BMS-986195 is a potent, covalent, irreversible inhibitor of Bruton’s tyrosine kinase (BTK).

DZD8586 is an oral, non-covalent, BBB penetrant LYN and BTK dual inhibitor, overcomes resistance mutations to the approved covalent and non-covalent BTK inhibitors.

ACP-5862 is a major metabolite of acalabrutinib and potent and selective covalent BTK inhibitor with IC50 of 5 nM.

GDC-0853 is orally available inhibitor of Bruton's tyrosine kinase (BTK) with potential antineoplastic activity.

BIIB091 is a novel reversible, selective, potent BTK inhibitor with Kd of 0.07 nM.

TAK-020 is a covalent Btk inhibitor, which becomes the clinical candidate.

Remibrutinib (LOU064) is a potent, highly selective covalent inhibitor of bruton tyrosine kinase (BTK) with IC50 of 1.3 nM, 2.5 nM and 18 nM for BTK, FcγR-induced IL8 and anti-IgM/IL4-induced CD69, respectively. Remibrutinib (LOU064) exhibits an exquisite kinase selectivity due to binding to an inactive conformation of BTK and has the potential for the treatment of autoimmune diseases.

AS-1763 is an orally available, potent, and selective BTK inhibitor and shows excellent potency against both wild/C481S mutant BTKs with IC50 of 0.85 nM/0.99 nM.

Zanubrutinib is a selective Bruton tyrosine kinase (BTK) inhibitor.

RN-486 is a Bruton's tyrosine kinase (Btk) inhibitor.

PCI-32765 (Ibrutinib) is a potent and highly selective Btk inhibitor with IC50 of 0.5 nM.

PCI 29732 is a selective and irreversible Btk inhibitor with IC50 of 8.2 nM in a FRET based biochemical enzymology assay.

ONO-4059 is a novel Small Molecule Dual Inhibitor Of Bruton’s Tyrosine Kinase (Btk) and Tec Kinase.

FM-A13 is a selective inhibitor of Bruton’s tyrosine kinase (BTK) – IC₅₀’s = 2.5 µM (recombinant BTK) and 17.2 µM (human BTK).

Evobrutinib is an inhibitor of Bruton's tyrosin kinase (Btk) inhibitor extracted from patent US20140162983 example 0174.

AVL-292 is a covalent, highly selective, orally active small molecule inhibitor of Btk currently being evaluated in a Phase 1b clinical trial in relapsed.

ARQ-531 is a potent, reversible, orally available inhibitor of both wild type and C481S-mutant BTK kinase with IC50 of 0.85 and 0.39 nM,

Acalabrutinib (ACP-196) is a second-generation, selective, irreversible inhibitor of BTK.

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.

(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.

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. N-piperidine Ibrutinib hydrochloride can be used as a BTK ligand in the synthesis of a series of PROTACs, such as SJF620. SJF620 is a potent PROTAC BTK degrader with a DC50 of 7.9 nM.

ONO-4059 is a highly selective, orally bioavailable BTK inhibitor with a potency (IC50) of 2.2 nM.

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.

XMU-MP-3 is a potent, selective, noncovalent BTK inhibitor with IC50 of 10.7 nM and 17.0 nM for BTK WT and BTK C481S mutation.XMU-MP-3 inhibited BTK‐transformed Ba/F3 cell proliferation with an IC50 of 11.4 nM, with negligible anti‐proliferative effects on parental wild‐type Ba/F3 cells (IC50>10 uM).XMU‐MP‐3 inhibited both the autophosphorylation and trans‐phosphorylation of BTK at residues Y223 and Y551, in a dose‐dependent manner in BTK‐transformed Ba/F3 cells at concentrations as low as 100 nM and completely suppressed at 1,000 nM.XMU‐MP‐3 was considerably less potent (IC50, 2,815 nM) against proliferation of BTK(T474M)‐transformed Ba/F3 cells.XMU‐MP‐3 inhibits the growth of malignant B‐cells, inhibited phosphorylation of PLCγ2 at Y1217 and Y759, substantially suppresses tumour growth in mouse xenograft models.XMU‐MP‐3 maintained inhibitory potency with an IC50 of 182.3 nM against BTK(C481S)‐Ba/F3 cells and with an IC50 of 17.0 nM in biochemical assays, suppressed ibrutinib‐resistant BTKC481S mutation in vivo.

TG-1701 (Edralbrutinib, TG1701) is a irreversible, orally available, potent and highly specific BTK inhibitor with Kd of 3 nM, IC50 of 6.7 nM, more selective than ibrutinib.TG-1701 exerts similar activity than the first-in-class BTKi ibrutinib, although with greater selectivity, in in vitro and in vivo models of B-NHL.TG-1701 impaired BCR downstream signaling in a concentration-dependent manner in IgM-stimulated cells, with maximal effects observed at 100 nM for TG-1701.TG-1701 shows mean GI50 of 6.4 uM in a set of 10 parental B-NHL cell lines (MCL cell lines GI50=4.3 uM).TG-1701 blunts Ikaros gene signature, including YES1 and MYC, in early-responder patients as well as in BTKi-sensitive B-NHL cell lines and xenografts.

KIN-8194 (KIN8194) is a highly potent dual HCK and BTK inhibitor with IC50 of <0.495 and 0.915 nM, respectively.KIN-8194 demonstrated greater selectivity compared with A419259 with no KIT, RET, PDGFRA, EPHB6, or CDPK1 inhibition.KIN-8194 binds to gatekeeper residue Thr333 of HCK, but not to Cys481 of BTK.KIN-8194 shows robust inhibition of both HCK and BTK activity in MYD88-mutated cells, showed robust inhibition of HCK Tyr410 phosphorylation; inhibits the growth and survival of MYD88-mutated WM and ABC DLBCL cells.KIN-8194 overcomes ibrutinib resistance relatedto BTK Cys481Ser-expressing MYD88-mutated B-cell lymphoma cells, synergizes with the BCL-2 inhibitor venetoclax.KIN-8194 shows superior activity over ibrutinib in MYD88-mutated TMD-8 ABC DLBCL xenograft mouse model.KIN-8194 is active against ibrutinib resistance in BTK Cys481Ser -expressing ABC DLBCL xenograft mouse model.

PRN473 (Atuzabrutinib, SAR 444727, PRN-473) is a potent, selective, covalent reversible BTK inhibitor.

BTK-IN-7 is a potent and selective inhibitor of BTK (IC50=4.0 nM). BTK-IN-7 has high selectivity in both enzymatic (ITK >250-fold, EGFR >2500-fold) and cellular levels(ITK >227-fold, EGFR 27-fold). BTK-IN-7 also has potent antitumor activity.

BLK-IN-1 (compound 1) is a selective and covalent inhibitor of B-Lymphoid tyrosine kinase (BLK) and BTK, with IC50s of 18.8 nM and 20.5 nM, respectively. BLK-IN-1 can be used for the research of cancer.

BTK-IN-8 is a potent selective peripheral covalent BTK inhibitor (IC50=0.22 nM; Kd=0.91 nM). BTK-IN-8 has good whole blood CD69 cellular potency (IC50=0.029 µM).