BML-190

BML-190
Identifiers
	IUPAC name 2-[1-(4-chlorobenzoyl)-5-methoxy-2-methylindol-3-yl]-1-morpholin-4-ylethanone;
CAS Number	2854-32-2 ;
PubChem CID	2415;
ChemSpider	2321 ;
CompTox Dashboard (EPA)	DTXSID50951230 ;
Chemical and physical data
Formula	C23H23ClN2O4
Molar mass	426.90 g·mol−1
3D model (JSmol)	Interactive image;
	SMILES C4COCCN4C(=O)Cc(c(c1cc2)cc2OC)c(C)n1C(=O)c3ccc(Cl)cc3;
	InChI InChI=1S/C23H23ClN2O4/c1-15-19(14-22(27)25-9-11-30-12-10-25)20-13-18(29-2)7-8-21(20)26(15)23(28)16-3-5-17(24)6-4-16/h3-8,13H,9-12,14H2,1-2H3 ; Key:BJSDNVVWJYDOLK-UHFFFAOYSA-N ;
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BML-190 (Indomethacin morpholinylamide) is a drug used in scientific research that acts as a selective CB₂ inverse agonist.^[1] BML-190 is structurally derived from the NSAID indomethacin but has a quite different biological activity.^[2] The activity produced by this compound is disputed, with some sources referring to it as a CB₂ agonist rather than an inverse agonist;^[3]^[4] this may reflect an error in classification, or alternatively it may produce different effects in different tissues, and more research is required to resolve this dispute.

References

^ New DC, Wong YH (February 2003). "BML-190 and AM251 act as inverse agonists at the human cannabinoid CB2 receptor: signalling via cAMP and inositol phosphates". FEBS Letters. 536 (1–3): 157–60. doi:10.1016/S0014-5793(03)00048-6. PMID 12586356. S2CID 38569901.
^ Klegeris A, Bissonnette CJ, McGeer PL (June 2003). "Reduction of human monocytic cell neurotoxicity and cytokine secretion by ligands of the cannabinoid-type CB2 receptor". British Journal of Pharmacology. 139 (4): 775–86. doi:10.1038/sj.bjp.0705304. PMC 1573900. PMID 12813001.
^ Melck D, De Petrocellis L, Orlando P, Bisogno T, Laezza C, Bifulco M, Di Marzo V (January 2000). "Suppression of nerve growth factor Trk receptors and prolactin receptors by endocannabinoids leads to inhibition of human breast and prostate cancer cell proliferation". Endocrinology. 141 (1): 118–26. doi:10.1210/endo.141.1.7239. PMID 10614630.
^ Scutt A, Williamson EM (January 2007). "Cannabinoids stimulate fibroblastic colony formation by bone marrow cells indirectly via CB2 receptors". Calcified Tissue International. 80 (1): 50–9. doi:10.1007/s00223-006-0171-7. PMID 17205329. S2CID 23624771.

[1] New DC, Wong YH (February 2003). "BML-190 and AM251 act as inverse agonists at the human cannabinoid CB2 receptor: signalling via cAMP and inositol phosphates". FEBS Letters. 536 (1–3): 157–60. doi:10.1016/S0014-5793(03)00048-6. PMID 12586356. S2CID 38569901.

[2] Klegeris A, Bissonnette CJ, McGeer PL (June 2003). "Reduction of human monocytic cell neurotoxicity and cytokine secretion by ligands of the cannabinoid-type CB2 receptor". British Journal of Pharmacology. 139 (4): 775–86. doi:10.1038/sj.bjp.0705304. PMC 1573900. PMID 12813001.

[3] Melck D, De Petrocellis L, Orlando P, Bisogno T, Laezza C, Bifulco M, Di Marzo V (January 2000). "Suppression of nerve growth factor Trk receptors and prolactin receptors by endocannabinoids leads to inhibition of human breast and prostate cancer cell proliferation". Endocrinology. 141 (1): 118–26. doi:10.1210/endo.141.1.7239. PMID 10614630.

[4] Scutt A, Williamson EM (January 2007). "Cannabinoids stimulate fibroblastic colony formation by bone marrow cells indirectly via CB2 receptors". Calcified Tissue International. 80 (1): 50–9. doi:10.1007/s00223-006-0171-7. PMID 17205329. S2CID 23624771.

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