JAK3/BTK-IN-3 is a potent inhibitor of JAK3/BTK. BTK and JAK3 are two important targets for autoimmune diseases. Simultaneous inhibition of the BTK/JAK3 signalling pathway exhibits synergistic effects. JAK3/BTK-IN-3 has the potential for the research of JAK3 kinase and/or BTK-related diseases (extracted from patent WO2021147952A1, compound 009)[1]
BMS-986195 is a potent, covalent, irreversible inhibitor of Bruton’s tyrosine kinase (BTK), with an IC50 of <1 nM.
BTK-IN-22 is a BTK inhibitor (IC50: 0.9 nM). BTK-IN-22 also inhibits BLX and BMX with IC50s of 1.4 and 1.2 nM respectively. BTK-IN-22 shows improved kinase selectivity compared to Ibrutinib (HY-10997)[1]
BTK-IN-24 (compound 195) is a potent BTK inhibitor via a ubiquitin proteolytic pathway[1].
BTK inhibitor 8 (Compound 27) is a Btk inhibitor with an IC50 of 0.11 nM. BTK inhibitor 8 inhibits B cell activation in hWB with an IC50 of 2 nM[1].
Larotinib mesylate hydrate is a potent broad-spectrum and orally active tyrosine kinase inhibitor (TKI) with EGFR as the main target with an IC50 of 0.6 nM[1].
BTK ligand 1 (compound 1) is a ligand targeting Bruton’s tyrosine kinase (Btk). BTK ligand 1 can combine with E3 ligase ligand (Ligand for E3 Ligase) through PROTAC Linker to form PROTAC. PROTACs targeting Btk can be used in the study of chronic lymphocytic leukemia (CLL) and other BK cell malignancies[1].
Remibrutinib, is a potent and orally active bruton tyrosine kinase (BTK) inhibitor with an IC50 value of 1 nM. Remibrutinib inhibits BTK activity with an IC50 value of 0.023 μM in blood[1]. Remibrutinib has the potential for Chronic urticaria (CU) treatment[2].
LFM-A13 is a potent BTK, JAK2, PLK inhibitor, inhibits recombinant BTK, Plx1 and PLK3 with IC50s of 2.5 μM, 10 μM and 61 μM; LFM-A13 shows no effects on JAK1 and JAK3, Src family kinase HCK, EGFR and IRK.
PTD10 is a highly potent PROTAC BTK degrader (DC50: 0.5 nM, KD: 2.28 nM). PTD10 degrades BTK in Ramos and JeKo-1 cells with DC50s of 0.5 and 0.6 nM respectively. PTD10 inhibits cell growth, and induces cell apoptosis via activation of the caspase-dependent pathway and mitochondrial pathway. PTD10 can be used for research of B-cell dysregulation[1].
CNX-774 is a potent, selective, and orally available small molecule inhibitor of Btk (IC50< 1 nM) that forms a ligand-directed covalent bond with Cys-481, a non-conserved amino acid within the active site of the enzyme.IC50 Value: <1 nM [1]Target: Btk KinaseIn biochemical assays, CNX-774 has demonstrated potent inhibition of Btk with an IC50 of <1nM in a continuous-read assay. The covalent bonding of CNX-774 to Btk was confirmed by incubating recombinant Btk protein with a 10-fold molar excess of CNX-774 for 1 hour at room temperature and analysis by MALDI-TOF MS. A shift of protein mass corresponding to the molecular weight of CNX-774 confirmed the covalent bonding of CNX-774 to Btk. Digestion of the covalently bonded Btk with pepsin followed by MSMS analysis established the bonding of CNX-774 to Cys-481. Cellular potency as well as prolonged duration of action of CNX-774 was demonstrated in Ramos cells by using a biotinylated covalent probe that targets the same Cysteine residue as CNX-774.CNX-774 was found to be >90% extractable after 2 hrs of incubation in both rat and human whole blood. These results demonstrate that CNX-774 has potent inhibitory activity towards the intended target, Btk, while achieving remarkable specificity in a variety of assays designed to assess off-target reactivity towards abundant cellular thiols and blood proteins.
TL-895 is a potent, orally active, ATP-competitive, and highly selective irreversible BTK inhibitor with an IC50 and a Ki of 1.5 nM and 11.9 nM, respectively[1]. TL-895 is used be for JAKi-relapsed/refractory myelofibrosis, acute myeloid leukemia, COVID-19 and cancer research[2][3][4].
BTK-IN-12 is a potent BTK inhibitor with IC50s of 1.2 nM and 0.8 nM for wild-type BTK or mutated BTK (C481S), respectively (WO2022037649A1; compound 8)[1].
BIIB091 is a highly selective, reversible BTK inhibitor for treating autoimmune diseases.
CHMFL-EGFR-202 is a potent, irreversible inhibitor of epidermal growth factor receptor (EGFR) mutant kinase, with IC50s of 5.3 nM and 8.3 nM for drug-resistant mutant EGFR T790M and WT EGFR kinases, respectively. CHMFL-EGFR-202 exhibits ∼10-fold selectivity for EGFR L858R/T790M against the EGFR wild-type in cells. CHMFL-EGFR-202 adopts a covalent “DFG-in-C-helix-out” inactive binding conformation with EGFR, with strong antiproliferative effects against EGFR mutant-driven nonsmall-cell lung cancer (NSCLC) cell lines[1].
PF-06250112 is a potent, highly selective, orally bioavailable BTK inhibitor with an IC50 of 0.5 nM, shows inhibitory effect toward BMX nonreceptor tyrosine kinase and TEC with IC50s of 0.9 nM and 1.2 nM, respectively[1].
Larotinib is a potent broad-spectrum and orally active tyrosine kinase inhibitor (TKI) with EGFR as the main target with an IC50 of 0.6 nM[1].
Tirabrutinib (ONO-4059) hydrochloride is a selective and novel inhibitor of BTK with IC50 2.2 nm, Tirabrutinib binds to BTK within B cells, thereby preventing B-cell receptor signaling and impeding B-cell development.
CGI-1746 is a potent and highly selective inhibitor of the Btk with IC50 of 1.9 nM.
N-piperidine Ibrutinib hydrochloride (Compound 1) is a reversible Ibrutinib derivative. N-piperidine Ibrutinib hydrochloride is a potent BTK inhibitor with IC50s of 51.0 and 30.7 nM for WT BTK and C481S BTK, respectively[1]. N-piperidine Ibrutinib hydrochloride can be used as a BTK ligand in the synthesis of a series of PROTACs, such as SJF620 (HY-133137). SJF620 is a potent PROTAC BTK degrader with a DC50 of 7.9 nM[2].
JAK3/BTK-IN-1 is a potent inhibitor of JAK3/BTK. BTK and JAK3 are two important targets for autoimmune diseases. Simultaneous inhibition of the BTK/JAK3 signalling pathway exhibits synergistic effects. JAK3/BTK-IN-1 has the potential for the research of JAK3 kinase and/or BTK-related diseases (extracted from patent WO2021147952A1, compound 002)[1].
The product is the analog of ONO-4059, ONO-4059 is a highly potent and selective Btk inhibitor with an IC50 in the sub-nM range. IC50 value: sub-nM range [2]Target: Btkin vitro: ONO-4059 ( analog ) is a selective, once-daily, oral inhibitor of BTK, which has been shown to play a role in the survival and proliferation of malignant B-cells. ONO-4059 (analog) shows a favourable safety profile along with promising efficacy in this difficult-to-treat patient population. [1]in vivo: ONO-4059 (analog) has demonstrated anti-tumour activity in several pre-clinical models.[1] ONO-4059 (analog) potently and dose-dependently reverse clinical arthritis and prevented bone damage in the CIA model.[2]
MT-802 is a potent BTK degrader based on PROTAC technology, with a DC50 of 1 nM. MT-802 has potential to treat C481S mutant chronic lymphocytic leukemia (CLL)[1].
JAK3/BTK-IN-2 is a potent inhibitor of JAK3/BTK. BTK and JAK3 are two important targets for autoimmune diseases. Simultaneous inhibition of the BTK/JAK3 signalling pathway exhibits synergistic effects. JAK3/BTK-IN-2 has the potential for the research of JAK3 kinase and/or BTK-related diseases (extracted from patent WO2021147952A1, compound 004)[1]
BTK-IN-14 is a potent inhibitor of BTK. BTK plays an important role in signaling mediated by B cell antigen receptor (BCR) and Fcγreceptor (FcγR) in B cells and myeloid cells, respectively. BTK-IN-14 has the potential for the research of related diseases, especially autoimmune diseases, inflammatory diseases or cancer (extracted from patent WO2022057894A1, compound 1)[1].
BTK inhibitor 19 is a highly selective, covalent BTK inhibitor (IC50 = 2.7 nM).
GDC-0834 is a potent and selective BTK inhibitor. GDC-0834 inhibits BTK with an in vitro IC50 of 5.9 and 6.4 nM in biochemical and cellular assays, respectively, and in vivo IC50 of 1.1 and 5.6 μM in mouse and rat, respectively.
Zanubrutinib is a selective Bruton tyrosine kinase (BTK) inhibitor.
CHMFL-BTK-01 (compound 9) is a highly selective irreversible BTK inhibitor, with an IC50 of 7 nM. CHMFL-BTK-01 (compound 9) potently inhibited BTK Y223 auto-phosphorylation[1].
BTK-IN-10 is a potent BTK inhibitor with IC50s of <5 nM for wild-type BTK or mutated BTK (C481S), respectively (WO2022012509A1; example 111)[1].