FAK-IN-26 

FAK-IN-26 is a BBB-penetrable Focal Adhesion Kinase (FAK) inhibitor (IC₅₀: 0.87 nM). FAK-IN-26 significantly suppresses tumor cell viability, cancer stem cell activity, and cell migration in A549 and SKOV-3 cell lines. FAK-IN-26 has potent anti-cancer activity in A549 and SKOV-3 tumor mice models with tumor inhibition rates of 59.15 % and 57.9 %^[1].

0.87 nM

FAK-IN-26 (Compound A8) has superior binding capacity on FAK with a K_d of 15 μM^[1].
FAK-IN-26 (1 μmol/L) has broad-spectrum inhibitory activity against multiple kinases, with FAK and FYNα being inhibited by more than 95 %^[1].
FAK-IN-26 (0.5-10 μM) significantly reduces the viability of A549 and SKOV-3 cells at lower concentrations compared to Defactinib (VS6063) (HY-12289). FAK-IN-26 (0.2-1.6 μM) dose-dependently reduces the cancer stem cell population in A549 and SKOV-3 cells^[1].
FAK-IN-26 (62.5-1000 nM, 72 h) significantly induces G2/M arrest in both A549 and SKOV-3 cell lines^[1].
FAK-IN-26 (0.1-10 nM, 6-48 h) dose-dependently decreases migration rates and distances of A549 and SKOV-3 cells with significant inhibition observed at concentrations of 1 nM and 10 nM^[1].
FAK-IN-26 (31.25-62.5 nM, 48 h) effectively inhibits FAK autophosphorylation in both A549 and SKOV-3 cells in a dose-dependent manner, with greater efficacy in A549 cells.

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

FAK-IN-26 (Compound A8) (25-50 mg/kg, p.o., once or twice a day for five days followed by two days off for 28 days) enhances anti-tumor effects compared to Defactinib (VS6063) (HY-12289), Erlotinib (HY-50896) and Paclitaxel (HY-B0015) in both A549 and SKOV-3 tumor mice models, and the combination therapy with Paclitaxel further enhances efficacy in the SKOV-3 tumor model^[1].
FAK-IN-26 (500-2000 mg/kg) is well-tolerated up to 2000 mg/kg in mice without causing acute toxicity^[1].
FAK-IN-26 has favorable tumor uptake and retention, with a peak uptake of 4.16 ID/g at 30 min post-injection in S180 tumor-bearing mice and efficiently penetrates the BBB, with brain uptake of 2.63 % ID/g at 15 min and 1.62 % ID/g at 120 min^[1].
FAK-IN-26 has favorable metabolic stability in human liver microsomes with CL_int and T_{1/2 of 31.8 μL/min/mg and 43.6 min^[1].}

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

460.30

C₂₀H₁₉BrFN₅O₂

2801785-12-4

O=C(NC)C1=CC=CC=C1NC2=NC(NC3=CC=C(OCCF)C=C3)=NC=C2Br

Room temperature in continental US; may vary elsewhere.

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

• [1]. Li Y, et al. Discovery of potent focal adhesion kinase (FAK) inhibitor A8 with enhanced antitumor activity. Eur J Med Chem. 2025 Jul 5; 291:117593.  [Content Brief]