ibrutinib

Ibrutinib (PCI-32765) is an irreversible inhibitor of BTK (IC50: 0.5 nM) that selectively blocks B cell activation.

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.

Ibrutinib D5 is a deuterium-labeled Ibrutinib. Ibrutinib is an irreversible Btk inhibitor.

Ibrutinib-MPEA is ibrutinib derivative. Ibrutinib is a covalent and irreversible BTK inhibitor that has been used to treat hematological malignancies.

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.

Ibrutinib is a selective, irreversible Btk inhibitor (IC50: 0.5 nM). Ibrutinib Racemate is the racemate of Ibrutinib.

Ibrutinib Interm 0441 is a piperidine derivative with an amine protecting group and may be used in the preparation of biologically active compounds.

Ibrutinib dimer is an impurity of Ibrutinib. IIbrutinib dimer is a Dimer of Ibrutinib. Ibrutinib is an irreversible Btk inhibitor (IC50: 0.5 nM).

Ibrutinib-biotin, a probe consisting of Ibrutinib linked to biotin via a long-chain linker, has an IC50 of 0.755-1.02 nM for BTK.

PCI 45227 is an active metabolite of the Bruton's tyrosine kinase inhibitor ibrutinib .1PCI 45227 is formed from ibrutinib by the cytochrome P450 (CYP) isoform CYP3A. 1.Veeraraghavan, S., Viswanadha, S., Thappali, S., et al.Simultaneous quantification of lenalidomide, ibrutinib and its active metabolite PCI-45227 in rat plasma by LC-MS/MS: Application to a pharmacokinetic studyJ. Pharm. Biomed. Anal.107151-158(2015)

Ibrutinib deacryloylpiperidine (IBT4A) is a highly selective Bruton's tyrosine kinase (BTK) irreversible inhibitor with an IC50 of 0.5 nM.

(Rac)-Ibrutinib alkyne (Compound 8) is a Btk inhibitor with an IC50 of 0.72 nM. This compound effectively inhibits B cell receptor signaling functions, with an IC50 of 9 nM for calcium flux inhibition in Ramos cells. (Rac)-Ibrutinib alkyne is applicable in research on diseases such as rheumatoid arthritis.

Ibrutinib (Standard) is a reference standard for research and analysis in studies involving Ibrutinib. Ibrutinib (PCI-32765) is a Bruton's tyrosine kinase (BTK) inhibitor (IC50=0.5 nM) with irreversible and selective properties. Ibrutinib blocks BTK to inhibit the proliferation and survival of B cells, and possesses antitumor activity, which can be used for the treatment of chronic lymphocytic leukemia, among others.

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.

IBT6A, an impurity of Ibrutinib, is a Btk inhibitor (IC50: 0.5 nM) that can be utilized in the synthesis of IBT6A Ibrutinib dimer and IBT6A adduct.

(Rac)-IBT6A hydrochloride is a racemate of IBT6A. IBT6A is an impurity of Ibrutinib. IBT6A can be used in the synthesis of IBT6A Ibrutinib dimer and IBT6A adduct. Ibrutinib is a Btk inhibitor (IC50: 0.5 nM).

IBT6A hydrochloride, an impurity of Ibrutinib, is relevant for synthesizing IBT6A Ibrutinib dimer and IBT6A adduct. Ibrutinib is a Btk inhibitor (IC50: 0.5 nM).

(Rac)-IBT6A is a racemate of IBT6A, an impurity of Ibrutinib that can be utilized in the synthesis of IBT6A Ibrutinib dimer and IBT6A adduct.

Propargyl-PEG1-acid, a PEG-based PROTAC linker, enables the synthesis of BTK-CRBN PROTACs, specifically Ibrutinib-based PROTAC 4 and PROTAC 5. At a concentration of 10 μM, PROTAC 5 facilitates the degradation of BTK and induces the degradation of CSK, LYN, and LAT2[1].

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].

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.

Abivertinib, also known as AC0010 and Avitinib, is a third-generation EGFR tyrosine kinase inhibitor and BTK Inhibitor that demonstrated clinical efficacy and manageable adverse events (AEs). Abivertinib inhibits cell proliferation, reduces colony-forming capacity, and induces apoptosis and cell cycle arrest in AML cells, especially those harboring FLT3-ITD mutations. Abivertinib was also found to be more sensitive than ibrutinib in treating AML. Abivertinib may be a promising novel agent for AML, with potential for combination treatment with HHT.

GNE-431 is a potent, selective and noncovalent Btk inhibitor with IC50 of 3.2 nM. GNE-431 showed excellent potency against the C481R, T474I, and T474M mutants. GNE-431 may provide a treatment option to patients, especially those who have acquired resistance to ibrutinib by mutation of Cys481 or Thr474.

BTK-IN-22, a BTK inhibitor (IC 50: 0.9 nM), also exhibits inhibition against BLX and BMX with IC 50 values of 1.4 and 1.2 nM, respectively. Demonstrating enhanced kinase selectivity, BTK-IN-22 outperforms Ibrutinib in this regard [1].