ALK

RIPK2-IN-1 is a selective inhibitor targeting RIPK2 and ALK2, with an IC50 of 51 nM and 5 nM, respectively. This compound demonstrates substantial efficacy in modulating RIPK2/NOD2 pathways, exhibiting an IC50 of 390 nM in cellular assays. RIPK2-IN-1 is suitable for research applications investigating pathways related to inflammation and immune response mechanisms.

ALKBH5-IN-5 is a selective inhibitor of ALKBH5 with an IC50 of 0.62 μM and a Kd of 804 nM. This compound disrupts the interaction between ALKBH5 and its substrates, m6A-RNA and 6mA-DNA, leading to enhanced differentiation and apoptosis in cancer cells, as well as G2-M phase arrest. Notably, ALKBH5-IN-5 reduces the protein levels of TACC3 and MYC while increasing cleaved caspase-3 levels, demonstrating significant antiproliferative effects. Furthermore, it exhibits antitumor activity in xenograft mouse models and is relevant for research into acute myeloid leukemia.

ALK-IN-26 is a selective inhibitor of the anaplastic lymphoma kinase (ALK) with an IC50 value of 7.0 μM for ALK tyrosine kinase. This compound exhibits favorable pharmacokinetic properties and demonstrates permeability across the blood-brain barrier. ALK-IN-26 has been shown to induce apoptosis, autophagy, and necrosis, making it a valuable tool in the study of glioblastoma and related malignancies.

Lorlatinib acetate is a selective and orally active inhibitor targeting ROS1 and ALK pathways. This compound exhibits potent anticancer activity with Kis of less than 0.025 nM for ROS1 and less than 0.07 nM for wild-type ALK, establishing it as a promising therapeutic candidate for ALK-driven cancers. Additionally, Lorlatinib acetate effectively inhibits ALK phosphorylation, demonstrated by IC50 values ranging from 15-43 nM for ALKL1196 and varying efficacy against multiple resistant mutations, making it a valuable tool for cancer research and drug discovery.

ALK/EGFR-IN-1 is a potent dual inhibitor targeting ALK and EGFR, effectively blocking their phosphorylation. This compound demonstrates high inhibitory activity against EGFR L858R T790M mutants in H1975 cells, with an IC50 of 4.3 nM, and EML4-ALK in BaF3 cells, with an IC50 of 3.6 nM. ALK/EGFR-IN-1 is particularly valuable for research in non-small cell lung cancer (NSCLC) and provides insights into the mechanisms of resistance in targeted therapies.

DDO-2728 is a selective inhibitor of AlkB homologue 5 (ALKBH5), demonstrating an IC50 of 2.97 μM. This compound enhances the levels of N6 methyladenosine (m6A) modifications, leading to increased cell apoptosis and cell cycle arrest. DDO-2728 has shown efficacy in suppressing tumor growth in the MV4 11 xenograft model, highlighting its potential application in cancer research and therapeutic strategies targeting ALKBH5.

Neladalkib is a potent oral selective inhibitor of anaplastic lymphoma kinase (ALK) with an IC50 of 2.8 nM. This compound induces apoptotic cell death and demonstrates anti-tumor activity, making it a valuable tool for cancer research. Neladalkib is particularly relevant in studies focused on ALK-driven malignancies and therapeutic resistance mechanisms.

Iruplinalkib (WX-0593) is an orally active and selective ALK/ROS1 inhibitor that effectively blocks tyrosine autophosphorylation of ALK, mutant ALK, and EGFR, with IC50 values ranging from 5.38 to 16.74 nM. Additionally, it inhibits the transport activity of MATE1, MATE2K, P-gp, and BCRP. Iruplinalkib is under investigation for the treatment of non-small cell lung cancer (NSCLC).

ALK/PI3K/AKT-IN-1 is a selective ALK inhibitor that demonstrates significant anti-proliferative effects on A549, H1975, and PC9 cancer cell lines with IC50 values of 0.44, 0.83, and 1.51 μM, respectively. This compound induces cell cycle arrest at the G1 phase by enhancing p21 and p27 expression while inhibiting CDK2 and phosphorylated Rb activity. Additionally, ALK/PI3K/AKT-IN-1 disrupts the ALK/PI3K/AKT signaling pathway, leading to mitochondrial membrane depolarization and apoptosis in A549 cells. It also effectively inhibits spheroid formation and growth in A549 cells, making it a valuable tool for cancer research.

ALK-IN-31 is an orally active inhibitor of anaplastic lymphoma kinase (ALK), with an IC50 of 1135 nM. This compound demonstrates significant antiproliferative activity against H2228 lung cancer cells, showing an IC50 of 1.35 μM. ALK-IN-31 induces apoptosis and halts cell cycle progression in the G0/G1 phase by modulating mitochondrial function. Furthermore, it attenuates tumor growth by downregulating p-AKT and p-mTOR within the PI3K-AKT-mTOR signaling pathway, making it a valuable tool for research in non-small cell lung cancer (NSCLC).

DA-0157 is a selective inhibitor of the epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), designed to address drug-resistant mutations, specifically EGFR C797S and ALK mutations in non-small cell lung cancer (NSCLC) models. It demonstrates potent antiproliferative activity in cells bearing EGFR Del19/T790M/C797S (IC50 = 6.9 nM), as well as in various ALK mutant forms, including Ba/F3-EML4-ALK-L1196M (IC50 = 5.5 nM). Additionally, DA-0157 has been shown to inhibit CYP2D6 with an IC50 of 5.26 μM, and exhibits promising antitumor efficacy in preclinical mouse models, making it a valuable tool for cancer research.

TSR-011-isomer is a potent anaplastic lymphoma kinase (ALK) inhibitor with an IC50 of 6 nM. This compound demonstrates significant biological activity by undergoing metabolic hydrolysis and NADPH-dependent metabolism, facilitating its clearance in biological systems. TSR-011-isomer is suitable for research focused on ALK-driven cancers, making it a valuable tool for studies in cancer biology and targeted therapy development.

XMU-MP-5 is a selective inhibitor of anaplastic lymphoma kinase (ALK), demonstrating potent inhibitory activity against ALK-mutated Ba/F3 cells with IC50 values ranging from 4 to 50 nM. This compound induces apoptosis specifically in EML4-ALK Ba/F3 cells and has shown notable antitumor efficacy in murine models. XMU-MP-5 serves as a valuable tool in cancer research, particularly in studies focused on ALK-driven malignancies.

Ceritinib mesylate is a selective ALK tyrosine kinase inhibitor that functions through ATP-competitive mechanisms, exhibiting an IC50 of 200 pM. In addition to its activity against ALK, Ceritinib mesylate also inhibits IGF-1R, InsR, and STK22D, with IC50 values of 8 nM, 7 nM, and 23 nM, respectively. This compound demonstrates significant antitumor potency, making it a valuable tool for research in cancer biology and targeted therapies.

A 83-01 sodium is a selective inhibitor of the transforming growth factor-beta (TGF-β) type I receptors ALK4, ALK5, and ALK7. With IC50 values of 12 nM, 45 nM, and 7.5 nM, it effectively blocks transcriptional activity induced by these kinases. This compound is valuable for research applications focused on TGF-β signaling pathways and regulation of cellular processes such as proliferation, differentiation, and epithelial-mesenchymal transition.

M4K-2009 is a potent inhibitor of ALK2, exhibiting an IC50 value of 13 nM, and is capable of penetrating the blood-brain barrier. In addition to its primary activity against ALK2, M4K-2009 demonstrates efficacy against the hERG potassium channel. This compound is valuable for research in the areas of bone morphogenetic protein signaling and related therapeutic applications.