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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
134 Results for "
diffuse large B cell lymphoma
" in MedChemExpress (MCE) Product Catalog:
Products (134)
134 Results for "diffuse large B cell lymphoma" in MCE Product Catalog:
Cat. No.: HY-156566
CAS No.: 2503036-46-0
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PROTAC BRD4 Degrader-21 is a BRD4-targeting PROTAC degrader with an IC50 value of 59 nM. PROTAC BRD4 Degrader-21 induces ubiquitination of BRD4, leading to its degradation via the proteasome. PROTAC BRD4 Degrader-21 binds to recombinant HSP90α protein with moderate affinity, having an IC50 of 100-1000 nM. PROTAC BRD4 Degrader-21 induces cancer cell death. PROTAC BRD4 Degrader-21 inhibits tumor growth in xenograft mouse models. PROTAC BRD4 Degrader-21 can be used for the research of acute myeloid leukemia, diffuse large B-cell lymphoma .
Cat. No.: HY-129179S
Synonyms: APG-2575-d8; Bcl-2/Bcl-xl inhibitor 1-d8
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Lisaftoclax-d8 is the deuterated-labeled Lisaftoclax (HY-129179). Lisaftoclax is an orally active, selective BCL-2 inhibitor with a Ki of < 0.1 nM against human BCL-2. Lisaftoclax selectively binds to BCL-2, disrupts the BCL-2:BIM complex, and antagonizes the antiapoptotic function of BCL-2. Lisaftoclax induces BAX/BAK-dependent, caspase-mediated apoptosis, upregulates the pro-death proteins BIM and Noxa, and downregulates mitochondrial respiratory function and ATP production. Lisaftoclax can be used in the research of hematological malignancies including chronic lymphocytic leukemia, multiple myeloma, and diffuse large B-cell lymphoma .
Cat. No.: HY-138834
CAS No.: 1042673-20-0
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JH-I-25 is an orally active IRAK1 and IRAK4 inhibitor. JH-I-25 inhibits LPS-induced IRAK4 phosphorylation, IRAK1 degradation, MAPK activation, and the expression of proinflammatory cytokines TNF-α and IL-6 in lung tissues. JH-I-25 improves the survival rate of LPS-induced septic mice and serves as an IRAK4 recruiter in the design of proteolysis-targeting chimeric molecules. JH-I-25 can be used in research related to diffuse large B-cell lymphoma, Waldenström's macroglobulinemia, septic shock, rheumatoid arthritis, atherosclerosis, Alzheimer's disease, acute lung injury, sepsis, and psoriasis .
Cat. No.: HY-157763
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Mal-PEG1-Val-Cit-PABC-diphosphate-BTK degrader-1 is a cleavable linker-payload conjugate and cereblon-binding BTK bifunctional degrader. Mal-PEG1-Val-Cit-PABC-diphosphate-BTK degrader-1 induces BTK degradation and exerts cytotoxic effects when delivered via CD79b monoclonal antibody. Mal-PEG1-Val-Cit-PABC-diphosphate-BTK degrader-1, when formulated as a CD79b antibody-drug conjugate, achieves sustained in vivo BTK degradation in tumor-bearing mice with reduced systemic payload exposure. Mal-PEG1-Val-Cit-PABC-diphosphate-BTK degrader-1 can be used for the research of activated b-cell-like diffuse large b-cell lymphoma (ADC linker: (HY-130944); PROTAC: (HY-163295)) .
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GBD-9 is a degrader based on the E3 ubiquitin ligase CRBN that targets BTK and the G1 to S phase transition protein GSPT1. GBD-9 has both PROTAC and molecular glue properties by inducing ubiquitination and proteasomal degradation of target proteins. GBD-9 can efficiently degrade wild-type and mutant BTK (such as C481S mutation) and GSPT1. GBD-9 significantly inhibits tumor cell proliferation by inducing G1 phase arrest in cancer cells, downregulating anti-apoptotic proteins (BCL-2, MCL-1) and activating Caspase-3 to induce apoptosis. GBD-9 is mainly used in the research of hematological tumors such as diffuse large B-cell lymphoma (DLBCL) and acute myeloid leukemia (AML) .
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MRT-2359 is an orally active and selective GSPT1 molecular glue degrader, with a DC50 of 5 nM. MRT-2359 induces CRBN/GSPT1 ternary complex formation to drive CRBN- and degron-dependent proteasomal GSPT1 degradation, with selectivity for wild-type GSPT1 over the GSPT1G575N mutant. MRT-2359 disrupts protein translation, induces ribosome stalling, downregulates MYC family proteins and their transcriptional output, reduces proliferation, and induces apoptosis in cancer cells. MRT-2359 can be used for the research of non-small cell lung cancer (NSCLC), small cell lung cancer (SCLC), neuroendocrine lung cancer, high grade neuroendocrine cancers, diffuse large B-cell lymphoma, prostate cancer, and MYC-driven solid tumors .
Cat. No.: HY-173333
CAS No.: 3081688-77-6
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PROTAC SMARCA2/4 degrader-38 is a SMARCA2/4 degrader (SMARCA2: DC50 = 3.0 nM; SMARCA4: 4.0 nM). PROTAC SMARCA2/4 degrader-38 binds to SMARCA2 and SMARCA4 bromodomains to induce degradation via the ubiquitin-proteasome system. PROTAC SMARCA2/4 degrader-38 induces G0/G1 phase cell cycle arrest and cell apoptosis in hematological cancer cells, blocks oncogenic activity of MYC and other disease-related genes in acute myeloid leukemia cells and inhibits proliferation of hematological cancer cell lines. PROTAC SMARCA2/4 degrader-38 can be used for the research of acute myeloid leukemia, diffuse large B-cell lymphoma, breast cancer, ovarian cancer, colorectal cancer, liver cancer, lung cancer .
Cat. No.: HY-153939S
Purity: 99.57%
Synonyms: RG7388-d3-1
Cat. No.: HY-15676R
CAS No.: 1229705-06-9
Synonyms: RG7388 (Standard)
Idasanutlin (Standard) (RG7388 (Standard)) is the analytical standard of Idasanutlin (HY-15676). This product is intended for research and analytical applications. Idasanutlin (RG7388) is an orally bioavailable MDM2 inhibitor with an IC50 of 6 nM. Idasanutlin disrupts MDM2-p53 binding, stabilizes and activates p53, triggering cell cycle arrest, apoptosis, and reduced cancer cell viability. Idasanutlin reduces EGFR protein expression and phosphorylation, suppresses downstream SHP2, MEK1/2, ERK1/2, AKT, mTOR, p70(S6K1), and S6 signaling. Idasanutlin induces mitochondrial ROS production, drives p38 MAPK phosphorylation, upregulates NOXA, and mediates caspase-3-dependent apoptosis and gasdermin E-mediated pyroptosis. Idasanutlin can be used for the research of TP53-mutant non-small cell lung cancer, T-cell acute lymphoblastic leukemia, colorectal carcinoma, melanoma, diffuse large B-cell lymphoma, mantle cell lymphoma, non-Hodgkin lymphoma, severe fever with thrombocytopenia syndrome, neuroblastoma, acute lymphoblastic leukemia, relapsed or refractory acute myeloid leukemia, osteosarcoma, solid tumors, and hematological tumors .
Cat. No.: HY-P11698
CAS No.: 476667-31-9
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NRX-0492 is an orally active BTK PROTAC degrader, with a binding IC50 of 1.2 nM for both wild-type BTK and BTK T474I, and 2.7 nM for BTK C481S, and exhibits cellular DC50 values of 0.1 nM and 0.2 nM against wild-type BTK and BTK C481S, respectively. NRX-0492 catalyzes the ubiquitination and proteasomal degradation of wild-type and drug-resistant mutant BTK by recruiting the CRBN E3 ubiquitin ligase complex. NRX-0492 inhibits the BCR signaling pathway and its downstream NF-κB/MYC transcriptional program, achieves rapid and sustained degradation in primary CLL cells, and exhibits extremely low cytotoxicity. NRX-0492 degrades BTK, inhibits tumor cell proliferation and activation, and significantly suppresses tumor growth in xenograft models. NRX-0492 can be used in research related to chronic lymphocytic leukemia and diffuse large B-cell lymphoma .
Cat. No.: HY-189126
CAS No.: 1240580-64-6
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YL064 is a multi-target STAT3-c-MYC inhibitor that directly binds to ATXN3 and inhibits its deubiquitinating activity, thereby promoting the ubiquitination and proteasomal degradation of oncogenic substrates of ATXN3. YL064 inhibits the phosphorylation of STAT3-Tyr705 without altering the total protein level of STAT3; meanwhile, it directly binds to the SH2 domain of STAT3 to block the dimerization, nuclear translocation, and DNA-binding activity of STAT3. YL064 directly targets the C-terminal HLH-Zip domain of c-Myc, upregulates the phosphorylation of c-Myc at the Thr58 site, and induces the ubiquitination and proteasome-dependent degradation of c-Myc. YL064 suppresses tumor cell proliferation, induces G2/M cell cycle arrest, reduces cell migration and invasion capacities, and triggers cancer cell apoptosis. YL064 can be used in related research on breast cancer, prostate cancer, diffuse large B-cell lymphoma, and multiple myeloma .
Cat. No.: HY-103019R
CAS No.: 1610408-97-3
Synonyms: (+)-BAY-1251152 (Standard); (+)-VIP152 (Standard); (S)-Enitociclib (Standard)
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Enitociclib (Standard) is the analytical standard of Enitociclib (HY-103019). This product is intended for research and analytical applications. Enitociclib ((+)-BAY-1251152; (+)-VIP152) is a selective CDK9 inhibitor (IC50=3 nM) that inhibits transcriptional elongation by blocking Ser2/Ser5 phosphorylation of RNA polymerase II. Enitociclib specifically depletes key short-lived proteins such as c-MYC, MCL-1 and induces tumor cell apoptosis. Enitociclib also interferes with the production of enhancer RNAs (eRNA) and enhancer-promoter interactions, and downregulates oncogene expression at the epigenetic level. Enitociclib exerts synergistic effects with agents including Bortezomib (HY-10227), Lenalidomide (HY-A0003), Pomalidomide (HY-10984), Venetoclax (HY-15531) and Paclitaxel (HY-B0015), and even reverses paclitaxel resistance. Enitociclib serves as a vital research tool for various malignancies such as double-hit diffuse large B-cell lymphoma, multiple myeloma and pancreatic ductal adenocarcinoma .
Cat. No.: HY-182959
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Hsp70TAC PD-1 Degrader-2 is a PD-L1 Hsp70TAC (Hsp70-targeting Chimeras) degrader with Kd values of 0.36 μM. Hsp70TAC PD-1 Degrader-2 forms a ternary complex with Hsp70 and PD-L1 to drive PD-L1 degradation. Hsp70TAC PD-1 Degrader-2 induces degradation of mature membrane-bound PD-L1 in an Hsp70-dependent manner and via caveolin-mediated endocytosis and lysosomal trafficking. Hsp70TAC PD-1 Degrader-2 accumulates preferentially in tumor cells with elevated Hsp70 expression for tumor-selective PD-L1 degradation. Hsp70TAC PD-1 Degrader-2 can be used for the research of cancer, such as breast invasive carcinoma, glioblastoma multiforme, diffuse large b-cell lymphoma . (Pink: PD-1/PD-L1 ligand (HY-19745A); Blue: Hsp70 ligand (HY-182979); Black: linker (HY-182982)).
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
