Gavestinel

Gavestinel
Clinical data
Other names	GV-150,526A
ATC code	none;
Identifiers
	IUPAC name 3-[(E)-3-anilino-3-oxoprop-1-enyl]-4,6-dichloro-1H-indole-2-carboxylic acid;
CAS Number	153436-22-7 ;
PubChem CID	6450546;
ChemSpider	4953148 ;
UNII	318X4QY113;
ChEMBL	ChEMBL419045 ;
CompTox Dashboard (EPA)	DTXSID90870012 ;
Chemical and physical data
Formula	C18H12Cl2N2O3
Molar mass	375.21 g·mol−1
3D model (JSmol)	Interactive image;
	SMILES OC(C1=C(/C=C/C(NC2=CC=CC=C2)=O)C3=C(Cl)C=C(Cl)C=C3N1)=O;
	InChI InChI=1S/C18H12Cl2N2O3/c19-10-8-13(20)16-12(17(18(24)25)22-14(16)9-10)6-7-15(23)21-11-4-2-1-3-5-11/h1-9,22H,(H,21,23)(H,24,25)/b7-6+ ; Key:WZBNEZWCNKUOSM-VOTSOKGWSA-N ;
	(what is this?) (verify)

Gavestinel (GV-150,526) was an investigational drug developed by GlaxoSmithKline for acute intracerebral hemorrhage, which in 2001 failed to show an effect in what was at the time, the largest clinical trial in stroke that had been conducted.^[1]^[2]

Gavestinel is an NMDA antagonist, binding selectively to the glycine site on the NMDA receptor complex, rather than the glutamate site many NMDA antagonists bind to.^[3]^[4]^[5]

^ Hauschildt E (3 April 2001). "No Benefit From Early Gavestinel Therapy For Acute Stroke Patients A DGReview of :"Glycine Antagonist in Neuroprotection for Patients With Acute Stroke GAIN Americas: A Randomized Controlled Trial" Journal of the American Medical Association (JAMA)". PSL. Archived from the original on 15 December 2014. Retrieved 9 December 2014.
^ Jeffrey S (4 April 2001). "GAIN Americas trial again shows no benefit from neuroprotectant agent in stroke". Medscape News.
^ Chopra B, Chazot PL, Stephenson FA (May 2000). "Characterization of the binding of two novel glycine site antagonists to cloned NMDA receptors: evidence for two pharmacological classes of antagonists". British Journal of Pharmacology. 130 (1): 65–72. doi:10.1038/sj.bjp.0703298. PMC 1572047. PMID 10780999.
^ Ikonomidou C, Turski L (October 2002). "Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury?". The Lancet. Neurology. 1 (6): 383–6. doi:10.1016/s1474-4422(02)00164-3. PMID 12849400. S2CID 31477519.
^ Hoyte L, Barber PA, Buchan AM, Hill MD (March 2004). "The rise and fall of NMDA antagonists for ischemic stroke". Current Molecular Medicine. 4 (2): 131–6. doi:10.2174/1566524043479248. PMID 15032709.

[1] Hauschildt E (3 April 2001). "No Benefit From Early Gavestinel Therapy For Acute Stroke Patients A DGReview of :"Glycine Antagonist in Neuroprotection for Patients With Acute Stroke GAIN Americas: A Randomized Controlled Trial" Journal of the American Medical Association (JAMA)". PSL. Archived from the original on 15 December 2014. Retrieved 9 December 2014.

[2] Jeffrey S (4 April 2001). "GAIN Americas trial again shows no benefit from neuroprotectant agent in stroke". Medscape News.

[pmid10780999-3] Chopra B, Chazot PL, Stephenson FA (May 2000). "Characterization of the binding of two novel glycine site antagonists to cloned NMDA receptors: evidence for two pharmacological classes of antagonists". British Journal of Pharmacology. 130 (1): 65–72. doi:10.1038/sj.bjp.0703298. PMC 1572047. PMID 10780999.

[pmid12849400-4] Ikonomidou C, Turski L (October 2002). "Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury?". The Lancet. Neurology. 1 (6): 383–6. doi:10.1016/s1474-4422(02)00164-3. PMID 12849400. S2CID 31477519.

[pmid15032709-5] Hoyte L, Barber PA, Buchan AM, Hill MD (March 2004). "The rise and fall of NMDA antagonists for ischemic stroke". Current Molecular Medicine. 4 (2): 131–6. doi:10.2174/1566524043479248. PMID 15032709.

[1]

[2]

[3]

[4]

[5]