BMS-754807 is a potent and reversibleIGF-1R/IRinhibitor (IC₅₀=1.8 and 1.7 nM, respectively;K_i=<2 nm for both). bms-754807 also shows potent activities againstMet, RON,TrkA,TrkB, AurA, and AurB withIC₅₀values of 6, 44, 7, 4, 9, and 25 nM, respectively^[1].

IC50: 1.7 nM (IR), 1.8 nM (IGF-1R), 4 nM (TrkB), 6 nM (Met), 7 nM (TrkA), 9 nM (AurA), 25 nM (AurB), 44 nM (RON)^[1]

BMS-754807 effectively inhibits the growth of a broad range of human tumor cell lines with IC₅₀values of ranging from 5 to 365 nM. BMS-754807 also inhibits the proliferation of human rhabdomyosarcoma tumor cells Rh41 and human colon carcinoma Geo with IC₅₀s of 7 and 5 nM, respectively. BMS-754807 shows inhibitory activity in the proliferation of Rh41 cells with IC₅₀of 5 nM^[1]. BMS-754807 inhibits the phosphorylation of IGF-1R (IC₅₀=13 nM) and the downstream targets Akt (IC₅₀=22 nM) and MAPK (IC₅₀=13 nM) in the IGF-Sal cell line with IC₅₀consistent with the antiproliferative IC₅₀(7 nM) in this cell line^[2]. BMS-754807 shows a median EC₅₀value of 0.62 μM against the PPTP cell lines. The median EC₅₀for the four Ewing sarcoma cell lines is less than that for the remaining PPTP cell lines (0.19 μM vs. 0.78 μM, P=0.0470)^[3]. BMS-754807 (0.25 and 0.5 μM) reduces the activated IGF-IR/IR (pIGF-IR/IR), causes a concurrent decrease in phosphorylated AKT in both lung cancer cell lines. BMS-754807 (0.5 μM) also reduces wound closure of lung cancer cells and reduces the ERK phosphorylation. BMS-754807 reduces cell viability in both A549 and NCI-H358 cells, with IC₅₀of 1.08 μM and 76 μM, respectively^[4].

BMS-754807 (3.125 and 12.5 mg/kg, p.o.) inhibits tumor growth in IGF-1R-Sal tumor-bearing nude mice. BMS-754807 inhibits tumor growth in a selected group of epithelial (IGF-1R-Sal, GEO, and Colo205), hematopoietic (JJN3), and mesenchymal (RD1 and Rh41) xenograft tumor models with TGI ranging from 53% to 115%. BMS-754807 is effective at a dose level of 3.125 mg/kg twice daily and as low as 6.25 mg/kg once daily, in the highly sensitive Rh41 rhabdomyosarcoma. BMS-754807 (25 mg/kg) also shows synergy when combined with targeted agents in human tumor cell lines and human xenograft models^[1]. Furthmore, BMS-754807 is active at doses from 3 mg/kg upward in the IGF-Sal tumor model^[2]. BMS-754807 (25 mg/kg, p.o.) induces significant differences in EFS distribution compared to controls in 18 of 32 evaluable solid tumor xenografts (56%) tested, but in none of the ALL xenografts studied^[3].

461.49

Solid

C₂₃H₂₄FN₉O

1001350-96-4

Room temperature in continental US; may vary elsewhere.

DMSO : ≥ 100 mg/mL(216.69 mM)

*"≥" means soluble, but saturation unknown.

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80℃, 6 months; -20℃, 1 month。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    90% (20%SBE-β-CDin saline)

  Solubility: 2.5 mg/mL (5.42 mM); Suspended solution; Need ultrasonic

  此方案可获得 2.5 mg/mL (5.42 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 2.

  请依序添加每种溶剂： 10% DMSO    40%PEG300   5%Tween-80   45% saline

  Solubility: ≥ 2.08 mg/mL (4.51 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (4.51 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH2O 中，得到澄清透明的生理盐水溶液
• 3.

  请依序添加每种溶剂： 10% DMSO    90%corn oil

  Solubility: ≥ 2.08 mg/mL (4.51 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (4.51 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。