DPPY (compound 6) is a potent PTK inhibitor with IC50 values of <10, <10, <10 nM for EGFR, BTK, JAK3, respectively. DPPY shows anti-proliferative activity against B-cell lymphoma cells. DPPY has the potential for the research of idiopathic pulmonary fibrosis (IPF)[1].
BTK-IN-20 (compound 283) is a BTK tyrosine kinase inhibitor and a 1H-pyrazolo[3,4-d]pyrimidine derivative. BTK-IN-20 can be used for the research of cancer and inflammation[1].
Sunvozertinib is a potent ErbBs (EGFR, Her2, especially mutant forms) and BTK inhibitor. Sunvozertinib shows IC50s of 20.4, 20.4, 1.1, 7.5, and 80.4 nM for EGFR exon 20 NPH insertion, EGFR exon 20 ASV insertion, EGFR L858R and T790M mutations, and Her2 Exon20 YVMA, and EGFR WT A431, respectively (patent WO2019149164A1, example 52)[1].
BCPyr is a new candidate BTK degrader (DC50 = 800 nM).
Poseltinib, an orally active, selective and irreversible Bruton’s tyrosine kinase (BTK) inhibitor (IC50 =1.95 nM), with 0.3, 2.3 and 2.4-fold selectivity for BTK over BMX, TEC and TXK, respectively. Poseltinib can covalently bind to the active site (cysteine 481 residue) of BTK, and reveales potent inhibition of B cell receptor (BCR), Fc receptor (FcR), Toll-like receptor (TLR) mediated signaling[1].
Ibrutinib deacryloylpiperidine (IBT4A) is an impurity of Ibrutinib[1]. Ibrutinib is a selective, irreversible Btk inhibitor with an IC50 of 0.5 nM[2].
Elsubrutinib (ABBV-105) is an orally active, potent, selective and irreversible Bruton's tyrosine kinase (BTK) inhibitor。The IC50 of Elsubrutinib for BTK catalytic domain is 0.18 μM. Elsubrutinib can be used for the research of inflammatory disease[1].
PCI 29732 is a selective and irreversible Btk inhibitor with IC50 of 8.2 nM in a FRET based biochemical enzymology assay.IC50 value: 8.2 nM [1]Target: Btk kinasePCI 29732(compound 1) has a 8.2 nM potency against Btk in a FRET based biochemical enzymology assay. PCI 29732 shows only modest inhibitory activity against Itk, another Tec family kinase, probably due to the difference at the “gatekeeper” residue [1].In human CD20+ B cells stimulated at the BCR, PCI-29732 blocked the transcriptional up-regulation of a panel of B-cell activation genes that occurs within 6 h of stimulation. Pulse exposure to the reversible inhibitor PCI-29732 did not result in BCR inhibition [2].
(R)-Elsubrutinib ((R)-ABBV-105) is a Btk inhibitor. (R)-Elsubrutinib can be used in studies of immune diseases (such as rheumatoid arthritis, psoriasis, ankylosing spondylitis, asthma, systemic lupus erythematosus) and cancer[1].
JNJ-64264681 is a potent, orally active, selective and irreversible covalent BTK inhibitor. JNJ-64264681 exhibits good pharmacokinetic characteristics and can be used for cancer and autoimmune diseases research[1].
RSH-7 is a potent Btk and FLT3 inhibitor with IC50s of 47, 12 nM, respectively. RSH-7 induces apoptosis and shows antiproliferative activities. RSH-7 inhibits BTK and FLT3 signaling and shows anti-tumor activity[1].
JAK3/BTK-IN-6 (compound 14h) is a potent BTK and JAK3 dual inhibitor, with IC50 values of 0.6 and 0.4 nM, respectively. JAK3/BTK-IN-6 shows good metabolic stability in human liver microsome. JAK3/BTK-IN-6 can be used for hematological and immune diseases research[1].
NX-2127 is an orally and potent BTK inhibitor, inducing degradation of the mutated BTKC481S in cells. NX-2127 inhibits proliferation of BTKC481S mutant TMD8 cells, more effectively than Ibrutinib (HY-10997). NX-2127 catalyzes the degradation of Ikaros (IKZF1) and Aiolos (IKZF3) with of 25 nM and 54 nM, respectively. NX-2127 stimulates T cell activation and increases IL-2 production in primary human T Cells[1][2].
QL47 is a potent, selective and irreversible BTK kinase inhibitor with IC50 of 7 nM.IC50 Value: 7 nMTarget: Btkin vitro: QL47 inhibits BTK kinase activity with an IC50 of 7 nM, inhibits autophosphorylation of BTK on Tyr223 in cells with an EC50 of 475 nM and inhibits phosphorylation of a downstream effector PLCγ2 (Tyr759) with an EC50 of 318 nM. In Ramos cells QL47 induces a G1 cell cycle arrest which is associated with pronounced degradation of BTK protein. QL47 inhibits the proliferation of B-cell lymphoma cancer cell lines at submicromolar concentrations [1].in vivo: N/A
GDC-0834 (S-enantiomer) is the S-enantiomer of GDC-0834. GDC-0834 is a potent and selective BTK inhibitor.
Luxeptinib (CG-806) is an orally active, reversible, first-in-class, non-covalent and potent pan-FLT3/pan-BTK inhibitor. Luxeptinib induces cell cycle arrest, apoptosis or autophagy in acute myeloid leukemia cells[1][2][3][4].
Topoisomerase I inhibitor 11 is a potent inhibitor of Topoisomerase I. Topoisomerase I inhibitor 11 can bind to BTK[1].
Atuzabrutinib is a potent BTK (Bruton's tyrosine kinase) inhibitor (patent WO2016100914A1)[1].
CNX-500 is a probe consisting of a covalent Btk inhibitor (CC-292) chemically linked to biotin. CNX-500 retains inhibitory activity against Btk (IC50 of 0.5 nM) and the ability to form a covalent bond with Btk. CNX-500 has low inhibitory effects on kinase epidermal growth factor receptor, and upstream Src-family kinases including Syk and Lyn[1].
Spebrutinib (AVL-292; CC-292) is a covalent, orally active, and highly selective with an IC50 of 0.5 nM.
Btk inhibitor 1R enantiomer Hcl is a pyrazolo[3,4-d]pyrimidine derivative as a Btk kinase inhibitor.IC50 value:Target: BtkFrom PCT Int. Appl. (2012), WO 2012158843 A2 20121122.
Cinsebrutinib is a Bruton's tyrosine kinase inhibitor, extracted from patent WO2021207549 (compound 5-6). Cinsebrutinib has the potential for cancer study.
JS25 is a potent, selective, covalent TEC family of non-receptor tyrosine kinases (BTK, ITK, TXK and BMX) inhibitor with IC50 of 3.5 and 5.8 nM for BMX and BTK, respectively.JS25 displays a strong binding affinity against all the members of TEC family, covalently inhibits BMX at Cys496. JS25 demonstrates intracellular target engagement in HEK293 cells (IC50=44.8 nM), 10 times greater than BMX-IN-1.JS25 inhibits androgen-receptor positive prostate-cancer cells with GI50 of 6.6 uM.JS25 shows synergistic anti-proliferative activity in LNCaP cells in combination with AKT1/2 (AKT inhibitor), Flutamide (androgen receptor antagonist) and LY293002 (PI3K inhibitor).
Tirabrutinib (ONO-4059) is a highly selective, orally bioavailable BTK inhibitor with an IC50 of 2.2 nM.
Avitinib (AC0010) is an irreversible, mutant-selective EGFR inhibitor that effectively inhibits EGFR T790M resistance mutations in non-small cell lung cancer (NSCLC). Abivertinib is also a novel BTK inhibitor.
EGFR-IN-40 (compound 3z) is a potent BTK, EGFR, and ITK inhibitor with IC50 values of 1.2 nM, 5.3 nM, and 46.1 nM, respectively[1].
GDC-0853 is a potent, selective, and noncovalent bruton's tyrosine kinase (Btk) inhibitor with a Ki of 0.91 nM.
BMX-IN-1 is a selective, irreversible inhibitor of bone marrow tyrosine kinase on chromosome X (BMX) that targets Cys496 in the BMX ATP binding domain with an IC50 of 8 nM, also targets the related Bruton’s tyrosine kinase (BTK) with an IC50 value of 10.4 nM, but is more than 47-656-fold less potent against Blk, JAK3, EGFR, Itk, or Tec activity.
BTK-030 is a novel BTK inhibitor.
PRN1008 is a reversible covalent inhibitor of Bruton’s Tyrosine Kinase (BTK), with an IC50 of 1.3 nM.