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the sci-wiki/effects/Brain

Brain

Every compound in the sci-wiki that affects brain; the ones you can source are floated to the front, then the reference-only entries. Tap any for the full entry, mechanism, and outlets.

2 sourced · 17 reference

←brain19/19filter this drawer by compound name

Idebenone

Idebenone is a synthetic analog of coenzyme Q10 (ubiquinone), a short-chain benzoquinone with antioxidant and mitochondrial properties. Originally developed by Takeda for Alzheimer's disease and other cognitive disorders, it is now used mainly as an approved treatment for Leber's hereditary optic neuropathy, a rare inherited cause of vision loss. It has also been studied in other mitochondrial and neuromuscular diseases and is used as an antioxidant ingredient in some skincare products.

Citicoline + Piracetam

Citicoline with piracetam is a combination of two nootropic compounds sometimes taken together for cognitive support. Citicoline, also called cytidine diphosphate choline, is a naturally occurring precursor used to build brain cell membranes and the neurotransmitter acetylcholine, while piracetam is a synthetic derivative of GABA and the original member of the racetam family. The pairing is popular in nootropic circles, although the two ingredients have been studied mainly on their own rather than as a fixed combination.

reference shelf; no outlet carries these yet

7,8,3'-Trihydroxyflavone

7,8,3'-Trihydroxyflavone is a close relative of 7,8-dihydroxyflavone with one extra hydroxyl, reported in the founding work on that compound to produce an even stronger effect on TrkB signalling. ⚠️ It has no measured binding affinity at TrkB. No Ki, Kd, IC50 or EC50 from a binding assay has ever been published for it, and the potency figures that circulate are fold-changes in signalling readouts, which are not measurements of target engagement. ⚠️ It was one of the compounds tested directly in an independent replication attempt, and it was inactive.

Neuroprotection

ATH-1105

ATH-1105 is an oral small molecule being developed for ALS, from the same company as fosgonimeton and on the same claimed mechanism of positive modulation of the hepatocyte growth factor system. It has completed a phase 1 and has the strongest target-validation evidence anyone in this chemical programme has produced. ⚠️ It is not, despite frequent description, an oral version of fosgonimeton. The published structure is a different chemical class entirely, and neither of its two papers mentions fosgonimeton or dihexa. The two compounds share a claimed mechanism, not a scaffold.

BnH-015B

BnH-015B is an oral compound from a Korean company, in a first-in-human trial for Alzheimer's disease. It is described by its sponsor as a positive modulator at the GluN2B site of the NMDA receptor. ⚠️ Nothing about it has ever been published. There is no structure, no CAS number, no chemistry record, no potency measurement, no pharmacokinetic data and no preclinical paper in the public record. This entry exists to say what is and is not known, because the compound appears in drug-pipeline listings in a form that reads like established pharmacology.

Neuroprotection

CAD-31

CAD-31 is a preclinical Alzheimer's candidate from the Salk Institute, selected for its ability to make neural precursor cells divide and then tested in aged Alzheimer's model mice, where it reduced memory deficits and brain inflammation. ⚠️ It has no known molecular target. No binding or potency measurement against any protein has ever been published for it, and its stated mechanism of fatty acid metabolism and inflammation is a description of what changed downstream rather than of what the molecule does. ⚠️ It is frequently grouped with CMS121 as a fisetin derivative. It is not one. Its own paper traces it back through J147 to curcumin, which is different chemistry from a different programme in the same laboratory.

CF3CN

CF3CN is a laboratory code for an optimised replacement for 7,8-dihydroxyflavone, redesigned to resist the metabolism that destroys the parent compound and to reach the brain better. Its catechol ring is swapped for a fused imidazole carrying a trifluoromethyl group, and a nitrile replaces the electron-donating group on the other ring. ⚠️ It is the one compound in this family with a real binding measurement. Surface plasmon resonance gave a dissociation constant of 80.2 nanomolar against the TrkB extracellular domain, measured alongside 7,8-dihydroxyflavone at 184.5 nanomolar in the same experiment. ⚠️ It also has no public registry identity at all: no CAS number, no PubChem record, no ChEMBL entry.

Cycloprolylglycine

Cycloprolylglycine is a small cyclic dipeptide found naturally in brain tissue, and the compound usually named as Noopept's active metabolite. It is studied under two names that describe the same molecule: Russian work calls it cycloprolylglycine, New Zealand work calls it cyclic glycine-proline. ⚠️ The active-metabolite claim is weaker than its popularity suggests. The primary source found the compound in untreated animals as well as treated ones, and reported a 2.5-fold rise at a single hour-long timepoint. The same institute later published that Noopept and this metabolite behave differently in a learning task, which is difficult to reconcile with a simple prodrug relationship.

Deoxygedunin

Deoxygedunin is a natural product from the Indian neem tree and from andiroba seed oil, a limonoid of the gedunin family. It is sold alongside the flavone TrkB compounds and is chemically unrelated to them; it appears in that group only because it came out of the same screen. ⚠️ Its literature is remarkably small. PubMed indexes six papers containing the word at all, one of which merely identifies it as a constituent of seed oil and has nothing to do with the nervous system. There is no second independent pharmacology programme anywhere.

ENT-A011

ENT-A011 is a synthetic derivative of DHEA reported to activate the TrkB receptor, the target of BDNF, without touching the related TrkA and TrkC receptors or the p75 receptor. It belongs to a Greek series of so-called microneurotrophins built from the same steroid backbone. ⚠️ It is a TrkB agonist, not a TrkA agonist, and that error is common enough to be worth flagging first. The same series contains ENT-A013, which is TrkA selective, and sources routinely confuse the two. Everything known about it comes from a single 2024 paper, entirely in cells, at one concentration.

Fosgonimeton

Fosgonimeton is an injectable prodrug of dihexa, developed for Alzheimer's disease and taken through a 549-patient phase 2/3 trial that missed every endpoint. It is the most thoroughly tested member of a family whose founding mechanism papers were retracted for fabricated data. The chemistry is worth stating plainly because it is rarely stated at all: fosgonimeton is dihexa carrying a phosphate group on one hydroxyl and nothing else. The phosphate makes it soluble enough to inject; the body removes it, and what circulates and enters the brain is dihexa. Anyone reading about dihexa is therefore reading about a molecule whose active form has already been given to hundreds of patients.

Neuroprotection

Gambogic amide

Gambogic amide is a derivative of gambogic acid, a caged xanthone from the resin of a Southeast Asian tree, reported as a selective agonist of TrkA, the nerve growth factor receptor. ⚠️ The problem with that claim is inside its own discovery paper. The binding site it describes is intracellular, on the part of the receptor inside the cell, which is not how an extracellular signalling molecule activates a receptor tyrosine kinase. ⚠️ An independent group later measured cytotoxicity at concentrations overlapping the ones used to call it an agonist, and showed that toxicity does not go through TrkA at all.

Neuroprotection

LM22B-10

LM22B-10 is a small molecule reported to activate both TrkB and TrkC, the receptors for BDNF and neurotrophin-3, from the same laboratory that produced LM22A-4. ⚠️ Two things about it deserve to come first. Chemically it is a triarylmethane, the same architecture as the leuco forms of malachite green and crystal violet, a class notorious for promiscuous and assay-interfering behaviour. And in recent literature the compound is used almost entirely as a generic activator of ERK signalling in non-neuronal cells, with no mention of TrkB or TrkC at all.

Nle1-Angiotensin IV

Nle1-Angiotensin IV is a six-amino-acid peptide, angiotensin IV with its first residue swapped for norleucine. It is the research compound the whole dihexa and fosgonimeton family grew out of, and it improved memory in rats in several laboratories through the late 1990s and 2000s. ⚠️ It is almost always described as an AT4 receptor agonist, and both halves of that are wrong. The AT4 receptor turned out to be IRAP, an enzyme rather than a receptor, and this peptide blocks its active site. It is an enzyme inhibitor that has been called a receptor agonist for thirty years out of habit. Every rodent experiment injected it directly into the brain, because it does not survive the bloodstream or cross into the brain on its own.

P7C3-A20

P7C3-A20 is the most-used member of the P7C3 family of aminopropyl carbazoles, a series that protects neurons in a striking range of animal injury models: traumatic brain injury, stroke, Parkinson's models, nerve injury and more. ⚠️ Its mechanism is described everywhere as activation of NAMPT, the enzyme that limits NAD regeneration. No binding or potency constant at that enzyme has ever been published for it, and the originating laboratory now describes the series as NAD-stabilising rather than NAMPT-activating. ⚠️ The only fully independent laboratory test of it in culture was negative twice: it failed to protect neurons in three separate systems, and it was toxic at higher concentrations.

Neuroprotection

P7C3-S243

P7C3-S243 is a single-enantiomer member of the P7C3 series, purified to 99 percent excess rather than used as a mixture. It protects dopamine neurons in a Parkinson's model and protects rats in an Alzheimer's model from behavioural and neurodegenerative decline without touching amyloid deposits. ⚠️ It carries the only sub-micromolar protein affinity ever measured for any compound in this series, and it is an off-target: 350 nanomolar at TSPO. That number matters because the series is routinely described as clean and selective.

R13

R13 is a prodrug of 7,8-dihydroxyflavone, built by capping both of the parent compound's hydroxyl groups with carbamate esters so it survives the gut better. It was the one candidate out of twenty screened derivatives that made it through to animal work. It roughly doubles oral bioavailability and half-life compared with the parent, and in Alzheimer's model mice it reduced amyloid deposition, protected synapses and improved maze performance. ⚠️ Its mechanism inherits an argument. R13 is assumed to work by releasing 7,8-dihydroxyflavone, which is assumed to activate the TrkB receptor, and that second assumption is contested, with independent groups having failed to reproduce receptor activation.

R7

R7 is a 7,8-dihydroxyflavone derivative that appears in research-chemical channels as a prodrug of that compound. ⚠️ It is a rejected candidate, and that is essentially the whole entry. R7 was one of twenty derivatives screened in a 2018 study, and it was eliminated before any animal work for a specific reason: it barely released 7,8-dihydroxyflavone in human liver preparations. A sibling from the same screen, R13, was the one that advanced. That single sentence is the entire published literature on R7. There is no structure, no formula, no measured affinity for anything, no animal study, no pharmacokinetics and no safety data.

Zidesamtinib

A ROS1-selective tyrosine kinase inhibitor approved by the FDA in July 2026 for locally advanced or metastatic ROS1-positive non-small cell lung cancer that has already progressed on a previous ROS1 inhibitor. It was designed to spare the TRK receptor family and to cross into the brain.