RANKL-IN-2 

RANKL-IN-2 is an orally active RANKL inhibitor with K_d values of 3.21 μM and 4.625 μM in the SPR and MST assays, respectively. RANKL-IN-2 binds to RANKL to interfere with RANKL-RANK interaction. RANKL-IN-2 suppresses osteoclastogenesis by inhibiting ROS, MAPK and NF-κB pathways. RANKL-IN-2 inhibits osteoclastogenesis via inhibition of RANKL-induced osteoclast formation, bone resorption, and osteoclast-specific gene and protein expressions in vitro.RANKL-IN-2 prevents bone loss in ovariectomized osteoporosis mice.RANKL-IN-2 can be used for the research of osteoporosis^[1].

RANKL-IN-2 (compound 3w) (1 μM；作用 4 天) 可在 1 μM 浓度下以强效活性抑制 RAW 264.7 细胞中 RANKL 诱导的破骨细胞生成^[1]。
RANKL-IN-2 (0.0625-2 μM；作用 5 天) 可呈剂量依赖性地抑制 RANKL 诱导的骨髓巨噬细胞 (BMMs) 破骨细胞生成，其 IC₅₀ 为 0.577 μM^[1]。
RANKL-IN-2 (0.5-2 μM；7 天) 以剂量依赖性方式抑制 RANKL 诱导的 BMM 中 F-actin 环的形成和骨吸收作用^[1]。
RANKL-IN-2 (0.5-2 μM；作用 5 天) 可呈剂量依赖性地抑制 RANKL 诱导的 BMMs 中破骨细胞标记基因和蛋白的表达^[1]。
RANKL-IN-2 (0.5-2 μM；作用 5 天) 可通过抑制 ROS 生成并促进抗氧化酶表达来调控 BMMs 中的 ROS 信号通路^[1]。
RANKL-IN-2 (0.5-2 μM；48 h) 可呈剂量依赖性抑制 RANKL 诱导的 BMMs 细胞内及线粒体 ROS 生成^[1]。
RANKL-IN-2 (1 μM；预处理 6 小时，RANKL 刺激 0-60 分钟) 可在 1 μM 浓度下抑制 BMMs 中 RANKL 诱导的 MAPK 和 NF-κB 信号通路^[1]。
RANKL-IN-2 (0.5-2 μM；作用 7 或 21 天) 对 MC3T3-E1 细胞的成骨细胞分化或矿化无影响^[1]。
RANKL-IN-2 在 PBS 和大鼠血浆中可稳定存在至少 12 小时^[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

RANKL-IN-2 (compound 3w) (10 mg/kg；灌胃；每两天一次；持续 8 周) 可通过提升骨结构参数、减少破骨细胞形成，预防小鼠卵巢切除诱导的骨丢失^[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

420.16

C₁₇H₁₃BrN₂OSe

2667022-87-7

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Yi L, et al. A novel RANKL-targeted selenyl quinolinamide alleviates ovariectomy-induced bone loss through inhibiting ROS, MAPK and NF-κB signaling pathways. Eur J Med Chem. 2026;305:118533.  [Content Brief]