c481s btk

N-piperidine Ibrutinib hydrochloride is a potent BTK inhibitor, a BTK ligand, inhibits WT BTK and C481S BTK, which can be used to synthesize a range of PROTAC molecules.N-piperidine Ibrutinib hydrochloride has potential anticancer N-piperidine Ibrutinib hydrochloride has potential anticancer activity, inhibiting the growth and proliferation of cancer cells.

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.

ARQ-531 is a potent and orally active BTK inhibitor with potential antineoplastic activity, with IC50s of 0.85 nM and 0.39 nM for WT-BTK and C481S-BTK, respectively.

N-piperidine Ibrutinib is a potent BTK inhibitor with IC50s of 51.0 for WT BTK and 30.7 nM for C481S BTK respectively. N-piperidine Ibrutinib 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.

MT-802 is an effective BTK degrader based on PROTAC technology (DC50: 1 nM). MT-802 has the potential to treat C481S mutant chronic lymphocytic leukemia (CLL).

WS-11 is a non-covalent reversible inhibitor of BTK, with IC50 values of 3.9 nM for the wild-type and 2.2 nM for the C481S mutant BTK. In addition to strong hydrogen bonding, WS-11 also forms robust π-π interactions with PHE540, and p-π interactions with LYS430 within the active pocket.

P131 is a PROTAC molecule consisting of a cereblon ligand based on Pomalidomide and IBT6A, linked via a PEG linker. P131 effectively degrades both wild-type and C481S mutant BTK with nanomolar potency.

TQ-3959 is an orally active BTKPROTAC degrader, with a DC50 of 14.6 nM. It exhibits antiproliferative activity against both wild-type BTK and BTK C481S mutant cell lines. TQ-3959 demonstrates tumor growth inhibition in female NOD-SCID mice with TMD-8 xenografts. This compound is applicable in the study of B-cell malignancies, such as lymphoma.

(R,R)-Birelentinib (Compound 14) is a potent BTK inhibitor with IC50 values of 0.7 nM for BTKWT and 0.86 nM for BTKC481S. It effectively inhibits BTK autophosphorylation with an IC50 of 24.3 nM. This compound exhibits significant antiproliferative activity against both wild-type and C481S mutant HEK293 cells, and is useful for studying resistant B-cell malignancies.

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.

XMU-MP-3 is a robust, non-covalent inhibitor of BTK, exhibiting exceptional potency with IC50 values of 10.7 nM and 17.0 nM for BTK WT and BTK C481S mutation, respectively, in the presence of 10 μM ATP. Moreover, XMU-MP-3 elicits apoptosis.

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).

RET-IN-14 is a potent inhibitor of RET, capable of acting on RET (WT) (IC50 < 0.51 nM), RET (G810R) (IC50: 9.3 nM), RET (V804M) (IC50: 1.3 nM), BTK (C481S) (IC50: 9.2 nM) and BTK (C481S) (IC50 : 15 nM). RET-IN-14 exhibits potential for tumor studies.

Rocbrutinib (LP-168) is a selective BTK kinase inhibitor that is effective against both wild-type and mutant forms (C481S, C481F, C481R, T474I, etc.), and has anti-tumor effects.

Fenebrutinib (GDC-0853) is a selective and noncovalent inhibitor of Bruton's tyrosine kinase (Btk) with a Ki of 0.91 nM.