| Bioactivity | MYLS22 is a first-in-class and selective optic atrophy 1 (OPA1) inhibitor. MYLS22 can target endothelial OPA1 to curtail tumor growth and inhibits angiogenesis by impinging on NFkB activity and on angiogenic gene expression. MYLS22 can inhibit mitochondrial fusion and exacerbate the mitochondrial damage[1][2]. | ||||||||||||
| Target | OPA1 | ||||||||||||
| Name | MYLS22 | ||||||||||||
| CAS | 306959-01-3 | ||||||||||||
| Formula | C24H21N5O2S | ||||||||||||
| Molar Mass | 443.52 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
|
||||||||||||
| Reference | [1]. Corrado M, et, al. Deletion of the mitochondria-shaping protein Opa1 during early thymocyte maturation impacts mature memory T cell metabolism. Cell Death Differ. 2021 Jul;28(7):2194-2206. [2]. Zhuang S, et, al. Targeting P2RX1 alleviates renal ischemia/reperfusion injury by preserving mitochondrial dynamics. Pharmacol Res. 2021 Aug;170:105712. |
MYLS22
CAS: 306959-01-3 F: C24H21N5O2S W: 443.52
MYLS22 is a first-in-class and selective optic atrophy 1 (OPA1) inhibitor. MYLS22 can target endothelial OPA1 to curtail
Data collection：peptidedb@qq.com
This product is for research use only, not for human use. We do not sell to patients.