btk in-1

BTK IN-1 [SNS062 analog] is an effective BTK inhibitor with an IC50 of less than 100 nM.

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.

BTK-IN-16 is a potential inhibitor of wild-type BTK and C481S mutants.BTK-IN-16 can be used to study various autoimmune diseases and cancers caused by BTK.

BTK-IN-19 is a reversible BTK inhibitor with an IC 50 of <0.001 μM .

BTK-IN-10 is a potent inhibitor of BTK, effective against both wild-type BTK (IC50<5 nM) and mutant BTK (C481S) (IC50<5 nM).

BTK-IN-15 is a novel, orally active Bruton's tyrosine kinase (BTK) inhibitor that inhibits BTK (IC50: 0.7 nM). BTK-IN-15 induces apoptosis in cancer cells and has good kinase selectivity and anti-tumour activity.

BTK-IN-11 is a potent BTK inhibitor with potential applications in research on autoimmune diseases, inflammatory diseases, and cancer.

BTK-IN-17 is a selective, orally active inhibitor of Bruton's Tyrosine Kinase (BTK) with an inhibition concentration (IC50) value of 13.7 nM. It effectively reduces the expression of phosphorylated BTK at Tyrosine 223 (p-BTK Y223) and phosphorylated Phospholipase C Gamma 2 at Tyrosine 1217 (p-PLCγ2 Y1217), demonstrating anti-inflammatory properties.

BTK-IN-18 is a potent, reversible inhibitor of Bruton's tyrosine kinase (BTK) with an IC50 of 0.002 µM, and it effectively suppresses CD69 and CD86 expression in vivo.

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.

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.

1,2-Bis(2-iodoethoxy)ethane is a PEG-based PROTAC linker used in the synthesis of MT802 and SJF620, which are potent PROTAC BTK degraders with DC50s of 1 nM and 7.9 nM, respectively [1].

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].

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.

JAK3-IN-1 is an orally active, selective and potent JAK3 inhibitor that can be used to study immune system diseases.

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.

Propargyl-PEG4-acid is a PEG-based PROTAC linker used in the synthesis of BTK-IAP PROTACs, including Ibrutinib-based PROTAC 2 and its analogue PROTAC 3. PROTAC 3 induces BTK degradation with a DC50 of 200 nM in THP-1 cells[1].

Lenalidomide-PEG3-iodine, an E3 ligase ligand-linker conjugate, consists of a cereblon-based Lenalidomide ligand and a 3-unit polyethylene glycol (PEG) linker. This compound is utilized in creating various proteolysis targeting chimeras (PROTACs), including the highly effective PROTAC BTK degrader SJF620, which has a degradation concentration 50 (DC50) of 7.9 nM[1].

FDU73 is a potent and selective BTK PROTAC degrader with a DC50 of 2.9 nM in JeKo-1 cells. It inhibits tumor cell proliferation and exhibits antitumor activity.

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.

1-(Piperidin-4-ylmethyl)piperidine is a PROTAC linker used in the synthesis of PROTAC molecules, such as PROTAC BTK Degrader-9.

Potent and selective BTK Degrader (IC50 = 5.1 nM); degrades BTK in a proteasome- and CRBN-dependent manner. Suppresses BTK signaling and proliferation in mantle cell lymphoma (MCL) cells by degrading BTK, IKFZ1, and IKFZ3 (3 validated targets in B-cell malignancies). Also degrades Ibrutinib (Cat. No. 6813) -resistant C481S-BTK mutant cancer cells. Exhibits no binding against a panel of 468 kinases at 1 μM. Reduces tumor burden and extends survival in lymphoma patient-derived xenograft models.

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.