TAK-020 is a covalent Btk inhibitor, which becomes the clinical candidate.
QL-X-138 is a selective and potent BTK/MNK dual kinase inhibitor with IC50 of 8, 107.4, and 26 nM for BTK, MNK1, and MNK2, respectively; exhibits covalent binding to BTK and noncovalent binding to MNK; enhances the antiproliferative efficacies in vitro against a variety of B-cell cancer cell lines, as well as AML and CLL primary patient cells; arrests cell cycle progression and strongly induces apoptosis.
PROTAC BTK Degrader-6 (Compound 15) is a PROTAC BTK degrader (DC50: 3.18 nM. PROTAC BTK Degrader-6 has anti-inflammatory activity, inhibits NF-κB activation, and inhibits the expression of pro-inflammatory cytokines (e.g. IL-1β, IL-6)[1].
CG-806 is a pan FLT3/BTK Multi-Kinase inhibitor.
CTA056 is an ITK (IL-2-inducible T-cell kinase) inhibitor with an IC50 of 0.1 μM. CTA056 selectively targets malignant T cells and modulates oncomirs. CTA056 induces apoptosis and is a potential therapeutic agent for the treatment of T-cell leukemia and lymphoma[1].
Ibrutinib dimer is a Dimer of Ibrutinib. Ibrutinib dimer is an impurity of Ibrutinib[1]. Ibrutinib is a selective, irreversible Btk inhibitor with an IC50 of 0.5 nM[2].
Orelabrutinib (ICP-022) is a potent, orally active, and irreversible Bruton's tyrosine kinase (BTK) inhibitor. Orelabrutinib has the potential for B-cell malignancies treatment[1].
BMS-986142 is a potent and highly selective reversible inhibitor of Bruton's tyrosine kinase (BTK) with an IC50 of 0.5 nM.
BMS-935177 is a potent and selective reversible inhibitor of Bruton’s tyrosine kinase (Btk) with an IC50 of 3 nM.
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 has antiproliferative activity and anticancer activity. LFM-A13 can be used in cancer-related research[1][3][4]
BTK-IN-5 is a covalent BTK inhibitor for treating medical conditions such as cardiovascular diseases, respiratory diseases, inflammation, and diabetes.
Btk inhibitor 2 is a Bruton's tyrosine kinase (BTK) inhibitor extracted from patent US 20170224688 A1.
BTK-IN-27 (example 8) is a BTK inhibitor (IC50: 0.2 nM). BTK-IN-27 shows anti-proliferative activity in TMD8 cells (IC50: < 5 nM). BTK-IN-27 can be used for research of cancer, lymphoma, leukemia and immunological diseases[1].
BTK-IN-19 (Compound 51) is a reversible BTK inhibitor with an IC50 of <0.001 μM[1].
JAK3/BTK-IN-5 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-5 has the potential for the research of JAK3 kinase and/or BTK-related diseases (extracted from patent WO2021147953A1, compound 35)[1]
Spebrutinib besylate (AVL-292 benzenesulfonate; CC-292 besylate) is a potent inhibitor of Btk kinase activity (IC50<0.5 nM, Kinact/Ki=7.69×104 M-1s-1s) in biochemical assays.
BTK IN-1 is a potent BTK inhibitor, with an IC50 of <100 nM.
BTK inhibitor 4b is a potent, highly selective inhibitors of BTK with IC50 of 4.2 and 0.9 nM against activated and unactivated BTK, respectively; demonstrates significant efficacy in models in vivo and good ADME and safety profiles.
GBD-9 is a double-mechanism degrader that efficiently degrades BTK and GSPT1 by recruiting the E3 ligase cereblon (CRBN). GBD-9 acts both as a PROTAC molecule to induce the degradation of BTK and as a molecular glue to degrade GSPT1. GBD-9 effectively inhibits cancer cell growth[1].
ACP-5862 is a major active, circulating, pyrrolidine ring-opened metabolite of Acalabrutinib with an IC50 of 5.0 nM for Bruton tyrosine kinase (BTK)[1]. Acalabrutinib is an orally active, irreversible, and highly selective BTK inhibitor, with an IC50 of 3 nM and EC50 of 8 nM[2].
XMU-MP-3 is a potent non-covalent BTK inhibitor with IC50s of 10.7 nM and 17.0 nM for BTK WT and BTK C481S mutation in the presence of 10 μM ATP, respectively. XMU-MP-3 also induces apoptosis[1].
ARQ 531 is a reversible non-covalent inhibitor of Bruton’s Tyrosine Kinase (BTK), with IC50s of 0.85 nM and 0.39 nM for WT-BTK and C481S-BTK, respectively.
RN486 is a selective Btk inhibitor with an IC50 Value of 4.0 nM.IC50 Value: 4.0 nM [1]Target: Btk Kinasein vitro: In the enzymatic assay, the compound potently inhibited Btk kinase activity with an IC50 of 4.0 nM. RN486 not only potently and selectively inhibited the Btk enzyme, but also displayed functional activities in human cell-based assays in multiple cell types, blocking Fcε receptor cross-linking-induced degranulation in mast cells (IC(50) = 2.9 nM), Fcγ receptor engagement-mediated tumor necrosis factor α production in monocytes (IC(50) = 7.0 nM), and B cell antigen receptor-induced expression of an activation marker, CD69, in B cells in whole blood (IC(50) = 21.0 nM) [1]. In a co-culture system consisting of human primary synovial FLS and activated human platelets, convulxin stimulation resulted in elevated production of pro-inflammatory cytokines, IL-6 and IL-8, an effect which was dose-dependently blocked by RN486 [2].in vivo: RN486 displayed similar functional activities in rodent models, effectively preventing type I and type III hypersensitivity responses. More importantly, RN486 produced robust anti-inflammatory and bone-protective effects in mouse CIA and rat adjuvant-induced arthritis (AIA) models. In the AIA model, RN486 inhibited both joint and systemic inflammation either alone or in combination with methotrexate, reducing both paw swelling and inflammatory markers in the blood [1]. The administration of RN486 completely stopped disease progression, as determined by histologic and functional analyses of glomerular nephritis. The efficacy was associated with striking inhibition of B cell activation, as demonstrated by a significant reduction in CD69 expression in response to BCR crosslinking. RN486 markedly reduced the secretion of IgG anti-double-stranded DNA (anti-dsDNA) secretion, as determined by enzyme-linked immunosorbent and enzyme-linked immunospot assays [3].
SJF620 is a potent PROTAC BTK degrader with a DC50 of 7.9 nM[1].
BMS-986143 is an orally active, reversible BTK inhibitor with an IC50 of 0.26 nM. BMS-986143 also inhibits TEC, BLK, BMX, TXK FGR, YES1, ITK with IC50s of 3 nM, 5 nM, 7 nM, 10 nM, 15 nM,19 nM, 21 nM, respectively. BMS-986143 can be used for the research of autoimmune diseases[1].
NRX-0492 is an orally active and potent degrader of BTK. NRX-0492 catalyzes ubiquitylation and proteasomal degradation of BTK with DC50≤0.2 nM and DC90≤0.5 nM, respectively. NRX-0492 inhibits B-cell receptor (BCR)-mediated signaling, transcriptional programs, and chemokine secretion. Moreover, NRX-0492 also links a noncovalent BTK-binding domain to Cereblon. Cereblon is an adaptor protein of the E3 ubiquitin ligase complex[1].
BI-1622 is an orally active, potent and highly selective HER2 (ERBB2) inhibitor, with an IC50 of 7 nM. BI-1622 shows greater than 25-fold selectivity over EGFR. BI-1622 shows high antitumor efficacy in vivo in xenograft mouse tumor models with engineered H2170 and PC9 cells and had a favorable drug metabolism and pharmacokinetics profile[1].
BTK-IN-11 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-11 has the potential for the research of related diseases, especially autoimmune diseases, inflammatory diseases or cancer (extracted from patent WO2022063101A1, compound Z2)[1].
BTK-IN-18 is a potent, reversible BTK inhibitor with an IC50 of 0.002 µM. BTK-IN-18 inhibits both CD69 and CD86 in vivo[1].
BTK-IN-23 is a BTK inhibitor (IC50: 12.8 nM). BTK-IN-23 also inhibits BLX and BMX with IC50s of 35.6 and 5.7 nM respectively. BTK-IN-23 shows improved kinase selectivity compared to Ibrutinib (HY-10997)[1].