Catalog No.
Product Name
Application
Product Information
Citations
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PROTAC KDM4 Degrader
PROTAC KDM4 Degrader-1 is a potent proteolysis targeting chimera (PROTAC) designed to selectively degrade KDM4A-C while sparing KDM4D. This compound demonstrates significant antiproliferative effects in esophageal cancer cells, inducing apoptosis and cell cycle arrest. Additionally, PROTAC KDM4 Degrader-1 effectively inhibits histone H3 lysine demethylation, making it a valuable tool for research into cancer biology and epigenetic regulation. -
IRAK4 PROTAC Degrader
PROTAC IRAK4 degrader-13 is a selective IRAK4-directed PROTAC degrader that effectively targets IRAK4 with DC50 values of 0.86 nM and 1.1 nM in monocytes and lymphocytes, respectively. This compound significantly activates TIR signaling and reduces the expression of proinflammatory cytokines in an Imiquimod-induced psoriasis mouse model. PROTAC IRAK4 degrader-13 is applicable in research focused on TLR- and IL-1R-driven inflammatory diseases, including hidradenitis suppurativa and atopic dermatitis. -
Ligands for E3 Ligase
XB2M54 is a selective antagonist of X-linked inhibitor of apoptosis protein (XIAP), functioning as a ligand for E3 ligases. It effectively inhibits NOD2-mediated inflammatory signaling pathways, making it a valuable tool in inflammation research. Additionally, XB2M54 can be employed in the synthesis of PROTAC ERĪ± Degrader-1, facilitating studies on targeted protein degradation and its implications in therapeutic applications. -
PD-L1 PROTAC Degrader
PROTAC PD-L1 degrader-2 is a selective degrader targeting PD-L1. It demonstrates a potent inhibitory effect with an IC50 of 197.4 nM and a binding affinity characterized by a Kd of 301 nM. This compound facilitates the internalization and subsequent degradation of PD-L1 through both proteasomal and lysosomal pathways, thereby enhancing immune system activation. Its efficacy has been validated in MC38 C57BL/6 mouse models, underscoring its potential for antitumor applications. -
Ligands for Target Protein for PROTAC
(Rac)-BMS-1 is a racemic compound that serves as a ligand for target proteins in the development of proteolysis-targeting chimeras (PROTACs). It plays a crucial role in synthesizing D5B PROTAC, facilitating targeted protein degradation. This compound is valuable for researchers investigating protein regulation and therapeutic applications in cancer and other diseases. -
Ligands for Target Protein for PROTAC
SHP2-IN-43 is a potent inhibitor of SHP2, demonstrating an IC50 of 98.7 nM. This compound serves as a valuable ligand for targeted protein degradation (PROTAC) applications, facilitating the synthesis of SHP2-D26. Researchers can utilize SHP2-IN-43 to explore the therapeutic potential of modulating SHP2 activity in various biological contexts. -
PROTAC VEGFR2 Degrader
PROTAC VEGFR-2 Degrader-1 is a targeted protein degradation compound designed to selectively degrade VEGFR-2. It demonstrates minimal VEGFR-2 inhibition with an IC50 exceeding 1 Ī¼M, and exhibits limited anti-proliferative activity against EA.hy926 cells, with an IC50 greater than 100 Ī¼M. This reagent is valuable for research applications focused on the regulation of VEGFR-2 and its role in vascular biology and related disease mechanisms. -
PROTAC VEGFR2 Degrader
PROTAC VEGFR-2 Degrader-2 primarily targets the vascular endothelial growth factor receptor 2 (VEGFR-2) for degradation through the PROTAC mechanism. This compound displays minimal inhibition of VEGFR-2 activity with an IC50 exceeding 1 Ī¼M and demonstrates anti-proliferative effects in EA.hy926 cells, with an IC50 greater than 100 Ī¼M. It serves as a valuable tool for studies focused on targeted protein degradation and the modulation of signaling pathways related to angiogenesis. -
LCK PROTAC Degrader
SJ45566 is a potent PROTAC-based degrader targeting LCK with a DC50 of 1.21 nM. This compound is designed for the selective degradation of LCK, providing a valuable tool for investigating T-Cell Acute Lymphoblastic Leukemia. Its efficacy in modulating LCK levels makes it applicable in studies aimed at understanding T-cell signaling pathways and cancer biology. -
Lck Molecular Glue Degrader
LCK degrader-2 is a Lck molecular glue degrader designed to selectively target and degrade the Lck protein. This compound demonstrates potent biological activity in disrupting Lck-mediated signaling pathways, making it a valuable tool for studying acute lymphoblastic leukemia (ALL) and other Lck-dependent malignancies. Its application in cancer research provides insights into therapeutic strategies for Lck-related diseases. -
Molecular Glue
Lck degrader-1 is a molecular glue degrader that targets lymphocyte-specific protein tyrosine kinase (LCK) with a DC50 of 23.1 nM. This compound plays a significant role in the degradation of LCK, making it a valuable tool for studying T-cell acute lymphoblastic leukemia (T-ALL). Researchers can utilize Lck degrader-1 to explore the molecular mechanisms underlying T-ALL and investigate potential therapeutic strategies. -
TRK PROTAC Degrader
CG428 is a potent CRBN-dependent PROTAC degrader specifically targeting tropomyosin receptor kinase (TRK). It effectively reduces levels of the TPM3-TRKA fusion protein in KM12 colorectal carcinoma cells with a DC50 of 0.36 nM and inhibits downstream PLCĪ³1 phosphorylation with an IC50 of 0.33 nM. CG428 demonstrates higher binding affinity for TRKA (Kd = 1 nM) compared to TRKB and TRKC, making it a valuable tool for research into colorectal carcinoma. -
Ligands for Target Protein for PROTAC
GNF-8625 is a potent TRK inhibitor that functions by targeting TRK receptor tyrosine kinases, specifically TRKA, TRKB, and TRKC, with IC50 values of 0.8 nM, 22 nM, and 5.4 nM, respectively. This compound can be utilized in conjunction with Thalidomide to create a PROTAC degrader, enabling targeted protein degradation. GNF-8625 is valuable in research applications investigating TRK-mediated pathways and offers potential in therapeutic strategies for cancers involving aberrant TRK signaling. -
RET PROTAC Degrader
PROTAC RET Degrader 1 is an orally bioavailable RET PROTAC degrader that effectively crosses the blood-brain barrier. It demonstrates remarkable potency with DC50 values for various RET mutations, including 1.7 nM for RET (WT) and 3 nM for RET (G810S). PROTAC RET Degrader 1 exhibits strong anti-proliferative effects in cancer cell lines harboring oncogenic RET fusions and mutations, and shows significant anti-tumor efficacy in patient-derived xenograft mouse models. This reagent is valuable for investigating RET-positive cancers and their therapeutic targeting. -
TLR4 Inhibitor/PROTAC Linker
TLR4-IN-C34-C2-COOH is a TLR4 inhibitor that serves as a PROTAC linker. It demonstrates significant potential in the modulation of inflammatory responses, particularly in studies involving acute myocardial injury. By targeting TLR4 in enterocytes and macrophages, TLR4-IN-C34-C2-COOH effectively reduces systemic inflammation in murine models of endotoxemia and necrotizing enterocolitis, making it a valuable tool for research in inflammation-related pathways. -
PROTAC Aurora-A/Aurora-B Degrader
dAurAB5 is a dual PROTAC degrader targeting Aurora-A (DC50 = 8.8 nM) and Aurora-B (DC50 = 6.1 nM). It effectively induces the degradation of these kinases, leading to reduced N-Myc levels and decreased viability in IMR32 neuroblastoma cells. dAurAB5 also downregulates AAK1, PTK2, GAK, and TTK, making it a valuable tool for investigating the molecular mechanisms in neuroblastoma and related cancers. -
FAK PROTAC degrader
FAK PROTAC B5 is a potent degrader targeting focal adhesion kinase (FAK) with an IC50 of 14.9 nM. This compound exhibits significant FAK degradation capabilities along with antiproliferative effects. Furthermore, it demonstrates notable plasma stability and moderate membrane permeability, effectively inhibiting cell migration and invasion. FAK PROTAC B5 is suitable for research applications focused on cancer biology and cellular signaling pathways. -
PROTAC FAK Degarder
BSJ-04-146 is a selective PROTAC that targets focal adhesion kinase (FAK) for degradation, exhibiting an IC50 of 26 nM. It demonstrates rapid and robust degradation of FAK in cancer cells while maintaining high specificity across the proteome, and it induces prolonged degradation in murine models. The activity of BSJ-04-146 relies on the ubiquitin-proteasome system, making it a valuable tool for investigating pathways associated with pancreatic cancer and triple-negative breast cancer. -
PTK2/FAK PROTAC Degrader
BI-0319 is a selective PROTAC degrader targeting PTK2/FAK, effectively promoting the degradation of these proteins. This compound has demonstrated the ability to reduce cancer cell viability, inhibit cellular proliferation, and curtail invasion, making it a valuable tool for cancer research, particularly in studies related to liver cancer. BI-0319 provides insights into therapeutic strategies focused on protein degradation in oncology. -
c-Met PROTAC Degrader
PROTAC c-Met degrader-1 is a selective and orally active degrader targeting c-Met, exhibiting a DC50 of 6.21 nM. This compound promotes CRBN-dependent ubiquitination and subsequent proteasomal degradation of c-Met, effectively inducing G0/G1 phase arrest in c-Met-dependent cancer cells. Furthermore, PROTAC c-Met degrader-1 demonstrates significant anticancer activity by killing c-Met-dependent cells and inhibiting tumor growth in animal models, making it a valuable tool for research in gastric cancer. -
PROTAC c-Met Degrader
PROTAC c-Met degrader-2 is a PROTAC-based degrader that selectively targets c-Met for degradation through the ubiquitin-proteasome pathway, exhibiting a DC50 of 50 nM. This compound employs a unique linkage incorporating a CRBN ligand derived from Thalidomide, facilitating targeted protein degradation. It serves as a valuable tool for researching c-Met-related pathways and their implications in various cancers, enhancing the understanding of therapeutic strategies involving c-Met modulation. -
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. -
PROTAC
L18I is a PROTAC designed to target Brutonās 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. -
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. -
Ligands for Target Protein for PROTAC
BTK ligand 12 is a potent ligand for Bruton's tyrosine kinase (BTK), functioning as a valuable component in the development of PROTACs targeting this protein. It exhibits strong binding affinity, facilitating the effective ubiquitination and degradation of BTK in various cellular contexts. This compound is essential for researchers investigating targeted protein degradation and the modulation of signaling pathways associated with BTK in therapeutic applications. -
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-ĪŗB activation and reducing the expression of pro-inflammatory cytokines, including IL-1Ī² 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 PROTAC Degrader
PROTAC BTK Degrader-2 is a highly effective proteolysis-targeting chimera (PROTAC) that selectively degrades Bruton's tyrosine kinase (BTK). By recruiting the Cullin-RING E3 ubiquitin ligase complex, it mediates the ubiquitination and subsequent degradation of BTK protein, leading to a marked reduction in its cellular levels. This compound is valuable in research focused on B-cell malignancies and autoimmune diseases, providing insights into BTK's role in signaling pathways and therapeutic interventions. -
PROTAC BTK Degrader
PROTAC BTK Degrader-10 is a PROTAC agent that targets Bruton's Tyrosine Kinase (BTK) for selective degradation. This compound is particularly useful in the study of chronic lymphocytic leukemia (CLL) due to its ability to modulate BTK levels, thereby influencing malignant cell survival and proliferation. The degrader is designed with a specific ligand for BTK and a linker, enabling effective recruitment of the E3 ubiquitin ligase Cereblon for targeted degradation. -
PROTAC Btk Degrader
SJF620 hydrochloride functions as a PROTAC designed for the degradation of Bruton's tyrosine kinase (Btk) via recruitment of the cereblon (CRBN) E3 ligase. With a DC50 value of 7.9 nM, SJF620 effectively mediates the targeted degradation of Btk, making it a valuable tool for research focused on Btk-related pathways. This compound is particularly relevant in studies of immune responses and various hematological malignancies. -
PROTAC BTK Degrader
PTD10 is a potent PROTAC degrader targeting Bruton's tyrosine kinase (BTK), exhibiting a DC50 of 0.5 nM and a KD of 2.28 nM. It effectively degrades BTK in Ramos and JeKo-1 cell lines, leading to the inhibition of cell growth and the induction of apoptosis through caspase activation and mitochondrial pathways. PTD10 is suitable for investigating mechanisms of B-cell dysregulation and related therapeutic strategies. -
BTK PROTAC Degrader
DDa-1 is a potent BTK PROTAC degrader with a DC50 of 90 nM, designed to facilitate the targeted degradation of Bruton's Tyrosine Kinase (BTK) in cellular systems. This compound effectively utilizes a novel mechanism involving DCAF1 binding, a distinct linker, and a specific BTK ligand to enhance selectivity and efficacy. DDa-1 is primarily utilized in research applications focusing on BTK-related signaling pathways and therapeutic strategies against B-cell malignancies. -
PROTAC BTK Degrader
BCPyr is a PROTAC-class degrader specifically targeting Brutonās Tyrosine Kinase (BTK), exhibiting a DC50 of 800 nM. This compound integrates a BTK ligand (ligand 11) and an E3 ubiquitin ligase ligand (ligand 20) through a pyrazinyl methanol linker. BCPyr facilitates the targeted degradation of BTK, making it a valuable tool for studying diseases where BTK is implicated, such as certain hematological malignancies. -
BTK/IKZF1/3 PROTAC Ligand
BTK/IKZF1/3 ligand 1 is a PROTAC ligand targeting Bruton's tyrosine kinase (BTK) and the Ikaros family zinc finger proteins (IKZF1/3). This compound can be conjugated with E3 ligase ligands and linkers to produce PROTAC BTK/IKZF1/3 Degrader-1, facilitating targeted protein degradation. It is valuable for cancer research, supporting investigations into therapeutic strategies aimed at modulating BTK and IKZF1/3 activity in malignant cells. -
BTK PROTAC Degrader
PROTAC BTK Degrader-12 is a PROTAC (Proteolysis Targeting Chimera) designed to selectively degrade Bruton's tyrosine kinase (BTK). It facilitates the targeted ubiquitination and subsequent proteasomal degradation of BTK, resulting in diminished signaling pathways associated with B-cell malignancies and autoimmune disorders. This compound serves as a valuable tool in research investigating BTK's role in disease mechanisms and therapeutic interventions. -
BTK PROTAC Degrader
TQ-3959 is an orally bioavailable BTK PROTAC degrader that demonstrates a DC50 of 14.6 nM. It exhibits potent antiproliferative effects on both wild-type BTK and the C481S mutant BTK cell lines. In vivo, TQ-3959 effectively inhibits tumor growth in female NOD-SCID mice bearing TMD-8 xenografts. This compound is valuable for investigating B-cell malignancies, including lymphoma. -
BTK/IKZF1/3 PROTAC Degrader
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
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 Ī¼M 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. -
BTK PROTAC Degrader
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 PROTAC Degrader
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. -
PROTAC ALK Degrader
SIAIS001 is a potent PROTAC degrader targeting anaplastic lymphoma kinase (ALK) with a DC50 of 3.9 nM. This compound induces G1/S phase cell cycle arrest and effectively inhibits the proliferation of SR cells with an IC50 of 0.9 nM. SIAIS001 is suitable for research in non-small cell lung cancer (NSCLC) and anaplastic large-cell lymphomas (ALCLs). -
NPM-ALK PROTAC Degrader
MS99-Ī²-Gal is a galactose-modified PROTAC degrader targeting the NPM-ALK fusion protein. This compound is selectively hydrolyzed by SA-Ī²-gal and esterase in senescent cancer cells, allowing the release of MS99, which effectively degrades the NPM-ALK protein. MS99-Ī²-Gal demonstrates an IC50 of 454.8 nM in aging Karpas 299 cells, showing improved potency compared to normal Karpas 299 cells with an IC50 of 2.162 Ī¼M. This reagent is valuable for cancer research, particularly in studies focused on targeted protein degradation. -
Ligands for Target Protein for PROTAC
ALK protein ligand-1 is a specific ligand for anaplastic lymphoma kinase (ALK) that plays a crucial role in targeted protein degradation using PROTAC technology. This compound exhibits potent inhibitory effects on ALK, making it a valuable tool for studying ALK-related signaling pathways and their implications in cancer biology. ALK protein ligand-1 is essential for the synthesis of AP-1, facilitating the exploration of novel therapeutic approaches in oncology research. -
EML4-ALK PROTAC Degrader
PROTAC EML4-ALK Degrader-2 is an advanced degrader specifically targeting the EML4-ALK fusion protein. With an IC50 of 1.6 nM, it exhibits potent selective inhibitory activity against ALK while maintaining selectivity over IGF1R, INSR, FLT3, and FGFR2. This compound demonstrates significant anti-cancer effects in both in vitro and in vivo models and is particularly relevant for research applications involving non-small cell lung cancer (NSCLC), as well as liver and cervical cancers. -
Brigatinib-PROTAC Degrader
SIAIS117 is a potent Brigatinib-PROTAC degrader that targets the ALK protein, specifically effective against the ALK G1202R point mutation. By utilizing a VHL-1 conjugation, SIAIS117 exhibits significant capability to induce protein degradation, leading to inhibited growth of SR and H2228 cancer cell lines. This compound holds potential for applications in anti-proliferative research, particularly in small cell lung cancer contexts. -
ALK PROTAC Degrader
PROTAC ALK degrader-5 is a targeted degrader composed of a small molecule that selectively degrades anaplastic lymphoma kinase (ALK). It demonstrates potent inhibitory activity against EML4-ALK and NPM-ALK, with IC50 values of 27.4 nM and 116.5 nM, respectively. This compound exhibits significant anti-proliferative effects against ALK-driven cancer cell lines, including H3122 and Karpas 299, and effectively inhibits ALK and STAT3 phosphorylation. PROTAC ALK degrader-5 is a valuable tool for investigating ALK-driven malignancies, particularly in the context of human non-small cell lung cancer and anaplastic large cell lymphoma research. -
ALK PROTAC Degrader
TD-004 is a highly effective ALK PROTAC degrader, demonstrating potent anti-ALK inhibitory activity with an IC50 of 0.11 ĀµM. This compound selectively hampers the proliferation of ALK-positive cancer cell lines, SU-DHL-1 and H3122, with IC50 values of 0.058 ĀµM and 0.28 ĀµM, respectively. TD-004 induces the degradation of ALK fusion proteins, including NPM-ALK and EML4-ALK, through the recruitment of the VHL E3 ligase and the proteasome pathway. Its significant tumor growth inhibition and favorable safety profile in vivo make TD-004 a valuable tool for researching anaplastic large cell lymphoma and non-small cell lung cancer. -
AURKA PROTAC Degrader
SK2187 is a selective degrader of Aurora kinase A (AURKA) utilizing the PROTAC technology, exhibiting a DC50 of approximately 10 nM. This compound demonstrates significant growth inhibition of NGP neuroblastoma cells, with an IC50 value of 101.5 nM. SK2187 is particularly relevant for research on MYCN-amplified neuroblastoma, enabling exploration of targeted degradation pathways in cancer therapy. -
Aurora-A/Aurora-B PROTAC Degrader
dAurAB2 is a dual-targeting PROTAC designed to degrade Aurora-A and Aurora-B, demonstrating potent efficacy with DC50 values of 59 nM and 39 nM, respectively. This compound effectively reduces N-Myc protein levels in MYCN-amplified IMR32 neuroblastoma cells, making it a valuable tool for neuroblastoma research. The unique design incorporates a specific Aurora ligand and an E3 ligase ligand connected by a tailored linker, facilitating targeted degradation and advancing studies in cancer biology. -
Aurora A PROTAC Degrader
AurAP14 is a PROTAC degrader specifically targeting Aurora A, with a DC50 of 120 nM. This compound exhibits potent inhibitory effects on various tumor cell lines, showing IC50 values of 0.294 Ī¼M in A549 cells and 0.534 Ī¼M in MCF-7 cells. AurAP14 induces apoptosis while effectively arresting A549 cells in the S and G2/M phases of the cell cycle. Additionally, AurAP14 demonstrates significant anti-tumor efficacy in nude mouse xenograft models of A549 and A549/PTR, making it a valuable tool for research focused on treating Aurora A-overexpressing non-small cell lung cancer (NSCLC).
