Aviandr
AVN-101, maritupirdine — an investigational multi-target CNS compound
Aviandr (AVN-101, maritupirdine — an investigational multi-target CNS compound) is a cognitive & mood research compound. Sold as a 5-HT6 antagonist, which is not what its own developers' binding data says. The published affinities are 5-HT7 at Ki 153 pM, histamine H1 at 0.58 nM, adrenergic alpha-2A, 2B and 2C at 0.41 to 3.6 nM, and only then 5-HT6, 5-HT2A and 5-HT2C at 1.2 to 2.0 nM. The receptor the product is named for is roughly eight to thirteen times weaker than its strongest target and is outranked by an antihistamine site and three adrenergic ones. Because receptors fill in order of affinity, any dose high enough to occupy 5-HT6 has already saturated the histamine and adrenergic targets — there is no selective window.
Aviandr quick facts
| Route | Oral |
| Frequency | Not established · Not established |
| Half-life | Not published. Good oral bioavailability and facilitated blood-brain barrier permeability are claimed; no half-life, clearance route or metabolizing enzyme is given |
| Forms | Oral |
| Evidence level | One phase I tolerability study, described inside a single paper by its developers. No efficacy trial in patients has been published in the ten years since. |
The catalog calls this a 5-HT6 antagonist. Its own developers' paper says the highest-affinity target is 5-HT7, and that histamine H1 at 0.58 nM binds tighter than 5-HT6 does — which is antihistamine territory and predicts sedation rather than sharpening. Meanwhile the 5-HT6 thesis itself has been tested at scale and failed twice: intepirdine in 1,315 patients at phase 3 and masupirdine in 564 at phase 2, both null. A class failure does not prove a particular molecule fails, but a product sold on that thesis is being sold on a losing record — and the entire human evidence for this one is a phase I in healthy volunteers.
How Aviandr works
Sold as a 5-HT6 antagonist, which is not what its own developers' binding data says. The published affinities are 5-HT7 at Ki 153 pM, histamine H1 at 0.58 nM, adrenergic alpha-2A, 2B and 2C at 0.41 to 3.6 nM, and only then 5-HT6, 5-HT2A and 5-HT2C at 1.2 to 2.0 nM. The receptor the product is named for is roughly eight to thirteen times weaker than its strongest target and is outranked by an antihistamine site and three adrenergic ones. Because receptors fill in order of affinity, any dose high enough to occupy 5-HT6 has already saturated the histamine and adrenergic targets — there is no selective window.
Proposed benefits
Researched for focus, memory, neuroprotection, mood and stress resilience.
Where to get Aviandr
Buy Aviandr at RUPharma →The evidence for Aviandr
Graded by what exists behind each claim.
✅ Clinically validated
- The entire human record is one phase I study, described inside a single paper by the people developing it (Ivachtchenko 2016). Its clinical claim is that the compound was well tolerated orally at doses up to 20 mg daily and did not prolong the QT interval. The product sold is a 20 mg tablet — the ceiling of the only tested range.
- No efficacy trial in patients has been published in the ten years since, in any of the five indications the 2016 paper proposed.
📊 Correlative data
- The mechanism it is sold on has been tested at scale and failed twice. MINDSET randomized 1,315 people with mild-to-moderate Alzheimer's dementia to intepirdine 35 mg or placebo on stable donepezil for 24 weeks: ADAS-Cog -0.36 (p=0.2249) and ADCS-ADL -0.09 (p=0.8260), neither significant (Lang 2021). Masupirdine in 564 randomized patients over 26 weeks was also non-significant on ADAS-Cog 11 (Nirogi 2022).
- A class failure is not proof a particular molecule fails, and the reviews still treat 5-HT6 as an open target (Nirogi 2023, Chagraoui 2025). What the trials establish is that the hypothesis has been given 1,879 randomized patients and returned nothing on the endpoints it was built to move.
🧪 Theoretical / extrapolated
- The catalog calls it a 5-HT6 antagonist and its own developers' binding data says otherwise: 5-HT7 at Ki 153 pM, histamine H1 at 0.58 nM, adrenergic alpha-2A/2B/2C at 0.41-3.6 nM, and only then 5-HT6, 5-HT2A and 5-HT2C at 1.2-2.0 nM.
- Because receptors fill in order of affinity, any dose high enough to occupy 5-HT6 has already saturated the histamine and adrenergic targets. There is no window in which this behaves as a selective 5-HT6 drug.
- Predicted downside: an H1 affinity of 0.58 nM is sedating-antihistamine territory, which predicts daytime drowsiness and additive effect with alcohol — the opposite of a cognitive enhancer. The paper reports affinity only and never states whether the compound is an agonist or antagonist at the alpha-2 sites, so the direction of its autonomic effect is genuinely unknown.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Aviandr actually does
The catalog calls this a 5-HT6 antagonist. Its own developers' paper says 5-HT6 is not its strongest target, and not its second or third either. Ivachtchenko 2016 reports the binding affinities directly: 5-HT7 at Ki = 153 pM, then histamine H1 at 0.58 nM, then adrenergic alpha-2A, 2B and 2C at 0.41 to 3.6 nM, and only then 5-HT6, 5-HT2A and 5-HT2C at 1.2 to 2.0 nM. On those numbers the receptor the product is named for is roughly eight to thirteen times weaker than the one it binds hardest, and it is outranked by an antihistamine target and three adrenergic ones. The paper's own title calls the molecule multi-target. The listing does not.
The histamine number is the one a buyer will actually feel. An H1 affinity of 0.58 nM is in the range of drugs prescribed as sedating antihistamines, and central H1 blockade is the standard pharmacological explanation for daytime sleepiness and weight gain in several psychiatric drug classes. Anyone taking this and reporting that it calms them down is describing an effect that the affinity table predicts without reference to serotonin at all.
One thing the paper does not say, and it matters. The abstract reports affinity at the adrenergic and histamine targets without stating whether the molecule is an agonist, an antagonist or an inverse agonist at each. Affinity says a drug binds; it does not say what happens next. For the alpha-2 receptors that distinction reverses the expected cardiovascular effect, so the published record leaves the direction of the drug's autonomic influence undetermined.
What is being sold. An investigational compound, 20 mg per tablet, at $57, with no marketing approval in any country. The reviews of the target class Nirogi 2023 Chagraoui 2025 treat 5-HT6 ligands as investigational agents, which is the correct description of everything in this family including this one.
Cell, rodent, human — and where it stops
The human record for this molecule is one phase I study, described inside a single paper written by the people developing it. Ivachtchenko 2016 reports molecular pharmacology, in vitro ADME, animal and human pharmacokinetics as part of the phase I program, biodistribution, animal efficacy and a safety profile. Its clinical claim is precisely this: the compound was well tolerated when taken orally at doses of up to 20 mg daily, did not markedly change plasma or urine biochemistry, and did not prolong the QT interval. That is a tolerability finding in healthy volunteers. There is no published efficacy trial in patients, and a search on 9 September 2026 returns none.
The tablet on sale is at the top of the tested range. The phase I statement covers doses up to 20 mg daily, and the product is a 20 mg tablet. A buyer taking one a day is at the ceiling of the only dose range any human data exists for; a buyer taking two is outside it entirely, with no published basis for what happens there.
Meanwhile the mechanism it is sold on was tested at scale and failed twice. Lang 2021 is MINDSET: a global double-blind randomized placebo-controlled phase 3 trial of the 5-HT6 antagonist intepirdine added to donepezil in 1,315 people with mild-to-moderate Alzheimer's dementia, 35 mg daily for 24 weeks. Neither co-primary endpoint moved: ADAS-Cog -0.36 (95% CI -0.95 to 0.22, p = 0.2249) and ADCS-ADL -0.09 (-0.90 to 0.72, p = 0.8260). Nirogi 2022 is masupirdine, a second 5-HT6 antagonist, in 564 randomized patients over 26 weeks on a donepezil and memantine background, with statistically non-significant differences on ADAS-Cog 11 and no significant effect on any secondary measure.
Read that the right way round. Those are two negative trials of other molecules, and a class failure is not proof that a particular compound fails — the reviews Nirogi 2023 Chagraoui 2025 are still written as accounts of an open research area rather than a closed one. What the trials do establish is that the 5-HT6 hypothesis has been given 1,879 randomized patients across two adequately sized studies and returned nothing on the endpoints it was built to move. A product sold on that hypothesis is being sold on a thesis with a losing record.
Aviandr pharmacokinetics — how much of it actually gets in
What the developers published, and what they did not. Ivachtchenko 2016 states good oral bioavailability and facilitated blood-brain barrier permeability, and reports pharmacokinetics in animals and in humans as part of phase I. It does not give a half-life, a time to peak, a clearance route or a metabolizing enzyme in its abstract. So the two qualitative claims a central nervous system drug most needs are present and every number that would let somebody design a schedule is absent.
The affinity table is the closest thing to a dose-response argument available. Occupancy rises with concentration, and receptors are recruited in order of affinity. At low exposure the 153 pM 5-HT7 site is engaged essentially alone; as concentration climbs, the 0.58 nM histamine H1 site and the 0.41 to 3.6 nM alpha-2 sites come in; 5-HT6 at 1.2 to 2.0 nM is among the last to fill Ivachtchenko 2016. The consequence is uncomfortable for the marketing: any dose high enough to meaningfully occupy 5-HT6 has already saturated the histamine and adrenergic targets. There is no window in which this behaves as a selective 5-HT6 drug.
The QT statement, read exactly. The phase I report says the compound does not prolong the QT interval at doses up to 20 mg daily Ivachtchenko 2016. That is a real and useful negative — QT prolongation is the failure mode that ends most multi-receptor central nervous system programs — and it is bounded by the dose studied. It says nothing about 40 mg, and nothing about 20 mg taken alongside another QT-active drug.
Why no schedule appears on this page. Without a half-life there is no accumulation estimate, without a clearance route there is no interaction map, and with a single phase I as the entire human dataset there is no exposure-response curve. This page states no dose.
What would have to be true, and how you would know it was not
Three predictions, and the first is testable by anybody on the first day.
1. Daytime sedation and reaction time, not memory. Given an H1 affinity of 0.58 nM Ivachtchenko 2016, the prediction is that a psychomotor vigilance test or a simple reaction-time task gets worse in the hours after a dose, and that most subjective reports describe calm and drowsiness. That is the opposite of a cognitive enhancer, it follows from the published binding data rather than from suspicion, and it is measured with a phone app.
2. Resting heart rate and a standing blood pressure, morning and evening, for two weeks. The alpha-2 affinities are high and the published record does not say whether the compound is an agonist or an antagonist there Ivachtchenko 2016, which means the direction of the autonomic effect is genuinely unknown. That makes this the single most informative cheap measurement available: agonism at alpha-2 lowers sympathetic outflow, antagonism raises it, and the two look nothing alike on a blood pressure cuff.
3. Against the product: MMSE or MoCA at baseline and 12 weeks. Two randomized trials totaling 1,879 patients found nothing on cognitive endpoints for two other drugs built on this target Lang 2021 Nirogi 2022. Prediction for a healthy adult on this one: no change beyond test-retest variation. Nobody has run a cognitive efficacy trial of this molecule in anybody, which is why the prediction is the honest content of the page.
What nobody has tested yet
Nobody has published a phase II of this compound. The 2016 paper says the primary therapeutic area to be tested in clinical trials would be Alzheimer's disease, and proposes generalized anxiety disorder, depression, schizophrenia and multiple sclerosis as further targets Ivachtchenko 2016. A search on 9 September 2026 returns no efficacy trial in any of the five, ten years later. A development program that publishes a phase I and then nothing is a fact a buyer is entitled to weigh.
Nobody has established the functional direction at the adrenergic and histamine sites. The abstract reports affinity only Ivachtchenko 2016. Whether the molecule blocks or activates alpha-2A determines whether it lowers or raises noradrenergic tone, which is the difference between a sedative and a stimulant on the autonomic side. A standard functional assay would settle it and none is published.
Nobody has separated the 5-HT7 effect from the rest. The highest-affinity target by an order of magnitude is 5-HT7 at 153 pM, a receptor with its own literature in circadian regulation and mood. If this molecule does anything in a person, that is the most likely site, and no study has tested a 5-HT7-relevant endpoint — sleep architecture, circadian phase, mood scale — in anyone taking it.
Extrapolation, labeled as such. If the class failures are about the target rather than the molecules Lang 2021 Nirogi 2022, then a fourth 5-HT6 antagonist should also fail, and this compound's multi-target profile is either its rescue or its confound. The experiment that would distinguish those is a trial that measures 5-HT7-mediated endpoints alongside cognition. The reviews of the field Nirogi 2023 Chagraoui 2025 describe the target as still open, and it will stay open until somebody runs that study.
Aviandr — its own safety story, not its class's
Three things this compound owns, and the first is a status rather than a side effect.
This is an investigational drug being sold at retail. It holds no marketing approval anywhere, which means no regulator has reviewed a manufacturing file, no pharmacopoeial monograph defines purity or impurity limits, and no adverse-event reporting system exists to collect what happens to the people taking it. The phase I tolerability statement Ivachtchenko 2016 describes a supervised study of a characterized batch. It does not transfer to a tablet bought online, because the thing being bought has not been shown to be the thing that was studied.
The sedation risk is predictable and the driving risk follows from it. Central histamine H1 occupancy at 0.58 nM affinity Ivachtchenko 2016 is the mechanism behind the drowsiness of first-generation antihistamines, and it compounds with alcohol and with every other sedating agent. Somebody who takes this expecting a nootropic and then drives has not been warned by anything on the product listing.
The absence of a QT problem is bounded by the dose that was tested. The phase I found no QT prolongation up to 20 mg daily Ivachtchenko 2016. Multi-receptor central nervous system compounds are the class where QT effects most often appear, the study was small and short as phase I studies are, and nothing at all is known about higher doses or about combination with the many common drugs that lengthen the interval. A negative in a small early study is a reason to keep looking, not a clearance.
Sources read for this page
- Ivachtchenko AV, Lavrovsky Y, Okun I. AVN-101: A Multi-Target Drug Candidate for the Treatment of CNS Disorders. Journal of Alzheimer's Disease 2016 · PMID 27232215
- Lang FM, Mo Y, Sabbagh M, et al. Intepirdine as adjunctive therapy to donepezil for mild-to-moderate Alzheimer's disease: a randomized, placebo-controlled, phase 3 clinical trial (MINDSET). Alzheimer's & Dementia: Translational Research & Clinical Interventions 2021 · PMID 34095437
- Nirogi R, Ieni J, Goyal VK, et al. Effect of masupirdine (SUVN-502) on cognition in patients with moderate Alzheimer's disease: a randomized, double-blind, phase 2, proof-of-concept study. Alzheimer's & Dementia: Translational Research & Clinical Interventions 2022 · PMID 35662833
- Nirogi R. Progress in Investigational Agents Targeting Serotonin-6 Receptors for the Treatment of Brain Disorders. Biomolecules 2023 · PMID 36830678
- Chagraoui A. 5-HT6 receptors: contemporary views on their neurobiological and pharmacological relevance in neuropsychiatric disorders. Dialogues in Clinical Neuroscience 2025 · PMID 40347153
Aviandr — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Aviandr moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Most of this class has no predicted marker movement at all, and saying so is more useful than listing markers that will not move.
What to do: A baseline liver panel is reasonable for anything taken daily and long-term. Beyond that there is nothing specific to chase.
- Dose range and how to work up to it
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Aviandr in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Aviandr
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| TSH (Thyroid-Stimulating Hormone) | Thyroid disease imitates every cognitive complaint there is |
| Vitamin B12 | Deficiency causes fog long before it causes anemia |
| Methylmalonic Acid (MMA) | Catches the deficiency a normal B12 hides |
| Ferritin | Low iron flattens cognition at levels most labs call fine |
| Vitamin D (25-Hydroxy) | Commonly low, cheap to correct, associated with mood |
The Brain Fog & Cognition panel covers these in one order — 12 markers, $233.06 with the discount applied.
Check results you already have → · All 103 markers A–Z
Aviandr — frequently asked questions
What is Aviandr?
Aviandr (AVN-101, maritupirdine — an investigational multi-target CNS compound) is a cognitive & mood research compound. Sold as a 5-HT6 antagonist, which is not what its own developers' binding data says. The published affinities are 5-HT7 at Ki 153 pM, histamine H1 at 0.58 nM, adrenergic alpha-2A, 2B and 2C at 0.41 to 3.6 nM, and only then 5-HT6, 5-HT2A and 5-HT2C at 1.2 to 2.0 nM. The receptor the product is named for is roughly eight to thirteen times weaker than its strongest target and is outranked by an antihistamine site and three adrenergic ones. Because receptors fill in order of affinity, any dose high enough to occupy 5-HT6 has already saturated the histamine and adrenergic targets — there is no selective window.
Where can I find Aviandr dosing and protocols?
Dosing, the reconstitution calculator and Coach Cam's full Aviandr protocol are available to members inside Skool. This public page covers what Aviandr is, how it works and the evidence.
What is the half-life of Aviandr?
Aviandr has an approximate half-life of Not published. Good oral bioavailability and facilitated blood-brain barrier permeability are claimed; no half-life, clearance route or metabolizing enzyme is given, which is part of what determines how often it's dosed.
What's the evidence behind Aviandr?
Current evidence level: One phase I tolerability study, described inside a single paper by its developers. No efficacy trial in patients has been published in the ten years since.. Aviandr is offered for research purposes only and is not an approved medicine.
What Aviandr is used for
Aviandr appears under 1 goal in the goal router.
Related Cognitive & Mood compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.