Batoprotafib (TNO155) 是一种有效的，选择性的，和具有口服活性野生型 SHP2 的变构抑制剂 (IC₅₀= 0.011 µM)。Batoprotafib 有研究 RTK 依赖性恶性肿瘤的潜力，尤其是晚期实体瘤。

Batoprotafib (TNO155) is a potent selective and orally active allosteric inhibitor of wild-type SHP2 (IC 50 =0.011 μM). Batoprotafib has the potential for the study of RTK-dependent malignancies, especially advanced solid tumors.

Solid

IC50: 0.011 μM (SHP2)

Batoprotafib shows an IC50 of 0.008 μM in KYSE520 pERK assay and shows an IC50 of 0.100 μM in KYSE520 5-day cell proliferation assay. The off-target IC50 values are 18 μM, 6.9 μM, and 11 μM for Cav1.2, VMAT, and SST3, respectively.
Batoprotafib (0-1000 nM; 6 days) inhibits the viability of NCI-H3255, HCC827, and PC9 cells with IC50 values lower than 1.5 μM. Batoprotafib is efficacious in EGFR-mutant NSCLC cell lines.
Batoprotafib is efficacious in acquired resistance models of EGFR inhibitors and demonstrates combination benefit with EGFR inhibitors.
Batoprotafib enhances the efficacy of KRAS inhibitors against KRAS lung and colorectal cancers.
Batoprotafib inhibits immune-suppressive macrophages and synergizes with PD1 blockade.

The oral bioavailability in mouse, rat and money are 78%, 86%, and 60%, respectively.
Batoprotafib (20 mg/kg; p.o.; twice daily for 40 days) inhibits tumor growth and is more effective when combined with Dabrafenib (HY-14660) plus Trametinib (HY-10999) in nude mice bearing HT-29 xenografts.
Batoprotafib (7.5 mg/kg; p.o.; b.i.d. or q.d. for 36 days) plus JDQ-443 (HY-139612) (100 mg/kg; p.o.; q.d.) improves the single-agent activity of JDQ443 in KRAS-mutated cell-derived (CDX) models in nude mice. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. TNO155: SHP2 inhibitor
[2]. Liu C, et al. Combinations with Allosteric SHP2 Inhibitor TNO155 to Block Receptor Tyrosine Kinase Signaling. Clin Cancer Res. 2021 Jan 1;27(1):342-354.
[3]. Weiss A, et al. Discovery, Preclinical Characterization, and Early Clinical Activity of JDQ443, a Structurally Novel, Potent, and Selective Covalent Oral Inhibitor of KR

In Vitro: DMSO : 100 mg/mL (236.99 mM; Need ultrasonic)配制储备液