BTK

ABBV-992 is a potent and selective Bruton's Tyrosine Kinase (BTK) inhibitor. It demonstrates significant inhibitory activity, making it a valuable tool for studying various hematological malignancies. This compound is primarily utilized in cancer research to investigate BTK signaling pathways and their roles in tumor progression and survival.

PROTAC BTK/IKZF1/3 Degrader-1 is a selective and orally bioavailable degrader targeting BTK, IKZF1, and IKZF3 through the PROTAC mechanism. This compound exhibits significant antitumor activity, making it a valuable tool for cancer research, particularly in the context of lymphoma. Its unique mechanism of action allows for the targeted degradation of specific oncogenic proteins, facilitating studies in therapeutic strategies and disease mechanisms.

PROTAC BTK Degrader-4 is a highly effective PROTAC designed to selectively degrade Bruton's tyrosine kinase (BTK) with a DC50 of less than 100 nM. This compound demonstrates minimal immunomodulatory imide drug (IMiD) activity, with a DC50 of 0.345 μM and a maximum degradation rate of 27.4%. PROTAC BTK Degrader-4 is suitable for investigating various pathologies, including cancers, autoimmune disorders, and inflammatory diseases associated with BTK dysregulation.

(R)-Acalabrutinib is a specific inhibitor of Bruton’s tyrosine kinase (BTK), a critical protein involved in B-cell receptor signaling. This compound serves as a valuable tool for research applications in hematological malignancies, particularly in the study of B-cell functions and the development of targeted therapies for conditions such as non-Hodgkin lymphoma and chronic lymphocytic leukemia. Its high selectivity for BTK allows for detailed investigations into BTK-mediated pathways and potential therapeutic interventions.

BTK-IN-19 is a reversible Bruton's tyrosine kinase (BTK) inhibitor with an IC50 of less than 0.001 μM. This compound demonstrates potent inhibitory activity against BTK, making it a valuable tool for studying B-cell signaling pathways. BTK-IN-19 is applicable in research focused on various hematological malignancies and autoimmune diseases, contributing to the understanding of therapeutic strategies targeting BTK.

BTK-IN-16 is a dual inhibitor targeting Bruton’s tyrosine kinase (BTK), specifically effective against both wild type and the C481S mutant, with IC50 values of 5.1 μM and 4.1 μM, respectively. This compound is crucial for research into autoimmune diseases and chronic lymphocytic leukemia, where BTK plays a significant role in disease progression. Its ability to inhibit both forms of BTK makes BTK-IN-16 a valuable tool for studying therapeutic strategies in these conditions.

PROTAC BTK Degrader-3 is a selective degrader targeting Bruton's tyrosine kinase (BTK) with a DC50 value of 10.9 nM for BTK degradation in Mino cells. This compound demonstrates significant biological activity and is applicable in research focusing on B-cell malignancies, particularly chronic lymphoid malignancies. Its mechanism of action offers potential pathways for therapeutic intervention in relevant disease models.

BTK-IN-3 is a selective inhibitor of Bruton's tyrosine kinase (BTK), a critical component in B-cell receptor signaling. This compound demonstrates significant biological activity by inhibiting BTK-mediated pathways, which are often implicated in various hematological malignancies. BTK-IN-3 is therefore utilized in research applications focused on cancer biology, particularly in the investigation of B-cell cancers and autoimmune disorders.

Ibrutinib dimer is a dimeric form of Ibrutinib, a selective and irreversible inhibitor of Bruton’s tyrosine kinase (Btk) with an IC50 of 0.5 nM. This compound serves as a valuable tool for studying Btk-mediated signaling pathways and its implications in various hematological malignancies. Researchers can utilize Ibrutinib dimer to investigate the effects of Btk inhibition in cellular models and to explore its potential therapeutic applications in cancer research.

(Rac)-IBT6A hydrochloride is a racemic mixture of IBT6A, a byproduct of Ibrutinib. This compound acts as a selective, irreversible Bruton's tyrosine kinase (Btk) inhibitor with an IC50 of 0.5 nM, making it useful for studying Btk-mediated signaling pathways. It serves as a valuable reagent in the synthesis of Ibrutinib derivatives and adducts, facilitating research into therapeutic strategies for diseases such as B-cell malignancies.

PROTAC BTK Degrader-14 is a targeted protein degrader that specifically degrades Bruton's tyrosine kinase (BTK) through the PROTAC mechanism of action. This compound is significant in cancer research, particularly for studies focused on malignancies where BTK plays a crucial role in signaling pathways. Its ability to effectively modulate BTK levels can provide insights into therapeutic strategies and disease mechanisms involving this key protein.

BTK Ligand 9 is a selective ligand for Bruton's tyrosine kinase (BTK), a critical regulator in B cell receptor signaling. This compound facilitates the development of PROTACs, specifically PROTAC DD-03-171, which are utilized in targeted protein degradation studies. Research applications include investigating the role of BTK in various hematological malignancies and exploring therapeutic strategies for B cell-related diseases.

(R,R)-Birelentinib is a potent Bruton's tyrosine kinase (BTK) inhibitor, achieving IC50 values of 0.7 nM for wild-type BTK and 0.86 nM for the C481S mutant. This compound effectively inhibits the self-phosphorylation of BTK, with an IC50 of 24.3 nM. (R,R)-Birelentinib demonstrates significant anti-proliferative effects against wild-type and C481S mutant HEK293 cells, making it valuable for research into drug-resistant B-cell malignancies.

BTK Degrader-1 Intermediate is a key precursor in the synthesis of BTK Degrader-1, a potent molecule targeting Bruton's tyrosine kinase (BTK). This compound serves as an essential building block for developing antibody-drug conjugates (ADCs), enabling targeted therapy for diseases associated with BTK dysregulation. Researchers utilize BTK Degrader-1 Intermediate in drug development processes to explore innovative treatment strategies in oncology and immunology.

CGI 560 is a potent inhibitor of Bruton's tyrosine kinase (BTK), exhibiting an IC50 value of 400 nM. This compound plays a significant role in the modulation of B-cell receptor signaling pathways, making it a valuable tool for research in hematological malignancies and autoimmune diseases. Its ability to selectively inhibit BTK can aid in elucidating the mechanistic underpinnings of various B-cell-related disorders.

Btk inhibitor 1 R enantiomer (Ibrutinib analog) (Compound 14) is a covalent and irreversible Bruton??s tyrosine kinase (BTK) inhibitor and can be used in synthesis of Ibrutinib and ibrutinib-based activity-based probes (ABPs).

Btk inhibitor 1 R enantiomer hydrochloride (Ibrutinib analog hydrochloride) (Compound 14) is a covalent and irreversible Bruton??s tyrosine kinase (BTK) inhibitor and can be used in synthesis of Ibrutinib and ibrutinib-based activity-based probes (ABPs).

Zanubrutinib (BGB-3111) is a selective Bruton tyrosine kinase (BTK) inhibitor.

Orelabrutinib (ICP-022) is a potent, orally active, and irreversible Bruton's tyrosine kinase (BTK) inhibitor with potential antineoplastic activity.

Remibrutinib, is a potent and orally active bruton tyrosine kinase (BTK) inhibitor with an IC50 value of 1 nM.

Tirabrutinib (ONO-4059) hydrochloride is a selective and novel inhibitor of BTK with IC50 2.2 nm, Tirabrutinib binds to BTK within B cells, thereby preventing B-cell receptor signaling and impeding B-cell development.

BTK inhibitor 1 (compound 27) is an inhibitor of BTK with an IC50 of 0.11 nM for Btk and inhibits B cell activation in hWB with an IC50 of 2 nM.

SJF620 is a PROTAC that targets Bruton's tyrosine kinase (Btk) for degradation through its ligands for Cereblon (CRBN). With a DC50 of 7.9 nM, SJF620 effectively recruits CRBN, facilitating selective protein degradation. This compound is primarily utilized in research applications focused on Btk-related signaling pathways and therapeutic development for B-cell malignancies.

NRX-0492 is an orally active PROTAC BTK degrader that promotes the ubiquitination and proteasomal degradation of Bruton's tyrosine kinase (BTK) with DC50 values as low as 0.2 nM. This compound effectively inhibits B cell receptor (BCR)-mediated signaling, transcriptional programs, and chemokine secretion, demonstrating significant antitumor activity against chronic lymphocytic leukemia. NRX-0492 comprises a BTK inhibitor, an E3 ligase ligand derived from Thalidomide, and a PROTAC linker, making it a valuable tool for studying BTK-related pathways and therapies.

TM471-1 is a potent and covalent inhibitor of Bruton's tyrosine kinase (BTK), demonstrating an IC50 of 1.3 nM against BTKWT and exhibiting selectivity with IC50 values of >40,000 nM for BTKC481S, 7.9 nM for TEC, and 12.4 nM for TXK. This compound effectively inhibits cell proliferation both in vivo and in vitro, induces apoptosis, and causes arrest in the G0/G1 phase of the cell cycle. TM471-1 is valuable for research into the roles of BTK in various cancer types and related signaling pathways.

DFCI-002-06 is an orally active PROTAC degrader targeting both HCK and BTK, demonstrating DC₅₀ values of 1.3 nM and 4.5 nM, respectively. This compound exhibits superior anti-tumor activity compared to a dual-target inhibitor, promoting apoptosis in cancer cells, particularly in MYD88 mutant B-cell malignancies. DFCI-002-06 serves as a valuable tool for researching mechanisms underlying these specific cancer types.

GBD-9 is a dual-action degrader that targets both BTK and GSPT1 by recruiting the E3 ligase cereblon (CRBN). It acts as a PROTAC to promote BTK degradation and functions as a molecular glue to induce GSPT1 degradation. GBD-9 exhibits significant antiproliferative activity in cancer cells, making it a promising candidate for cancer research.

Avitinib (Abivertinib) maleate is a third-generation, irreversible, and orally active selective EGFR inhibitor with IC50 values of 0.18 nM for both EGFR^L858R and EGFR^T790M, and 7.68 nM for wild-type EGFR. In addition to its EGFR-targeting activity, Avitinib maleate also inhibits BTK phosphorylation and induces apoptosis in mantle cell lymphoma models, demonstrating broad-spectrum anticancer efficacy.

Sunvozertinib (DZD9008) is a potent, orally active inhibitor of ErbB family kinases, including mutant forms of EGFR and HER2, as well as Bruton's tyrosine kinase (BTK). It demonstrates strong inhibitory activity against a range of clinically relevant EGFR mutations, with IC₅₀ values of 20.4 nM for EGFR exon 20 NPH insertion, 20.4 nM for EGFR exon 20 ASV insertion, 1.1 nM for EGFR L858R/T790M, and 7.5 nM for HER2 exon 20 YVMA mutation. It exhibits reduced activity against wild-type EGFR (IC₅₀ = 80.4 nM in A431 cells), supporting its selectivity for mutant forms. Sunvozertinib is being investigated as a targeted therapy for non-small cell lung cancers harboring EGFR or HER2 exon 20 alterations.

NX-5948 (BTK-IN-24) is an orally bioavailable, blood-brain barrier-penetrant PROTAC degrader targeting Bruton's tyrosine kinase (BTK). It induces BTK degradation via the cereblon E3 ligase pathway, effectively inhibiting B cell activation. NX-5948 exhibits both anti-inflammatory and antitumor activities, supporting its use in cancer and immune-related research.

Zelebrudomide (NX-2127) is a novel, potent BTK degrader that induces proteasomal degradation through targeted ubiquitination, rather than direct inhibition. In addition to degrading BTK, Zelebrudomide (NX-2127) enhances immune responses by stimulating T cell activation and increasing IL-2 production in primary human T cells, supporting its potential in cancer and immunotherapy research.

PLS-123 is a covalent, irreversible inhibitor of Bruton's tyrosine kinase (BTK), displaying an IC50 of less than 5 nM. It effectively disrupts BTK's catalytic activity at Tyr551 and self-activation at Tyr223, leading to the inhibition of key signaling pathways, including AKT/mTOR and MAPK, as well as blocking PLCγ2 activation. PLS-123 exhibits potent anti-proliferative effects against a range of B-cell lymphoma cell lines, inducing apoptosis through a caspase-dependent mechanism. Additionally, it demonstrates substantial antitumor efficacy in the OCI-Ly7 xenograft model, making it a valuable tool for research in lymphoma.

TL-895 is a potent, orally bioavailable, irreversible inhibitor of Bruton's tyrosine kinase (BTK) that functions as an ATP-competitive agent. It demonstrates high selectivity with an average IC50 of 1.5 nM against recombinant BTK and minimal activity against BLK, BMX, and TXK. TL-895 effectively inhibits BTK auto-phosphorylation at the Y223 site (IC50: 1-10 nM) and suppresses the production of inflammatory cytokines such as IL-8, IL-1β, MCP-1, and TNF-α in monocytes and macrophages. This compound is valuable for investigating chronic lymphocytic leukemia (CLL), myelofibrosis (MF), and various B-cell malignancies.

XMU-MP-3 is a potent non-covalent inhibitor of Bruton's tyrosine kinase (BTK), exhibiting IC50 values of 10.7 nM for wild-type BTK and 17.0 nM for the C481S mutation in the presence of 10 μM ATP. This compound is known to induce apoptosis in BTK-dependent cells, making it a valuable tool for investigating B-cell receptor signaling and related pathways. XMU-MP-3 is applicable in research focused on hematological malignancies and immune responses.

EGFR-IN-40 is a selective inhibitor targeting Bruton's tyrosine kinase (BTK), epidermal growth factor receptor (EGFR), and IL-2-inducible T-cell kinase (ITK). It exhibits potent inhibitory activity with IC50 values of 1.2 nM for BTK, 5.3 nM for EGFR, and 46.1 nM for ITK. This compound is valuable for research applications focusing on cancer therapeutics and signaling pathways related to these kinases.

(S)-Sunvozertinib, the S-enantiomer of Sunvozertinib, acts as a selective inhibitor of the ErbB family of receptors and Bruton's tyrosine kinase (BTK). It demonstrates potent inhibitory activity against multiple oncogenic variants of EGFR, including exon 20 insertions and the L858R/T790M mutation, with IC50 values of 51.2 nM, 51.9 nM, 1 nM, and 21.2 nM, respectively. Due to its dual action on both ErbBs and BTK, (S)-Sunvozertinib is poised for applications in targeted cancer therapy and research into mechanisms of resistance in EGFR-driven malignancies.

Rocbrutinib is a highly selective Bruton's tyrosine kinase (BTK) inhibitor, exhibiting an IC50 of 0.11 nM for wild-type BTK and 1.0 nM for the C481S-mutated variant. It demonstrates significant anti-leukemic activity by reducing cell viability, inducing cytotoxic effects, and inhibiting cell migration. This compound is applicable in research surrounding chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and mantle cell lymphoma.

BTK-IN-48 is a potent inhibitor of Bruton's tyrosine kinase (BTK) with an IC50 of 1.14 μM. This compound effectively inhibits recombinant BTK and c-Src, demonstrating moderate activity against LCK, BMX/ETK, FLT3, and PIM1. BTK-IN-48 is valuable for research related to B-cell malignancies and autoimmune diseases, making it a useful tool for understanding the underlying mechanisms of these conditions.