SHP2-IN-13 

SHP2-IN-13 is a highly selective and orally active SHP2 “tunnel site” allosteric inhibitor with an IC50 of 83.0 nM. SHP2-IN-13 has the potential for cancers bearing RTK oncogenic drivers and SHP2-related diseases research.

SHP2-IN-13 (compound 129) potently inhibits the pERK signaling in a dose-dependent manner with IC₅₀ values of 0.59 μM and 0.63 ± 0.32 μM in NSCLC cells and NCI–H1975-OR cells, respectively.^[1].
SHP2-IN-13 (0-30 μM; 24 hours) inhibited pERK levels and receptor tyrosine kinase (RTK)-driven cancer cell proliferation in NCI–H1975 cells, . And it also inhibits phosphorylated ERK (pERK) levels in receptor tyrosine kinase (RTK)-resistant NSCLC cells^[1].

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

In vivo pharmacokinetics studies, SHP2-IN-13 (compound 129) (IV/PO; 5mg/kg) demonstrates high clearance, a high volume of distribution (13.9 L/kg), a moderate half-life (T_1/2=5.31 h). Additionally, SHP2-IN-13 shows a higher oral bioavailability (F =55.07 ± 7.93%) than SHP099 (F =46%) and is suitable for further in vivo anti-tumor evaluation^[1].
SHP2-IN-13 (oral gavage; 20 mg/kg; daily) exhibits an anti-leukaemic efficacy and causes significant reduction of leukemia burden. Additionally, it near completely eradicated human CD45⁺ leukaemic cells in blood and spleen^[1].

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

327.38

C₁₆H₂₁N₇O

2951854-02-5

CC1(CCN(CC1)C2=NC=C(C(N)=N2)C(NC3=CN=CC=C3)=O)N

Room temperature in continental US; may vary elsewhere.

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

• [1]. Ruixiang Luo, et al. Discovery of a potent and selective allosteric inhibitor targeting the SHP2 tunnel site for RTK-driven cancer treatment. Eur J Med Chem. 2023 May 5;253:115305.  [Content Brief]