Catalog No.
Product Name
Application
Product Information
Citations
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PROTAC BTK Degrader
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. -
BTK Inhibitor
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. -
BTK Inhibitor
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. -
BTK/EGFR/ITK Inhibitor
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. -
ErbBs/BTK Inhibitor
(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. -
BTK Inhibitor
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 Inhibitor
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. -
BTK Inhibitor
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. -
HCK/BTK PROTAC Degrader
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. -
Pan-FLT3/Pan-BTK Inhibitor
Luxeptinib is a first-in-class, non-covalent pan-FLT3 and pan-BTK inhibitor that exhibits potent oral activity. This compound effectively induces cell cycle arrest, apoptosis, or autophagy in acute myeloid leukemia cells, making it a significant tool for cancer research. Its dual-targeting mechanism positions Luxeptinib as a potential therapeutic candidate in the treatment of hematological malignancies. -
Btk Inhibitor
LFM-A13 is a selective Bruton's tyrosine kinase (BTK) inhibitor known for its capacity to inhibit JAK2 and PLK. With IC50 values of 2.5 μM for recombinant BTK, 10 μM for JAK2, and 61 μM for PLK3, LFM-A13 exhibits significant antiproliferative and anticancer properties. This compound is valuable for research applications focused on cancer biology and therapeutic interventions targeting BTK and related signaling pathways. -
JAK3/BTK Inhibitor
JAK3/BTK-IN-3 is a selective inhibitor of Janus kinase 3 (JAK3) and Bruton's tyrosine kinase (BTK). Targeting both JAK3 and BTK can provide synergistic effects beneficial for the therapeutic intervention of autoimmune diseases. This compound is suitable for research applications focused on elucidating the roles of JAK3 and BTK in various disease mechanisms, facilitating the development of novel treatment strategies. -
JAK3/BTK Inhibitor
JAK3/BTK-IN-7 is a potent inhibitor targeting Janus kinase 3 (JAK3) and Bruton’s tyrosine kinase (BTK), demonstrating IC50 values of 2 nM and 14 nM, respectively. This compound exhibits significant anti-inflammatory activity, making it a valuable tool for investigating the underlying mechanisms of rheumatoid arthritis. Its efficacy in modulating inflammatory pathways highlights its potential in related therapeutic research applications. -
JAK3/BTK Inhibitor
JAK3/BTK-IN-2 is a potent dual inhibitor of Janus kinase 3 (JAK3) and Bruton's tyrosine kinase (BTK). By simultaneously targeting the BTK/JAK3 signaling pathway, this compound demonstrates synergistic effects that may enhance therapeutic outcomes in autoimmune diseases. JAK3/BTK-IN-2 is suitable for research applications focused on JAK3 and BTK-related pathologies, facilitating studies on their roles in immune regulation and disease progression. -
JAK3/BTK Inhibitor
JAK3/BTK-IN-5 is a potent dual inhibitor targeting Janus kinase 3 (JAK3) and Bruton's tyrosine kinase (BTK). This compound effectively disrupts the BTK/JAK3 signaling pathway, demonstrating potential synergistic effects advantageous for the treatment of autoimmune diseases. JAK3/BTK-IN-5 is valuable for research into conditions related to JAK3 kinase and BTK, making it a crucial tool for studying the pathophysiology of these targets. -
BTK/JAK3 Inhibitor
JAK3/BTK-IN-6 is a potent dual inhibitor targeting Bruton's Tyrosine Kinase (BTK) and Janus Kinase 3 (JAK3), exhibiting IC50 values of 0.6 nM and 0.4 nM, respectively. This compound demonstrates excellent metabolic stability in human liver microsomes, making it suitable for in vitro studies. JAK3/BTK-IN-6 is valuable in research applications related to hematological disorders and immune system dysfunctions. -
JAK3/BTK Inhibitor
JAK3/BTK-IN-4 is a potent inhibitor targeting both JAK3 and BTK kinases, which are critical in the modulation of immune responses involved in autoimmune diseases. By simultaneously inhibiting the BTK/JAK3 signaling pathway, JAK3/BTK-IN-4 demonstrates synergistic effects, making it a valuable tool for studying JAK3 and BTK-related pathologies. This compound is particularly relevant for research applications focused on therapeutic strategies for autoimmune disorders. -
JAK3/BTK Inhibitor
JAK3/BTK-IN-1 is a potent dual inhibitor targeting JAK3 and BTK, key proteins implicated in autoimmune diseases. By simultaneously blocking the BTK/JAK3 signaling pathway, this compound demonstrates synergistic effects that could enhance therapeutic outcomes. JAK3/BTK-IN-1 is suitable for research into JAK3 kinase and BTK-related diseases, facilitating the exploration of innovative treatment strategies in immunology and related fields. -
BTK/FLT3 Inhibitor
RSH-7 is a potent inhibitor of Bruton's tyrosine kinase (BTK) and Fms-like tyrosine kinase 3 (FLT3), exhibiting IC50 values of 47 nM and 12 nM, respectively. This compound induces apoptosis and demonstrates significant antiproliferative activity. By inhibiting BTK and FLT3 signaling pathways, RSH-7 is a valuable tool for research in oncology and targeted therapies for hematological malignancies. -
BTK Inhibitor
BTK-IN-7 is a potent and selective Bruton’s Tyrosine Kinase (BTK) inhibitor, exhibiting an IC50 of 4.0 nM. This compound demonstrates exceptional selectivity in enzymatic assays, with over 250-fold selectivity for ITK and over 2500-fold for EGFR, as well as in cellular contexts with a 227-fold and 27-fold selectivity respectively. BTK-IN-7 exhibits significant antitumor activity, making it a valuable tool for research in cancer biology and the development of targeted therapies. -
BTK Inhibitor
BTK-IN-9 is a reversible Bruton's tyrosine kinase (BTK) inhibitor known for its potent antiproliferative effects against mantle cell lymphoma. This compound disrupts mitochondrial membrane potential and elevates reactive oxygen species levels in Z138 cells, leading to increased apoptotic activity. BTK-IN-9 is valuable for research applications focusing on lymphoma biology and the mechanisms of apoptosis. -
BTK Inhibitor
Pirtobrutinib is a highly selective, non-covalent inhibitor of Bruton's tyrosine kinase (BTK). It effectively targets diverse BTK C481 substitution mutations, demonstrating strong antitumor activity in BTK-dependent lymphoma models in vivo. Pirtobrutinib exhibits over 300-fold selectivity for BTK compared to a panel of 370 other kinases and shows minimal inhibition of non-kinase off-targets at 1 μM. This specificity makes it a valuable tool for studying BTK-related signaling pathways and therapeutic applications in hematological malignancies. -
BTK Inhibitor
2-(Bromomethyl)acrylic acid functions as a selective inhibitor of Bruton's tyrosine kinase (BTK). It covalently modifies the cysteine 481 residue of BTK through a nucleophilic addition-elimination mechanism, leading to the inhibition of the B-cell receptor signaling pathway. This compound promotes immunogenic cell death in BTK-expressing B-cell lymphoma cells by triggering the release of damage-associated molecular patterns like extracellular ATP and HMGB1. It exhibits significant cytotoxicity against BTK-expressing cells while demonstrating minimal toxicity to BTK-negative counterparts, making it valuable for research into B-cell lymphoma. -
BTK Inhibitor
Acalabrutinib maleate is an oral, irreversible, and highly selective BTK inhibitor targeting cysteine residue Cys481 in the ATP-binding pocket of BTK. This compound exhibits potent activity against chronic lymphocytic leukemia (CLL) in mouse models, making it a valuable tool for CLL research. Additionally, Acalabrutinib maleate features an alkyne group, enabling it to participate in copper-catalyzed azide-alkyne cycloaddition (CuAAc), facilitating its use in click chemistry applications. -
BTK Inhibitor
Tolebrutinib, a selective inhibitor of Bruton tyrosine kinase (BTK), demonstrates potent activity with IC50 values of 0.4 nM in Ramos B cells and 0.7 nM in HMC microglia cells. Its ability to penetrate the blood-brain barrier underscores its relevance in studying central nervous system immunity. Tolebrutinib is a valuable tool for research into multiple sclerosis (MS) and other neurological conditions influenced by BTK activity. -
BTK Degrader
Catadegbrutinib is a selective chimeric degradation activator compound targeting Bruton's tyrosine kinase (BTK), with an IC50 of 0.69 nM. By facilitating the recruitment of BTK to E3 ubiquitin ligase, Catadegbrutinib promotes polyubiquitination and subsequent proteasomal degradation of BTK, effectively reducing its activity. This compound is valuable for investigating B-cell malignancies, including chronic lymphocytic leukemia, small lymphocytic lymphoma, and mantle cell lymphoma. -
Btk Inhibitor
BIIB091 is a selective and potent reversible Bruton’s tyrosine kinase (BTK) inhibitor, demonstrating an IC50 of less than 0.5 nM. By binding to the BTK protein and inducing an inactive conformation via sequestering of TYR-551, BIIB091 effectively obstructs BTK signaling pathways. This compound is valuable for research applications in multiple sclerosis and other immune-mediated disorders. -
PROTAC BTK Degrader
PROTAC BTK Degrader-1 is an innovative PROTAC-based compound designed for the selective degradation of Bruton's tyrosine kinase (BTK), exhibiting IC50 values of 34.51 nM for wild-type BTK and 64.56 nM for the BTK-481S mutant. This compound effectively lowers BTK protein levels, thereby inhibiting tumor growth. Additionally, PROTAC BTK Degrader-1 features an alkyne group facilitating its application in copper-catalyzed azide-alkyne cycloaddition (CuAAc) for advanced chemical research and targeted therapies. -
BTK Inhibitor
Elsubrutinib is a potent and selective irreversible inhibitor of Bruton's tyrosine kinase (BTK). With an IC50 value of 0.18 μM for the BTK catalytic domain, it demonstrates strong inhibitory activity. Elsubrutinib is utilized in research related to inflammatory diseases, providing valuable insights into BTK's role in various cellular processes. -
HCK/BTK Inhibitor
KIN-8194 is an orally active dual inhibitor targeting HCK and BTK, exhibiting IC50 values of 0.915 nM and <0.495 nM, respectively. It effectively disrupts growth and integrin-mediated adhesion in BTK inhibitor-resistant mantle cell lymphoma (MCL). KIN-8194 demonstrates the ability to overcome ibrutinib resistance, providing a survival advantage in TMD-8 ABC DLBCL xenograft models, making it a valuable tool for research in hematologic malignancies and therapeutic resistance mechanisms. -
BTK Inhibitor
PF-06658607 is an alkynylated irreversible inhibitor of Bruton's tyrosine kinase (BTK), designed to covalently bind to active site cysteines in the ATP-binding pocket. This compound effectively serves as a research tool for identifying off-target effects of covalent kinase inhibitors in cancer cell models. Its unique alkyne functionality facilitates the use of azide-based detection probes through copper-catalyzed click chemistry, enhancing the study of BTK-related signaling pathways. -
BTK/MNK Dual Inhibitor
QL-X-138 is a selective dual inhibitor of Bruton's tyrosine kinase (BTK) and MAPK-interacting kinase (MNK), demonstrating potent covalent binding to BTK and non-covalent binding to MNK. It exhibits IC50 values of 9.4 nM for BTK, and 107.4 nM and 26 nM for MNK1 and MNK2, respectively. Additionally, QL-X-138 displays antiviral activity against dengue virus serotype 2, with an IC50 of 3.5 μM. This compound is valuable for research involving B-cell malignancies and related therapeutic investigations. -
PROTAC
L18I is a PROTAC designed to target Bruton’s tyrosine kinase (Btk), facilitating the degradation of this protein and thereby mitigating inflammation associated with autoimmune diseases, such as lupus erythematosus induced by BM12 splenocytes. This compound comprises the IBT6A ligand, a linker moiety (Propargyl-PEG3-alcohol), and an E3 ubiquitin ligase ligand (Lenalidomide-Br), effectively promoting the destruction of Btk. L18I serves as a valuable tool for investigating Btk's role in autoimmunity and offers potential pathways for therapeutic intervention. -
BTK Degrader
BTK degrader-1 is a bifunctional degrader targeting Bruton’s tyrosine kinase (BTK) through its conjugation with CD79b. This compound facilitates the targeted degradation of BTK, leading to significant anti-tumor effects. It serves as a valuable tool for research applications focused on therapeutic strategies for hematological malignancies. -
BLK Inhibitor
BLK-IN-2 is a potent and selective irreversible inhibitor of B-Lymphoid tyrosine kinase (BLK), exhibiting an IC50 of 5.9 nM. In addition, it inhibits Bruton’s tyrosine kinase (BTK) with an IC50 of 202 nM. This compound demonstrates strong antiproliferative activity against various lymphoma cell lines, making it a valuable tool for research in B-cell malignancies and related signaling pathways. -
Covalent Probe/Btk Inhibitor
CNX-500 is a covalent probe that targets Bruton's tyrosine kinase (Btk) through a potent inhibitor (CC-292) chemically linked to biotin. With an IC50 of 0.5 nM, CNX-500 exhibits strong inhibitory activity against Btk while forming a stable covalent bond. The compound demonstrates low off-target effects on epidermal growth factor receptor and upstream Src-family kinases such as Syk and Lyn, making it suitable for research applications focused on Btk-related pathways in cellular signaling and disease models. -
BTK Inhibitor
N-piperidine Ibrutinib hydrochloride is a reversible derivative of Ibrutinib, functionally acting as a potent Bruton Tyrosine Kinase (BTK) inhibitor. It demonstrates IC50 values of 51.0 nM for wild-type BTK and 30.7 nM for the C481S mutant. This compound serves as a valuable BTK ligand in the synthesis of PROTACs, including SJF620, which has shown a DC50 of 7.9 nM, highlighting its potential utility in targeted protein degradation research applications. -
BTK Inhibitor
BIIB129 is a covalent and selectively targeting inhibitor of Bruton's tyrosine kinase (BTK), designed to penetrate the blood-brain barrier effectively. By covalently binding to Cys481 in BTK, BIIB129 disrupts the signaling pathways in B cells and myeloid cells. This compound is particularly relevant for research applications in multiple sclerosis (MS), providing insights into the modulation of immune responses associated with the disease. -
BTK Inhibitor
ACP-5862 is a potent Bruton tyrosine kinase (BTK) inhibitor, exhibiting an IC50 of 5.0 nM. As a major circulating metabolite of Acalabrutinib, it maintains high selectivity for BTK, which is critical for the modulation of B-cell signaling pathways. ACP-5862 is also a weak time-dependent inactivator of CYP3A4 and CYP2C8. This compound is widely utilized in research focused on hematological malignancies and B-cell related disorders, facilitating insights into targeted therapies. -
PROTAC BTK Degrader
DD-03-171 is a selective PROTAC BTK degrader that targets Bruton's tyrosine kinase (BTK) for degradation. This compound demonstrates significant anti-proliferative effects on mantle cell lymphoma (MCL) cells with an IC50 of 5.1 nM and enhances survival in murine models bearing patient-derived xenograft (PDX) lymphoma. Additionally, DD-03-171 inhibits platelet function and thrombosis, making it a valuable tool for research in cancer and hematological disorders. -
Stable Isotope
Acalabrutinib-d4 is a deuterated derivative of Acalabrutinib, an orally active and irreversible second-generation Bruton Tyrosine Kinase (BTK) inhibitor. This stable isotope labeled compound serves as a valuable tool for studying BTK inhibition in biological systems. Additionally, Acalabrutinib-d4 features an alkyne group, facilitating its use as a click chemistry reagent through copper-catalyzed azide-alkyne cycloaddition (CuAAc). Its applications extend to exploring therapeutic potential and pharmacokinetic properties in research settings. -
BTK Degrader
(R)-Zelebrudomide is a Bruton’s Tyrosine Kinase (BTK) degrader synthesized as an isomer of the PROTAC compound Zelebrudomide. It selectively induces the degradation of BTK, a crucial target in the treatment of various hematological malignancies. This compound is utilized in research to investigate its potential therapeutic applications in autoimmune diseases and cancers where BTK is implicated. -
Ibrutinib Derivative
Ibrutinib-MPEA is an Ibrutinib derivative targeting Bruton's tyrosine kinase (BTK), a key regulator in B cell receptor signaling. As a covalent and irreversible inhibitor, Ibrutinib-MPEA demonstrates significant biological activity against various hematological malignancies. This compound is primarily utilized in research applications focusing on cancer biology and the study of BTK-related signaling pathways. -
BTK Inhibitor
Edralbrutinib is a selective Bruton’s tyrosine kinase (BTK) inhibitor with a high potency for targeting BTK signaling pathways. This compound demonstrates significant inhibition of B-cell receptor (BCR) signaling, making it a valuable tool for studying diseases such as B-cell malignancies and autoimmune disorders. Research applications include investigation of B-cell signaling dynamics and therapeutic development for BTK-dependent pathologies. -
Btk Inhibtior
Atuzabrutinib is a selective reversible inhibitor of Bruton's tyrosine kinase (Btk), which plays a crucial role in B-cell receptor signaling. This compound demonstrates significant inhibition of neutrophil recruitment through the modulation of macrophage antigen-1 signaling pathways. Atuzabrutinib is primarily utilized in research focused on B-cell mediated autoimmunity, chronic inflammatory diseases, and various malignancies. Its targeted action on Btk makes it valuable in studying therapeutics aimed at B-cell related disorders. -
Btk Inhibitor
TAK-020 is a covalent inhibitor of Bruton's tyrosine kinase (Btk), demonstrating potent activity in targeting the Btk pathway. It is designed for use in research applications related to Btk-associated signaling in various hematological malignancies and autoimmune disorders. This compound serves as a valuable tool for investigating the role of Btk in cell proliferation and survival, making it a significant candidate for therapeutic development in these areas. -
BTK Inhibitor
JNJ-64264681 is a selective, irreversible covalent inhibitor of Bruton's Tyrosine Kinase (BTK). This compound demonstrates potent inhibition and favorable pharmacokinetic properties, making it suitable for research applications in cancer and autoimmune diseases. Its specificity for BTK allows for the exploration of pathways regulated by this critical enzyme in disease models. -
PROTAC BTK Degrader
PROTAC BTK Degrader-6 is a potent PROTAC degrader targeting Bruton's tyrosine kinase (BTK) with a DC50 of 3.18 nM. This compound exhibits anti-inflammatory activity by inhibiting NF-κB activation and reducing the expression of pro-inflammatory cytokines, including IL-1β and IL-6. It serves as a valuable tool for research into the modulation of immune responses and the development of therapies for inflammatory diseases. -
BTK PROTAC Degrader
UBX-382 is an orally active BTK PROTAC degrader with a DC50 of 4.56 nM, specifically designed to target Bruton's tyrosine kinase (BTK). It effectively disrupts B-cell receptor signaling and demonstrates robust degradation of both wild-type and mutant BTK proteins, including the C481S mutation. UBX-382 has been shown to inhibit tumor growth in murine xenograft models with BTK-expressing TMD-8 cells, making it a valuable tool for investigating B-cell-related malignancies and therapeutic strategies. -
Btk Inhibitor
BIIB068 is a potent and selective reversible Bruton’s Tyrosine Kinase (Btk) inhibitor, demonstrating an IC50 of 1 nM and a Kd of 0.3 nM. With over 400-fold selectivity for Btk compared to other kinases, BIIB068 is well-suited for research into autoimmune diseases. Its oral bioactivity opens avenues for studies focusing on Btk-mediated pathways and therapeutic interventions.
