Quick Comparison
| B-Complex | Fasoracetam | |
|---|---|---|
| Half-Life | Water-soluble; excreted daily (except B12 which is stored) | 1.5-2.5 hours |
| Typical Dosage | Standard: A quality B-complex providing 25-100 mg of B1, B2, B3, B5, B6, plus 400-800 mcg folate (as methylfolate) and 500-1000 mcg B12 (as methylcobalamin). Methylated forms preferred for B9 and B12 (folate → methylfolate, B12 → methylcobalamin). Take in the morning — B vitamins can be mildly energizing. | Standard: 20-100 mg sublingually or orally, 1-3 times daily. Many users find 20-40 mg effective. Clinical trials for ADHD used 100-400 mg twice daily. |
| Administration | Oral (capsules, tablets, sublingual). Methylated forms preferred for B9 and B12. Take with breakfast. | Oral or sublingual. Sublingual may provide better absorption. |
| Research Papers | 10 papers | 5 papers |
| Categories |
Mechanism of Action
B-Complex
Each B vitamin serves specific neurological functions: B1 (thiamine) — cofactor for transketolase (pentose phosphate pathway), pyruvate dehydrogenase, and alpha-ketoglutarate dehydrogenase; essential for glucose metabolism and ATP production in neurons. B2 (riboflavin) — precursor to FAD/FMN, cofactors for Complex I and II of the electron transport chain, and glutathione reductase. B3 (niacin/niacinamide) — precursor to NAD+/NADPH via the salvage pathway; NAD+ is substrate for sirtuins, PARP, and 400+ dehydrogenases. B5 (pantothenic acid) — component of coenzyme A, required for acetylcholine synthesis via choline acetyltransferase and for fatty acid oxidation. B6 (pyridoxine) — cofactor for AADC (5-HTP to serotonin, L-DOPA to dopamine), GABA synthesis (GAD), and homocysteine metabolism. B9 (folate) — tetrahydrofolate donates methyl groups for dTMP and purine synthesis, and for homocysteine remethylation. B12 (cobalamin) — cofactor for methionine synthase (myelin maintenance) and methylmalonyl-CoA mutase.
Fasoracetam
Fasoracetam upregulates GABA-B receptor (GABA-B1/GABA-B2 heterodimer) expression and function, which is unique among racetams — this receptor upregulation is potentially beneficial for restoring GABAergic sensitivity after prolonged benzodiazepine or phenibut use. It enhances group II metabotropic glutamate receptor (mGluR2/mGluR3) signaling, which modulates presynaptic glutamate release and reduces excitotoxicity. Fasoracetam increases acetylcholine release in the cerebral cortex via modulation of choline acetyltransferase activity and vesicular acetylcholine transporter function. It may also modulate the glutamatergic system through mGluR5. The combination of GABAergic (GABA-B-mediated inhibition), glutamatergic (mGluR modulation), and cholinergic enhancement provides anxiolytic effects alongside cognitive enhancement. Clinical trials focus on ADHD patients with GRM (glutamate receptor) gene variants.
Risks & Safety
B-Complex
Common
Bright yellow urine (harmless — riboflavin excretion), mild nausea.
Serious
Very safe at standard doses. B6 can cause peripheral neuropathy at >200 mg daily for extended periods.
Rare
Flushing from niacin (B3) if non-flush form is not used.
Fasoracetam
Common
Headache, fatigue, mild digestive discomfort.
Serious
Limited long-term human safety data.
Rare
Low mood, brain fog, loss of motivation at very high doses.
Full Profiles
B-Complex →
The B vitamins (B1, B2, B3, B5, B6, B9, B12) are essential coenzymes in brain energy metabolism, neurotransmitter synthesis, and methylation reactions. Deficiency in any B vitamin impairs cognitive function. B12 and folate deficiency specifically cause irreversible neurological damage if untreated. A high-quality B-complex is foundational for any nootropic regimen, particularly for vegetarians, older adults, and those under chronic stress.
Fasoracetam →
A newer racetam that uniquely upregulates GABA-B receptors, making it potentially useful for people who have developed tolerance to GABAergic substances like Phenibut or benzodiazepines. It also enhances glutamate and acetylcholine signaling. Being studied in clinical trials for ADHD in adolescents with specific glutamate receptor gene mutations.