Bioactivity | LSD1-IN-32 (compound 11e) is a potent LSD1 inhibitor with an IC50 value of 0.99 µM. LSD1-IN-32 inhibits RANKL-induced osteoclastogenesis, bone resorption and F-actin belt formation. LSD1-IN-32 has the potential for the research of osteoporosis[1]. |
Target | IC50: 0.99 µM (LSD1) |
Invitro | LSD1-IN-32 (compound 11e) (1.25, 2.5, 5 µM) 以剂量依赖性方式增加破骨细胞生成过程中的甲基化水平[1]。LSD1-IN-32 (0.25, 0.5, 1, 2, 4 µM) 抑制 RANKL 诱导的破骨细胞生成、骨吸收和 F-肌动蛋白带形成[1]。LSD1-IN-32 (2 µM; 0, 1, 2, 4 days) 降低 RANKL 诱导的 Acp5、Nfatc1、Oscar、Dc-stamp、Atp6v0d2 和 Ctsk 基因的 mRNA 表达水平[1]。LSD1-IN-32 (0.5, 1, 2, 4 µM) 可抑制 RANKL 诱导的破骨细胞生成中 p-LSD1、p-IκB 和 p-NFκB 的表达[1]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> LSD1-IN-32 相关抗体: RT-PCR[1] Cell Line: |
In Vivo | LSD1-IN-32 (5, 10 mg/kg) 抑制了小鼠 OVX 诱导的破骨细胞性骨质流失[1]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: |
Formula | C36H56N2O3Si2 |
Molar Mass | 621.01 |
Transport | Room temperature in continental US; may vary elsewhere. |
Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
Reference | [1]. Chen Z, et al. Discovery of TCP-(MP)-caffeic acid analogs as a new class of agents for treatment of osteoclastic bone loss. Bioorg Chem. 2024 Sep;150:107603. |