. H1 affinity approximately 2 nM; secondary 5-HT2A antagonism (Ki approximately 10 nM) and weak D2 antagonism contribute to the anxiolytic profile. The principal active metabolite cetirizine retains H1 antagonism but loses CNS penetration owing to addition of a carboxylic acid group, and is marketed separately as a non-sedating antihistamine (Zyrtec). Plasma half-life is 14 to 25 hours; metabolism is hepatic. Approved for anxiety, pruritus, and as a preoperative sedative; off-label use in insomnia and as a benzodiazepine-sparing anxiolytic. Used as the canonical first-generation H1 antihistamine in mechanism studies.

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

May 9, 2026
Gaboxadol (THIP)

Our opinion on this compoundNiche research probe

61/100

The canonical extrasynaptic delta-GABA-A probe; therapeutically abandoned but mechanistically irreplaceable for tonic inhibition research

Look, gaboxadol is a weird one to rate because it exists in two completely separate stories simultaneously. The first story is a clinical failure: Lundbeck and Merck took it through Phase 3 in primary insomnia, watched patients experience disorientation and hallucinations, and pulled the plug in 2007. That story is over. The second story is the interesting one, and its the reason gaboxadol belongs in this library at all.

Here’s the thing about the mechanism. Most GABA pharmacology targets synaptic receptors, the alpha1/2/3-beta-gamma2 isoforms that benzodiazepines and z-drugs hit. Those receptors mediate phasic inhibition, fast transient signals. Gaboxadol does something different: it’s a superagonist at extrasynaptic GABA-A receptors bearing the delta subunit, primarily alpha4-beta3-delta and alpha6-beta3-delta, and those receptors mediate tonic inhibition, the continuous low-amplitude background current that sets the excitability baseline of a neuron. Thats a genuinely different biological variable, and most of the GABA pharmacology toolkit doesn’t let you isolate it cleanly.

We think the differentiation here is underappreciated. Muscimol hits both synaptic and extrasynaptic receptors indiscriminately. DS2, a delta-selective PAM, modulates the receptor but doesn’t agonize it directly. If you want to study what delta-subunit tonic GABA-A current actually does in a circuit, gaboxadol is effectively the only clean pharmacological lever. That’s a real niche, and it’s gotten more interesting since the brexanolone and zuranolone data validated the delta-subunit angle for neurosteroid-sensitive states. Labs working on PMDD biology, alcohol use disorder, stress-related changes in inhibitory tone, or sleep architecture at the subunit level are going to want this compound on the shelf.

The evidence picture is decent for a failed drug. Multiple Phase 3 trials ran to completion before the adverse event signal emerged. That means there’s actual human pharmacology data: real EEG effects, real sleep architecture changes, real CNS penetration confirmed by the adverse events themselves. Preclinical literature is solid and multi-lab. The translational signal is real but it points toward a wall therapeutically, which is why the score here isn’t higher overall.

Honestly, if you’re not working on GABA-A subunit biology specifically, this compound probably isn’t your priority. The clinical failure isn’t a reason to ignore it, but it does mean the research community actively using it is a specialist one. For those investigators, it’s close to indispensable. For everyone else, it’s a footnote in GABA pharmacology history with a genuinely interesting mechanism they probably won’t have occasion to use.

Novelty

48

Mechanism promise

68

In-category differentiation

72

Evidence quality

60

Translational signal

45

Research bench value

75

Rationale Gaboxadol failed Phase 3 as a hypnotic due to adverse psychiatric events, but the mechanism is intact and validated; it scores high on differentiation and bench value because no other compound selectively probes extrasynaptic delta-containing GABA-A receptors with the same precision, making it indispensable for labs working on tonic inhibition, neurosteroid sensitivity, or delta-subunit biology specifically.

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

Selective extrasynaptic GABA-A delta-subunit agonist

A 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol agonist selective for extrasynaptic GABA-A receptors containing the delta subunit; investigated as a hypnotic.

Abstract

Gaboxadol (THIP; 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol; CAS 64603-91-4; molecular formula C6H8N2O2; molecular weight 140.14) is a selective extrasynaptic GABA-A receptor agonist developed at Lundbeck and Merck through the 1990s and 2000s. Distinct from benzodiazepines and barbiturates by selective binding to GABA-A receptor isoforms containing the delta subunit (alpha4-beta3-delta and alpha6-beta3-delta), which are predominantly extrasynaptic and mediate tonic (continuous, low-amplitude) inhibition rather than the phasic (high-amplitude, transient) inhibition mediated by synaptic alpha1/2/3-beta-gamma2 receptors. The compound is a superagonist at delta-containing receptors (efficacy greater than that of GABA itself). Phase 3 trials in primary insomnia (2007) were halted following adverse psychiatric events including disorientation and hallucinations; development was abandoned. The compound retains research utility as the canonical extrasynaptic delta-GABA-A agonist for academic GABA pharmacology and sleep architecture studies. Plasma half-life is approximately 1.5 to 2 hours.

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

May 9, 2026
Tofisopam

Plain-language summaryIntrigue 56 / 100

Tofisopam (Grandaxin) is an unusual benzodiazepine from EGIS in Hungary, registered in the 1960s. The chemistry is technically a benzodiazepine, but the substitution pattern (a 2,3-fused ring rather than the standard 1,4-fused ring of diazepam and lorazepam) means it does not bind the classic GABA-A benzodiazepine site at all. As a result it produces anxiolysis without sedation, muscle relaxation, cognitive impairment, or dependence. The actual mechanism is not fully worked out, with proposals including phosphodiesterase inhibition and dopaminergic modulation. Approved across Europe and parts of Asia for anxiety and autonomic dysfunction; never approved in the US. Genuinely interesting pharmacologically because it shows that the benzodiazepine scaffold can do more than activate GABA-A. 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

51/100

A structurally distinct non-GABA-A anxiolytic with real probe value and an incompletely mapped mechanism worth investigating

Here’s the thing about tofisopam: it’s not a benzodiazepine in the way that word usually lands. Yes, the diazepine ring is there, but the nitrogen positions are at the 2,3 carbons rather than the 1,4 positions of diazepam or lorazepam, and that single structural difference eliminates binding at the classical benzodiazepine allosteric site on GABA-A receptors entirely. That means no sedation from GABA current potentiation, no muscle relaxation from that pathway, and by most accounts no physical dependence profile that mirrors classical benzos. EGIS Pharmaceuticals in Hungary developed it in the 1960s, and it’s been marketed as Grandaxin in Hungary, France, and several Asian markets for decades under indications that include anxiety, autonomic instability, and post-stress recovery. For a compound this old to still have an incompletely characterized mechanism is either a red flag or a research opportunity depending on how you look at it.

We lean toward opportunity, cautiously. The leading hypotheses for tofisopam’s activity include phosphodiesterase IV (PDE4) inhibition and some form of dopaminergic modulation, possibly both operating in parallel. PDE4 inhibition is not a trivial mechanism: roflumilast got approved for COPD on that axis, and the neuroimmune and cognitive implications of PDE4 in the CNS have attracted serious attention over the last decade. If tofisopam genuinely hits PDE4 with relevant potency in neural tissue, thats a more interesting story than it usually gets credit for. The dopaminergic angle is less characterized but could explain the reported antifatigue and mood-brightening effects that dont fit a pure anxiolytic profile. What we dont have is a clean pharmacological dissection confirming which target drives which effect at clinically relevant concentrations.

The evidence base is the main drag on the score. Tofisopam has human approval, which is real, but the supporting literature is heavily weighted toward Eastern European clinical work from the 1970s through the 1990s, published in journals that dont make modern replication standards easy to verify. There isnt a modern phase 2 or phase 3 RCT benchmarking it against placebo or active comparators with current methodology. The preclinical literature is sparse compared to what you’d want before building a research program around it.

Where tofisopam earns its keep is as a reference tool. If your lab is trying to understand what non-GABAergic, non-serotonergic anxiolysis looks like pharmacologically, it’s essentially the only 2,3-benzodiazepine with a usable human history and commercial availability. That niche is real but narrow. Honestly, it scores where it scores because it’s genuinely interesting as a probe without being important enough in any active research conversation to rank higher. Investigators in autonomic pharmacology or PDE4 neuroimmunology should know it exists.

Novelty

42

Mechanism promise

55

In-category differentiation

60

Evidence quality

40

Translational signal

48

Research bench value

60

Rationale Tofisopam’s 2,3-benzodiazepine scaffold genuinely sidesteps classical GABA-A activity, making it the reference probe for non-sedating, non-dependence-forming anxiolysis via a mechanism that still isn’t fully nailed down; the European approval provides a real human signal, but the evidence base is dominated by older Eastern European literature with limited modern replication, keeping differentiation and bench value from pulling the score higher.

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

2,3-benzodiazepine atypical anxiolytic

A 2,3-benzodiazepine without classical GABA-A activity; a non-sedating anxiolytic marketed in Europe.

Abstract

Tofisopam (1-(3,4-dimethoxyphenyl)-5-ethyl-7,8-dimethoxy-4-methyl-5H-2,3-benzodiazepine; CAS 22345-47-7; molecular formula C22H26N2O4; molecular weight 382.46) is a 2,3-benzodiazepine developed at EGIS (Hungary) in the 1960s and approved in Hungary, France, and other European and Asian markets under the trade name Grandaxin. Distinct from the 1,4-benzodiazepine class (diazepam, lorazepam, etc.) by the position of the nitrogens in the diazepine ring: the 2,3 isomer does not bind the classical benzodiazepine site on GABA-A receptors and lacks the GABA-A-mediated sedation, anxiolysis, and dependence of conventional benzodiazepines. The mechanism is incompletely characterized; possibilities include phosphodiesterase IV inhibition and modulation of dopaminergic signaling. Plasma half-life is approximately 6 to 8 hours; metabolism is hepatic. Approved indications in markets where registered include anxiety disorders, autonomic instability, and post-stress recovery; off-label use in fatigue and reactive depression. Not approved in the US. Used as a reference 2,3-benzodiazepine.

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

May 9, 2026
Propranolol

Plain-language summaryIntrigue 73 / 100

Propranolol (Inderal) is the first commercially successful beta-blocker, developed by James Black at ICI and approved by the FDA in 1967. Black’s work on it earned him the Nobel Prize and reshaped cardiovascular medicine. It blocks both subtypes of beta-adrenergic receptor, dampening the heart’s response to adrenaline as well as the bronchial and metabolic effects. Beyond its many cardiovascular uses, it has a substantial second life in psychiatry and neurology: it is the standard prescription for performance anxiety (one or two tablets before public speaking blunts the heart-pounding and tremor without affecting cognition), is first-line for migraine prevention, and has been studied for trauma memory reconsolidation in PTSD. Lipophilic enough to cross into the brain, which contributes to both its therapeutic and side effects. 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

41/100

Historical cornerstone with almost no remaining research novelty; valuable as a canonical non-selective beta-blocker probe

Look, propranolol is one of the most consequential drugs in the history of pharmacology. James Black’s Nobel Prize was built partly on it. And yet, as a research target in 2026, it’s almost entirely spent. That’s the tension the score reflects, and it’s not a close call.

The cardiovascular evidence base is airtight. Hypertension, angina, atrial fibrillation, migraine prophylaxis, essential tremor — six approved indications and decades of replicated RCTs sitting behind each of them. The pharmacokinetics have been characterized exhaustively: non-selective beta-1 and beta-2 blockade, 3-to-6 hour half-life, high lipophilicity giving CNS penetration that hydrophilic competitors like atenolol and nadolol simply lack. Those properties earned it permanent status as the reference non-selective beta-blocker. That reference-compound identity is essentially its only remaining research value — real, but narrow.

The most interesting live research angle is the PTSD memory reconsolidation work, and we want to be honest about what that actually is. The mechanistic logic is genuinely clever: noradrenergic signaling in the basolateral amygdala is required for fear memory reconsolidation, so blocking beta-adrenergic receptors during a deliberate recall event should attenuate reconsolidation and weaken the traumatic memory. Pitman’s Harvard MGH group published the original proof-of-concept in 2002. Alain Brunet’s Montreal lab has been the most persistent investigator, including a 2018 randomized trial in PTSD patients showing meaningful symptom reduction. The signal is real. But the 2019 Cochrane review found the evidence base insufficient, effect sizes across studies are modest, and its been 24 years since the founding paper. Calling this novel would be a stretch.

The novelty problem is fundamental. Beta-adrenergic blockade has been understood mechanistically since the 1960s. No new chemistry, no new mechanisms, no structural innovations. For reconsolidation paradigms specifically, metoprolol covers most of the same ground, and timolol is another option with similar CNS access. Propranolol has first-mover advantage in this niche and a denser associated literature, but its not uniquely irreplaceable in most bench designs.

What we like: the translational track record is definitive, and for performance anxiety studies, adrenergic probe work, or reconsolidation paradigms, its the right tool and the right reference. What we don’t like: the mechanism is fully characterized, the novelty is gone, and the questions propranolol can uniquely answer are getting fewer every year. A serious investigator building a new research program around propranolol in 2026 would need a very specific reason. This is a historical cornerstone, not a frontier compound.

Novelty

10

Mechanism promise

20

In-category differentiation

30

Evidence quality

80

Translational signal

80

Research bench value

50

Rationale Propranolol scores extremely low on novelty and mechanism — it’s a 1967 drug with single-receptor, fully-characterized pharmacology and no new chemistry — but pulls evidence and translational scores high owing to its approved-drug status across six indications and 60 years of clinical use; the PTSD memory reconsolidation angle is the most interesting current research use case, but Pitman’s foundational work is 24 years old and replication remains mixed, preventing a meaningful novelty rescue.

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

Non-selective beta-adrenergic antagonist

A non-selective beta-adrenergic antagonist; the first beta-blocker, repurposed for performance anxiety and migraine prophylaxis.

Abstract

Propranolol (1-(naphthalen-1-yloxy)-3-(propan-2-ylamino)propan-2-ol; CAS 525-66-6; molecular formula C16H21NO2; molecular weight 259.34) is a non-selective beta-adrenergic antagonist developed by James Black at ICI and approved by the FDA in 1967 under the trade name Inderal. The compound is the first commercially successful beta-blocker, foundational to modern cardiovascular pharmacology. Beta-1 affinity is approximately equal to beta-2 affinity (non-selective). Plasma half-life is 3 to 6 hours; the lipophilic structure produces high CNS penetration, distinguishing propranolol from hydrophilic beta-blockers (atenolol, nadolol) for indications requiring central effect. Approved indications include hypertension, angina, atrial fibrillation, migraine prophylaxis, essential tremor, and hypertrophic cardiomyopathy. Off-label use is extensive: performance anxiety (most common psychiatric indication), PTSD memory reconsolidation, akathisia, hyperthyroid tachycardia. The 5-HT receptor partial agonism (weak) was a former curiosity but is not clinically meaningful at standard doses. Used as the canonical non-selective beta-blocker reference compound.

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May 9, 2026
Pindolol

Plain-language summaryIntrigue 48 / 100

Pindolol is an old beta-blocker, FDA-approved in 1982, that lowers blood pressure by quieting the heart. What makes it interesting outside cardiology is a side activity: it binds tightly to a serotonin receptor (5-HT1A) that normally throttles serotonin release. By turning off that throttle alongside an SSRI antidepressant, pindolol was hypothesized to make the SSRI kick in faster (days rather than weeks). Trials produced mixed results, with some studies showing accelerated response in depression and others showing nothing. It is still used occasionally in psychiatry as an SSRI booster, but never became standard practice. 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

37/100

Old beta-blocker with real 5-HT1A probe value, but inconsistent clinical signal limits excitement

Look, pindolol is one of those compounds where the mechanism is more interesting than the compound itself. Approved for hypertension in 1982, it spent years as a fairly unremarkable non-selective beta-blocker until researchers noticed something: it binds 5-HT1A receptors with real affinity (Ki around 50 nM) and acts as a partial agonist there. That property got it drafted into psychiatric research as an SSRI augmentor in the 1990s, and for a while it was genuinely intriguing.

The hypothesis was elegant. SSRIs lose their first two weeks to autoreceptor-mediated negative feedback at the raphe. Add a 5-HT1A partial agonist like pindolol, and you desensitize those presynaptic autoreceptors faster, in theory compressing the latency to antidepressant effect. Multiple placebo-controlled trials tested this through the late 1990s and into the 2000s. Some showed a real 1-2 week acceleration. Others did not. The meta-analyses are frustrating reading: positive signal on onset, weaker or null signal on overall efficacy. That inconsistency is the core problem with this compound as a research target, and we think it explains why the field mostly moved on.

Where pindolol still earns its place in a serious library is as a probe. Its specific combination of beta-blockade plus 5-HT1A partial agonism is hard to replicate with other tools. If you’re running mechanistic work on presynaptic serotonin autoreceptor desensitization, or trying to parse the cardiovascular from the serotonergic components of a drug interaction, pindolol gives you a handle thats difficult to replace. Its been called the canonical 5-HT1A binding beta-blocker in mechanism studies for good reason. Buspirone is more selective at 5-HT1A but lacks the beta component entirely. That combination makes pindolol genuinely useful for dissecting receptor contributions in mixed-pharmacology contexts.

What we dont love: the SSRI augmentation question is basically settled as disappointing, the compound is old enough that most interesting questions about it have been asked, and the short half-life (3-4 hours) is a practical nuisance in research designs. Its not a novel mechanism, not a novel compound, and the translational arrow from preclinical to clinical is pointing in different directions depending on which trial you read.

Honestly, if youre building a research program around serotonin autoreceptor biology and need a pharmacological tool with a specific dual profile, pindolol is worth having. As a primary research target in its own right? The case is thin. The probe utility is real but narrow, and the clinical inconsistency means the translational story never really closed.

Novelty

20

Mechanism promise

42

In-category differentiation

35

Evidence quality

45

Translational signal

35

Research bench value

52

Rationale Pindolol scores as a niche probe because its 5-HT1A autoreceptor work is genuinely useful for serotonin pharmacology, but the compound is a 1982 FDA approval with mixed augmentation trial data; bench utility saves it from obscurity, novelty and translational inconsistency drag the overall down.

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

Non-selective beta-adrenergic antagonist with 5-HT1A partial agonism

A non-selective beta-blocker with intrinsic 5-HT1A partial agonism; investigated as an SSRI augmenting agent.

Abstract

Pindolol (1-(1H-indol-4-yloxy)-3-(propan-2-ylamino)propan-2-ol; CAS 13523-86-9; molecular formula C14H20N2O2; molecular weight 248.32) is a non-selective beta-adrenergic antagonist with intrinsic sympathomimetic activity (partial agonism) and 5-HT1A partial agonism, approved by the FDA in 1982. The compound’s distinguishing pharmacological feature in psychiatric research is high-affinity 5-HT1A binding (Ki approximately 50 nM) with partial agonist activity at presynaptic autoreceptors; concurrent administration with an SSRI desensitizes the autoreceptor more rapidly than the SSRI alone, hypothetically accelerating the antidepressant response. Multiple placebo-controlled trials in the 1990s and 2000s reported faster onset (1 to 2 weeks shorter latency) but inconsistent overall efficacy improvement. Plasma half-life is 3 to 4 hours; metabolism is hepatic. Approved indications in cardiology include hypertension and angina; the SSRI augmentation use remains off-label. Used as the canonical 5-HT1A binding beta-blocker in mechanism studies.

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

May 9, 2026
Clonidine

Plain-language summaryIntrigue 60 / 100

Clonidine is a 1960s blood-pressure drug (sold as Catapres) that turned out to be unexpectedly versatile. It works by activating alpha-2 adrenergic receptors in the brainstem, dampening the sympathetic nervous system, the body’s stress response. That single mechanism explains why it lowers blood pressure, blunts opioid withdrawal symptoms, calms tics in Tourette syndrome, and reduces hyperactivity in ADHD (often as a non-stimulant alternative or add-on to stimulants in children). It is also used to manage hot flashes and as a sedating premedication. The drug is cheap, generic, and well-characterized, with sedation and rebound hypertension on abrupt discontinuation as the main downsides. Not stocked by Kodiac. This monograph is provided for research and educational reference.

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

Our opinion on this compoundResearch workhorse

45/100

Prototype alpha-2 agonist with real bench utility but essentially zero research novelty

Look, clonidine is not a research compound in any contemporary sense of the word. Boehringer Ingelheim synthesized it in the 1960s looking for a nasal decongestant, stumbled onto a central antihypertensive, and the FDA approved it in 1974. That backstory tells you a lot about where this thing sits in 2025: its mechanism was characterized before most of today’s investigators were born, and the pharmacology has not moved since.

The mechanism is presynaptic alpha-2A autoreceptor activation in the locus coeruleus, which dials down central noradrenergic tone. Secondary imidazoline I1 activity contributes to the blood pressure effect. Both of those stories are closed chapters in the literature. Theres nothing here that opens a new question; every pathway clonidine touches has been characterized to death, and the interesting molecular biology has moved to more selective tools. Dexmedetomidine is far more alpha-2A selective. Guanfacine has a cleaner CNS profile and is now the preferred agent for ADHD in most treatment algorithms. In differentiation terms, clonidine is the prototype that got superseded.

Where we do give clonidine some credit is bench utility. It remains the canonical alpha-2 reference standard for studies of noradrenergic regulation, locus coeruleus physiology, and sympathetic nervous system modulation. If you’re designing a study that needs a clean alpha-2 agonist as a positive control or pharmacological probe, clonidine is still what most labs reach for, partly because the literature comparator base is enormous. The PTSD-associated hyperarousal work, particularly the fear consolidation studies out of Pitman and Cahill’s groups, used clonidine as the reference intervention precisely because any new agent has to beat a known standard. That kind of indispensable-comparator role keeps the bench value score from cratering.

The translational and evidence scores are the only numbers that look strong here, and honestly they should, because this is an approved drug with decades of clinical use across four labeled indications. The rebound hypertension on abrupt discontinuation is one of the best-characterized discontinuation effects in all of pharmacology. But evidence quality for a research library score is about how much we’ve learned, not how much we’ve confirmed; at this point clonidine is all confirmation, no discovery.

We think this compound belongs in the library as a reference entry, not as something an investigator would build a program around in 2025. The score of 45 reflects that: real clinical and bench-utility credit, close-to-zero novelty and mechanism credit. Use it as the comparator arm, not the experimental arm.

Novelty

18

Mechanism promise

28

In-category differentiation

35

Evidence quality

78

Translational signal

72

Research bench value

65

Rationale Clonidine scores moderate overall on the strength of its well-validated clinical record and genuine utility as the reference alpha-2 agonist in noradrenergic research, but novelty and mechanism scores drag hard because this is a 1960s compound with a fully mapped single-receptor mechanism; more selective successors like dexmedetomidine and guanfacine have largely displaced it in both clinic and bench contexts.

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

Central alpha-2 adrenergic agonist

An imidazoline alpha-2 adrenergic receptor agonist; an antihypertensive repurposed for ADHD, opioid withdrawal, and Tourette syndrome.

Abstract

Clonidine (N-(2,6-dichlorophenyl)-4,5-dihydro-1H-imidazol-2-amine; CAS 4205-90-7; molecular formula C9H9Cl2N3; molecular weight 230.10) is an imidazoline alpha-2 adrenergic agonist developed at Boehringer Ingelheim in the 1960s and approved by the FDA in 1974 under the trade name Catapres. The compound activates presynaptic alpha-2A adrenergic autoreceptors in the locus coeruleus, reducing central noradrenergic outflow and producing centrally mediated reductions in sympathetic tone, blood pressure, and heart rate. Secondary imidazoline I1 receptor activity contributes to the antihypertensive effect. Plasma half-life is 12 to 16 hours; renal excretion is the principal clearance pathway. Approved indications include hypertension, ADHD (extended-release Kapvay), opioid withdrawal, and Tourette syndrome; off-label use in insomnia, hot flashes, and PTSD-associated hyperarousal. Rebound hypertension on abrupt discontinuation is a characteristic adverse effect. The compound is widely used in academic neuroscience as the prototype alpha-2 agonist for studies of noradrenergic regulation.

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

May 9, 2026
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.

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May 9, 2026
HMB (β-Hydroxy-β-methylbutyrate)

Our opinion on this compoundEstablished workhorse

37/100

Mature anti-catabolic metabolite with real catabolic-state signal but low novelty as a research target

Look, HMB has been around since the early 1990s, and the core story hasn’t changed much. It’s a metabolite of leucine, produced via alpha-ketoisocaproate during roughly 5% of leucine catabolism, and the proposed mechanism is straightforward: reduce protein breakdown through ubiquitin-proteasome pathway inhibition while nudging mTOR signaling upward. Thats a real mechanism. Just not a particularly exciting one. We’ve known how the proteasome works for decades, and HMB’s interaction with it is well-characterized to the point of being textbook.

The evidence picture is better than you’d expect from something marketed this aggressively. In catabolic states, the signal is genuine. HIV wasting trials, cancer cachexia cohorts, bedrest-induced atrophy protocols, and post-surgical recovery studies all show meaningful lean mass preservation at 3 g/day. The Vukovich group, Flakoll et al., and several independent labs replicated this in sarcopenic and hospitalized populations. That is the compound at its best. In healthy resistance-trained athletes, the effect size compresses fast. The meta-analyses in athletic populations are messy, and the dramatic early claims from Wilson et al. didn’t survive independent replication at scale.

The free acid form (HMB-FA) has better pharmacokinetics than the calcium salt, faster absorption and higher peak plasma concentration. Interesting story in theory. But most of the foundational clinical work used Ca-HMB, so the HMB-FA literature is thinner, and the practical effect-size advantage looks modest when you read the head-to-head data carefully. Not a reason to deprioritize the compound, but not a reason to get excited either.

What we don’t like about HMB as a research target: the mechanism doesn’t point at anything that isn’t already well-mapped. If you’re trying to understand proteasome biology, you’re reaching for more specific chemical probes. If you’re trying to build an anti-catabolic protocol, you’re comparing HMB to leucine supplementation, essential amino acid formulations, and the newer mitochondrial peptide work, and HMB doesn’t come out ahead on bench utility. The probe value is real but narrow. It works best as a comparator arm in muscle-wasting trial design. That’s about its ceiling.

For investigators in catabolic biology, it earns a place as a reference compound: well-sourced, defined pharmacokinetics, clean mechanism. For anyone focused on the frontier of muscle-sparing or anti-aging research, the interesting signals are coming from myostatin pathway modulators, mitochondrial peptides, and GLP-1 adjacent compounds. HMB is the baseline you measure against, not the signal you’re chasing. Honest assessment: score this one and move on.

Novelty

22

Mechanism promise

28

In-category differentiation

35

Evidence quality

52

Translational signal

52

Research bench value

40

Rationale HMB lands just under the foundational-metabolite ceiling on its own calculated merit: the catabolic-state evidence base is genuine and multi-lab replicated, but the mechanism is unremarkable, novelty is low, and differentiation from leucine itself or EAA protocols is modest. No cap binds because the axes score it there naturally.

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

Leucine metabolite (anti-catabolic supplement)

Beta-hydroxy-beta-methylbutyrate; a leucine metabolite that reduces muscle protein breakdown; used in catabolic states and as a supplement.

Abstract

HMB (beta-hydroxy-beta-methylbutyric acid; CAS 625-08-1; molecular formula C5H10O3; molecular weight 118.13; Ca-HMB salt CAS 135236-72-5) is a metabolite of the branched-chain amino acid leucine, produced by approximately 5 percent of leucine catabolism via alpha-ketoisocaproate. Mechanism: HMB reduces muscle protein breakdown via inhibition of the ubiquitin-proteasome pathway and enhanced cell membrane integrity; secondary effects on muscle protein synthesis through mTOR pathway activation. The clinical evidence is strongest in catabolic states (HIV wasting, cancer cachexia, sarcopenia of aging, bedrest, post-surgical recovery) where 3 g/day reduces protein breakdown and preserves lean mass. In healthy resistance-trained athletes, the effect is small. The free acid form (HMB-FA) has improved pharmacokinetics over the calcium salt (Ca-HMB) but most research uses Ca-HMB. Plasma half-life is approximately 2 hours. Used as a reference anti-catabolic supplement.

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May 9, 2026

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