ba/f3 cells

Osimertinib (AZD-9291) is an EGFR third-generation inhibitor that inhibits the T790M resistance mutation produced by second-generation EGFR inhibitors with irreversible and oral activity. Osimertinib has antitumor activity for the treatment of EGFR-mutated non-small-cell lung cancer.

ALK ROS1 inhibitor 2e HCL possesses anti-apoptotic, anti-proliferative and anti-tumour activities.

Osimertinib mesylate (AZD-9291 mesylate) is an EGFR third-generation inhibitor that inhibits the T790M resistance mutation produced by second-generation EGFR inhibitors with irreversible and oral activity. Osimertinib mesylate has antitumor activity for the treatment of EGFR-mutated non-small-cell lung cancer.

(S,R,S)-AHPC TFA (VHL ligand 1 TFA) (VH032-NH2 TFA) is a VH032-based ligand designed for von Hippel-Lindau (VHL) protein recruitment. This compound can be linked to protein ligands (e.g., BCR-ABL1) using a linker to create PROTACs (e.g., GMB-475), which effectively induce the degradation of BCR-ABL1, demonstrated by an IC50 of 1.11 μM in Ba F3 cells.

Reslizumab (Sch 55700) is a humanized immunoglobulin G (IgG)4 κ monoclonal antibody that binds to human interleukin 5, thereby decreasing eosinophil production and survival.Reslizumab improves lung function, induces a decrease in eosinophil production and maturation, and may be used in the study of asthma.

HG6-64-1 is a potent and selective inhibitor of B-Raf, with an IC50 of 0.09 μM on B-raf V600E-transformed Ba F3 cells.

JAK3-IN-1 is an orally active, selective and potent JAK3 inhibitor that can be used to study immune system diseases.

MerTK Axl-IN-1 (Compound A-910) is a potent and selective dual inhibitor of MerTK Axl, exhibiting IC50 values of 4.2 nM and 8.8 nM in Ba F3 cells, and 0.2 nM and 0.9 nM in HTRF cells, respectively. It effectively inhibits pMerTK in vivo and possesses a long half-life and high oral bioavailability.

DS06652923 is an orally active inhibitor targeting EGFR triple mutations. It exhibits growth-inhibitory effects on Ba F3EGFRdel19 T90M C795S cells, with a GI50 value of 9.4 nM. Additionally, DS06652923 induces tumor regression in the Ba F3 syngeneic transplantation model.

JBJ-07-149 is an inhibitor of EGFRL858R T790M with an IC50 of 1.1 nM. It suppresses the proliferation of Ba F3 cells with IC50 values of 4.9 μM when used alone, and 0.148 μM when combined with Cetuximab. Additionally, JBJ-07-149 can serve as a target protein ligand for synthesizing [DDC-01-163].

EGFR-IN-140 (Compound 31) is an inhibitor of EGFR, effectively targeting both wild-type EGFR and the EGFRL858R T790M C797S mutant, with Ki values of 0.95 nM and 2.1 nM, respectively. Additionally, it inhibits EGFRdel19 T790M C797S in Ba F3 cells with an IC50 of 56.9 nM and demonstrates antitumor activity in mouse models.

JAK-IN-40 (Compound 46) is an inhibitor of JAK, effectively targeting JAK1, JAK2, and JAK3 with IC50 values of 0.022, 0.759, and 1.601 μM, respectively. It reduces the phosphorylation of STAT3 and inhibits the proliferation of cancer cells Ba F3 and JAK1-TEL Ba F3 with GI50 values of 0.614 μM and 0.193 μM. JAK-IN-40 arrests cell cycle progression at the G2 M phase in H1975 and H2087 cells, leading to apoptosis. Additionally, JAK-IN-40 exhibits a synergistic anti-tumor effect when used in combination with Osimertinib.

JAK2-IN-7, a selective inhibitor targeting Janus Kinase 2 (JAK2), exhibits inhibitory concentrations (IC50) of 3 nM for JAK2, 11.7 nM for SET-2 cells, and 41 nM for Ba F3 V617F cells, indicative of its potency and selectivity. This compound demonstrates more than 14-fold selectivity against JAK1, JAK3, and FLT3, underlining its specificity. JAK2-IN-7 effectively induces cell cycle arrest at the G0 G1 phase and promotes apoptosis in tumor cells, manifesting significant antitumor activities [1].

Aspochalasin D, a co-metabolite originally isolated from A. microcysticus along with aspochalasins A, B, and C, has antibacterial activity against Gram-positive and Gram-negative bacteria at a concentration of 1 mg ml. Aspochalasin D is more cytotoxic via apoptosis to Ba F3-V12 cells in an IL-3-free medium [IC50 = 0.49 μg ml] than in an IL-3-containing medium [IC50 = 1.9 μg ml].

BCR-ABL-IN-3 is a highly effective, irreversible inhibitor of Bcr-Abl, with an IC50 value of ≤100 nM for Ba F3 Bcr-Abl T3151, displaying significant anti-cancer activity.

WF-47-JS03 is a selective and potent inhibitor of RET kinase that crosses the blood-brain barrier and is more than 500-fold more selective for the kinase insertion domain receptor (KDR).WF-47-JS03 acts on Ba F3 cells transfected with KIF5B-RET (IC50: 1.7 nM) and LC-2 ad lung cancer cells transfected with CCDC6-RET (IC50: 5.3 nM). cells (IC50: 5.3 nM).

BCR-ABL-IN-4 is a BCR-ABL inhibitor exhibiting anticancer activity with an inhibitory effect on cancer cell growth, specifically on K562 cells (IC50: 0.67 nM) and BCR-ABL T315I-transfected Ba F3 cells (IC50: 16 nM).

AP23464 is a potent adenosine 5'-triphosphate (ATP)-based inhibitor of Src and Abl kinases, displays antiproliferative activity against a human CML cell line and Bcr-Abl-transduced Ba F3 cells (IC(50) = 14 nM. AP23464 ablates Bcr-Abl tyrosine phosphorylation, blocks cell cycle progression, and promotes apoptosis of Bcr-Abl-expressing cells. Biochemical assays with purified glutathione S transferase (GST)-Abl kinase domain confirmed that AP23464 directly inhibits Abl activity. Importantly, the low nanomolar cellular and biochemical inhibitory properties of AP23464 extend to frequently observed imatinib mesylate-resistant Bcr-Abl mutants, including nucleotide binding P-loop mutants Q252H, Y253F, E255K, C-terminal loop mutant M351T, and activation loop mutant H396P. AP23464 was ineffective against mutant T315I, an imatinib mesylate contact residue. The potency of AP23464 against imatinib mesylate-refractory Bcr-Abl and its distinct binding mode relative to imatinib mesylate warr......

Type II TRK Inhibitor 1 is a potent inhibitor targeting multiple tropomyosin receptor kinase (TRK) fusion protein variants as well as the wild type. It demonstrates notable antiproliferative effects on Ba F3 cells expressing CD74-TRKA G667C and ETV6-TRKC G696C, with half-maximal inhibitory concentrations (IC50s) of 6 nM and 1.7 nM, respectively [1].

TRK-IN-23 (compound 24b) is a potent, orally active TRK inhibitor with IC50s of 0.5 nM for TRKA, 9 nM for TRKC, 14 nM for TRKA G595R, 4.4 nM for TRKA F589L, and 4.8 nM for TRKA G667C. It induces apoptosis in Ba F3-TRKAG595R and Ba F3-TRKAG667C cells [1].

FLT3-IN-22 (compound 22f) is a potent FLT3 inhibitor with IC50 values of 0.941 nM for FLT3 and 0.199 nM for the FLT3 D835Y mutant. It demonstrates significant antiproliferative effects against MV4-11 cells and Ba F3 cell lines expressing mutant FLT kinase variants, including FLT-D835Y and FLT3-F691L [1].

TRK-IN-24 (compound 10g) is a selective inhibitor of Trk receptors, effectively targeting TRKA, TRKC, and mutant forms TRKA G595R, TRKA G667C, and TRKA F589L, with corresponding IC50 values of 5.21, 4.51, 6.77, 1.42, and 6.13 nM. It demonstrates antitumor activity in BaF3-CD74-NTRK1 G595R and BaF3-CD74-NTRK1 G667C xenograft models and inhibits the proliferation of Ba F3 cells expressing single mutants SF, GK, and xDFG, with an IC50 range of 1.43-47.56 nM [1].

AKE-72 is a Pan-BCR-ABL inhibitor with anti-leukemic activity.AKE-72 inhibits the proliferation of Ba F3 cells expressing natural BCR-ABL or its T315I mutant.

Neladalkib (NVL-655) is a selective and brain-permeable ALK inhibitor with antitumor activity that inhibits a variety of ALK-mutant oncoproteins, and may be useful in the study of non-small cell cancers.