Chemistry:Cetyl-GABA

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Cetyl-GABA, or CEGABA, also known as hexadecyl 4-aminobutanoate or as γ-aminobutyric acid (GABA) cetyl ester, is a GABA receptor agonist which has been used in scientific research.[1][2][3] It is the cetyl (hexadecyl) ester of the major inhibitory neurotransmitter γ-aminobutyric acid (GABA).[1][2]

The drug is a centrally penetrant and orally active prodrug of GABA with profoundly increased potency and has been shown to increase brain GABA levels.[1][2] Whereas GABA itself is unable to cross the blood–brain barrier easily, cetyl-GABA is lipophilic and readily able to cross into the brain.[1][2][4] In addition, it has a longer duration than GABA, thought to be due to delayed ester cleavage.[2] Cetyl-GABA produces sedation and anticonvulsant effects in rodents.[1][2][5][6][7] In addition, it inhibits muricidal behavior in mice similarly to muscimol.[5][6] The drug is about 500-fold more potent than GABA on a molar basis as an anticonvulsant and in terms of brain GABA elevation in rodents.[1][2] It is said to be highly potent in vivo, being surpassed in potency only by muscimol and gaboxadol in one study.[2]

Cetyl-GABA is described as a "soap-like drug" and as being fairly toxic by intravenous and intraperitoneal routes in rodents, but as being well-tolerated when given orally.[1]

Cetyl-GABA was first described in the scientific literature by 1978.[5][6] It was of interest as a potential anticonvulsant for therapeutic use to treat epilepsy, but was never marketed.[2]

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 "Cetyl GABA: effect on convulsant thresholds in mice and acute toxicity". Neuropharmacology 19 (2): 217–220. February 1980. doi:10.1016/0028-3908(80)90141-0. PMID 7360336. 
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 "Comparative assay of anticonvulsant and toxic potencies of sixteen GABAmimetic drugs". Neuropharmacology 21 (8): 803–810. August 1982. doi:10.1016/0028-3908(82)90068-5. PMID 7121752. 
  3. ↑ "[GABA-ergic cortical component in the action of piracetam and cetyl GABA]" (in Russian). Biulleten' Eksperimental'noi Biologii I Meditsiny 93 (4): 62–64. April 1982. PMID 7082805. 
  4. ↑ "United States Pharmacopeia (USP) Safety Review of Gamma-Aminobutyric Acid (GABA)". Nutrients 13 (8): 2742. August 2021. doi:10.3390/nu13082742. PMID 34444905. "Because GABA is a key neurotransmitter in the CNS, it is important to understand how much of the administered amount may traverse the blood-brain barrier (BBB) when it is ingested orally as a dietary supplement. So far, evidence indicates that very low amounts of GABA cross from the plasma into the brain through the BBB even when GABA is exogenously administered orally or intravenously [97,98,102,103,104,105,106,107,108].". 
  5. ↑ 5.0 5.1 5.2 "Modulatory effects of baclofen muscimol and GABA on interspecific aggressive behaviour in the rat". Neuropharmacology 17 (12): 1063–1065. December 1978. doi:10.1016/0028-3908(78)90039-4. PMID 570649. 
  6. ↑ 6.0 6.1 6.2 "Influence of baclofen and GABA-minetic agents on spontaneous and olfactory-bulb-ablation-induced muricidal behaviour in the rat". Arzneimittel-Forschung 28 (9): 1508–1509. 1978. PMID 582545. 
  7. ↑ "High anticonvulsant potency of gamma-aminobutyric acid (GABA)mimetic drugs in gerbils with genetically determined epilepsy". The Journal of Pharmacology and Experimental Therapeutics 226 (3): 839–844. September 1983. doi:10.1016/S0022-3565(25)21841-9. PMID 6411901. 

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See also
Receptor/signaling modulators
GABAA receptor positive modulators
GABA metabolism/transport modulators

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