This page describes pharmacological agents that may have legal restrictions, side effects, and drug interactions in your jurisdiction. Information is for educational research only — consult a clinician before considering any compound.

High-risk compound

Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.

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AF710B

Extensively Studied

Anavex's M1-PAM + sigma-1 dual agonist, originally synthesized at Israel's IIBR by Abraham Fisher's group, then licensed worldwide to…

Aliases (6)

ANAVEX 3-71 · ANAVEX®3-71 · AF710-B · AVN-101 (do-not-confuse — different compound) · CAS 1235733-73-9 (racemic) · 1-(2, 8-Dimethyl-1-thia-3, "8-diazaspiro[4.5]dec-3-yl)-3-(1H-indol-3-yl)propan-1-one (B-enantiomer)

TYPICAL DOSE

10 µg/kg

Daily

ROUTE

Oral (tablet)

Oral

CYCLE

N/A — do not cycle a compound you shouldn't be …

As prescribed

STORAGE

Room temp; original container

Room temp

Overview

What is AF710B?

AF710B is an investigational orally-active allosteric M1 muscarinic acetylcholine receptor agonist with sigma-1 receptor activity, developed for Alzheimer's disease. It is designed to restore cholinergic signaling without the side-effect profile of classical M1 agonists.

Key Benefits

Preclinical reduction of amyloid-beta and tau pathology, improvement in cognitive performance in AD rat models, and restoration of cholinergic function — all at doses well below those that cause classical muscarinic side effects.

Mechanism of Action

Bitopic / allosteric M1 muscarinic agonist with concurrent sigma-1 receptor agonism. Restores cholinergic transmission and modulates intracellular calcium handling and ER stress responses, reducing tau hyperphosphorylation and amyloid burden in preclinical models.

▸Brand options2 known

ANAVEX 3-71AF710-B

StatusNot scheduled (investigational); research-use-only at MedChemExpress / TargetMol; no Rx pathway anywhere

Research Indications

Most Effective

1. M1 muscarinic positive allosteric modulator (PAM)

The M1 muscarinic acetylcholine receptor is concentrated on cortical and hippocampal pyramidal neurons and is the primary postsynaptic ch…

Effective

2. Sigma-1 receptor agonist

Sigma-1 is not a classical neurotransmitter receptor — it's a chaperone protein at the mitochondria-associated ER membrane (MAM). Under c…

Investigational

Convergence

The dual-receptor pitch: M1 amplification fixes the symptomatic cholinergic deficit *and* shifts APP toward non-amyloidogenic processing,…

Peptide Interactions

cerebrolysin

Synergistic

TrkA/TrkB neurotrophic + M1/sigma-1 chaperone is a clean theoretical pair (different pathways, both pro-survival, both disease-modifying-claim). No data.

acd-856

Synergistic

Trk-PAM amplifies BDNF/NGF signaling; M1-PAM amplifies ACh signaling. Two PAM mechanisms aimed at different transmitter systems with overlapping plasticity o…

citicoline / alpha-GPC

Synergistic

provides ACh substrate; M1-PAM amplifies whatever ACh is produced. Mechanistically clean.

Strong serotonergic agents (SSRIs, MAOIs, tramadol, MDMA)

Avoid

sigma-1 + 5-HT additive risk, theoretical.

Donepezil / galantamine / huperzine A

Avoid

stacking M1-PAM on top of cholinesterase inhibitors is a redundant double-hit on cholinergic signaling and may produce peripheral muscarinic AE that neither …

High-dose anticholinergics (diphenhydramine, scopolamine, tricyclic antidepressants)

Avoid

would functionally cancel the M1-PAM action.

Quality Indicators

✓

Pharmacy-dispensed, intact packaging

Prescription tablets in original sealed packaging from a licensed pharmacy.

Generic vs branded

Generics are usually fine but bioavailability can vary slightly; track if you switch.

✗

Unbranded blister or counterfeit risk

Counterfeit pharmaceuticals are a known issue; verify pharmacy and lot if buying internationally.

What to Expect

Day 1
PK-driven acute peak per administration. Verify dose tolerated.
Week 1
Steady-state reached for most daily-dosed pharma.
Week 2-4
Therapeutic effect established; titration window if needed.
Long-term
Periodic monitoring per drug class (labs, BP, ECG as applicable).

Side Effects & Safety

From human trials to date (limited disclosure)

Common (>10%): Not separately disclosed in available press releases; framed as "well-tolerated" with no severe TEAEs in Phase 2.
Less common (1-10%): Unknown — Phase 1 AE table not published in detail.
Rare-serious (<1%): None reported. No QTc signal, no EPS, no severe muscarinic peripheral effects, no liver enzyme red flag in published commentary.

Theoretical / mechanism-derived concerns

M1-PAM peripheral muscarinic spillover (sweating, GI, bradycardia) — minimized by allosteric design and M1 selectivity, not eliminated. Watch in any self-trial would be HR + GI + sweating.
Sigma-1 agonism + serotonergic compounds — sigma-1 modulates 5-HT release and has theoretical serotonergic-syndrome additive risk with strong serotonergic agents (SSRIs, MDMA, MAOIs). No documented case for AF710B but mechanistically plausible.
Cognitive blunting / paradoxical amnestic effects in non-AD brains — pure speculation, but cholinergic over-signaling in healthy adults can occasionally produce attentional narrowing or REM-like sedation. Galantamine has reported this; AF710B has not, but n is small.
Drug-development class signal — multiple M1 orthosteric agonists (xanomeline alone, GSK1034702, MK-7622) failed for AE burden or efficacy. The PAM design is supposed to fix this; it hasn't been clinically proven yet at scale.