btk inhibitor 1

BTK inhibitor 1 (Compound 27) is a BTK inhibitor (IC50: 0.11 nM) with an inhibitory effect on B-cell activation in hWB with an IC50 of 2 nM.

Btk inhibitor 1 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. [1]. PCT Int. Appl. (2012), WO 2012158843 A2 20121122.

BTK inhibitor 10 is a potent and orally active compound with potential applications in rheumatoid arthritis treatment.

BTK inhibitor 13 (compound 8) is a potent and selective BTK inhibitor with an IC50 of 1.2 nM.

BTK inhibitor 19 is a highly selective, covalent BTK inhibitor (IC 50 = 2.7 nM).

BTK inhibitor 18 is a selective, potent, covalent, orally active Btk inhibitor (IC50: 142 nM) that exhibits anti-inflammatory effects.

BTK inhibitor 17 is a potent irreversible Bruton's tyrosine kinase (BTK) inhibitor with an IC50 value of 2.1 nM, suitable for use in rheumatoid arthritis studies.

Remibrutinib inhibits BTK activity with an IC50 value of 0.023 μM in blood. Remibrutinib is an effective and orally active Bruton tyrosine kinase inhibitor (IC50: 1 nM). Remibrutinib has the potential for Chronic urticaria (CU) treatment.

JAK3/ BTk-in-1 is a dual JAK3/BTK inhibitor that specifically targets and inhibits Janus kinase 3 (JAK3) and Bruton's tyrosine kinase (BTK), two important targets in autoimmune diseases. JAK3/ BTk-in-1 simultaneously inhibited the BTK/JAK3 signaling pathway, showing a synergistic effect. JAK3/ BTK-in-1 is a potential compound for the treatment of immune-related diseases, such as autoimmune diseases, certain types of cancer (including lymphoma and leukemia), and other diseases that may be characterized by an unbalanced immune response.

Tirabrutinib hydrochloride is a potent, highly selective, and irreversible oral BTK inhibitor. Tirabrutinib hydrochloride irreversibly covalently binds to Bruton tyrosine kinase (BTK) in B cells and exhibits potent in vitro cytotoxicity against many types of B cell malignancies, as well as in vivo antitumor activity in mouse models [1].

(Rac)-PF-06250112 is a racemic form of PF-06250112, a potent and highly selective BTK inhibitor that is orally bioavailable; it also inhibits BMX non-receptor tyrosine kinase and TEC [1].

AZ7550, an active metabolite of AZD9291, inhibits the activity of IGF1R (IC50: 1.6 μM).

AZ7550 hydrochloride (AZ7550 hydrochloride ), an active metabolite of AZD9291, inhibits the activity of IGF1R (IC50: 1.6 μM).

Spebrutinib besylate (AVL-292 benzenesulfonate; CC-292 besylate) is a Btk kinase activity inhibitor with an IC50 of less than 0.5 nM and a Kinact/Ki of 7.69×10^4 M^-1s^-1.

BMX-IN-1 (BMX kinase inhibitor) is a selective inhibitor of bone marrow tyrosine kinase on chromosome X (BMX, IC50 = 8 nM) and the related Bruton's tyrosine kinase (BTK, IC50 = 10.4 nM), but BMX-IN-1 is more than 47-656 fold less potent against Blk, JAK3, EGFR, Itk, or Tec activity.

PF-06465469 is a covalent ITK inhibitor (IC₅₀ = 2 nM) that also inhibits BTK. PF-06465469 suppresses CXCL12-mediated cell migration, decreases PD-1 and LAG-3 expression. PF-06465469 shows strong potential application in leukemia and T-cell lymphoma research.

I-As-1 is a potent inhibitor of Bruton's tyrosine kinase (BTK) with an IC50 of 2.35 nM. It exhibits antiproliferative activity against Ramos cells and OCI-LY10 cells, with IC50 values of 0.52 μM and 0.11 μM, respectively.

TM471-1 is an orally active, covalent Bruton’s tyrosine kinase (BTK) inhibitor displaying an IC0 value of 1.3 nM for BTKWT, > 40000 nM for BTKC481S, 7.9 nM for TEC, and 12.4 nM for TXK. It inhibits cell growth both in vitro and in vivo, arrests the cell cycle at the G0/G1 phase, and induces apoptosis.

CFON-026 is a selective, orally active, non-covalent BTK inhibitor with an IC50 of 0.27 nM. It demonstrates significant antitumor activity against wild-type BTK (TMD8 and REC-1) as well as all clinically relevant BTK resistance mutations (BTKC481S, T474I, L528W, and V416L). CFON-026 induces complete tumor regression in the TMD8 xenograft mouse model. This compound is applicable for research into hematologic cancers, such as chronic lymphocytic leukemia and Waldenström's macroglobulinemia.

CNX-774 is a highly specific, irreversible, and orally active BTK inhibitor (IC50<1 nM).

Avitinib (AC0010), also known as AC0010 or AC0010MA, is an orally available, irreversible, epidermal growth factor receptor (EGFR) mutant-selective inhibitor, with potential antineoplastic activity. Upon oral administration, avitinib covalently binds to and inhibits the activity of mutant forms of EGFR, including the drug-resistant T790M EGFR mutant, which prevents signaling mediated by mutant forms of EGFR. This may both induce cell death and inhibit tumor growth in EGFR-mutated tumor cells. EGFR, a receptor tyrosine kinase that is mutated in a variety of Ys, plays a key role in tumor cell proliferation and tumor vascularization. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced when compared to non-selective EGFR inhibitors, which also inhibit wild-type EGFR.

(R)-Pirtobrutinib ((R)-LOXO-305) is the less active enantiomer of Pirtobrutinib, a highly selective, non-covalent, next-generation BTK inhibitor that effectively inhibits diverse BTK C481 substitution mutations [1].

Pirtobrutinib (LOXO-305) is an advanced BTK inhibitor that displays high selectivity and operates through a non-covalent mechanism. This compound effectively inhibits various BTK C481 substitution mutations, leading to tumor regression in BTK-dependent lymphoma tumors in mouse xenograft models. Furthermore, Pirtobrutinib exhibits remarkable selectivity for BTK, with more than a 300-fold difference compared to 370 other kinases tested. Notably, at a concentration of 1 μM, Pirtobrutinib demonstrates no significant inhibition of non-kinase off-targets.

Luxeptinib (CG-806) is a novel pan-FLT3/pan-BTK inhibitor that is administered orally. It exhibits potent and reversible inhibition of these enzymes, acting through a non-covalent mechanism. Luxeptinib effectively induces cell cycle arrest, apoptosis, or autophagy in acute myeloid leukemia cells [1][2][3][4].