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 ;
Chemical and physical data
Formula	C23H23ClN2O4
Molar mass	426.892 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.

Lead optimization of the parent structure resulted in L-768,242 & L-759,787.

References

New, DC; Wong, YH (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.
Klegeris, A; Bissonnette, CJ; McGeer, PL (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 (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/en.141.1.118. PMID 10614630.
Scutt, A; Williamson, EM (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.

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[1] New, DC; Wong, YH (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.

[2] Klegeris, A; Bissonnette, CJ; McGeer, PL (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 (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/en.141.1.118. PMID 10614630.

[4] Scutt, A; Williamson, EM (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.