UBX-382
Based on 1 Customer Validation
UBX-382 is an orally active BTK PROTAC degrader with a DC50 of 4.56 nM. UBX-382 inhibits B-cell receptor signaling by targeting BTK. UBX-382 shows superior degradation activity for wild-type and mutant BTK proteins. UBX-382 inhibits tumor growth in murine xenograft models harboring wild-type or C481S mutant BTK-expressing TMD-8 cells. UBX-382 can be used for the study of B-cell-related blood cancers.
For research use only. We do not sell to patients.
- Purity : 96.20%
- CAS No.: 2884554-45-2
- Formula: C42H44N10O4
- Molecular Weight:752.86
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
Biological Activity
Description
IC50 & Target
[1]|
Cereblon |
In Vitro
UBX-382 (0.00001-10 nM, 0.5-48 h) induces potent BTK degradation with a DC 50 of 4.56 nM in TMD-8 cells[1].
UBX-382 (0.0001-10 μM, 3-5 days) inhibits the proliferation of TMD8 (IC50 = 14 nM), WSU-DLCL2 (IC50 = 18 nM), OCI-Ly3 (IC50 = 199 nM) and U2932 (IC50 = 21 nM) measured by the Cell Titer-Glo assay in duplicates[1].
UBX-382 (10 nM, 24 h) significantly inhibits CCL3 and CCL4 secretion induced by BCR signal activation in TMD-8 cells[1].
UBX-382 (100 nM, 6-24 h) inhibits the phosphorylation of BTK Y223, SYK, MEK, and ERK in U2932 cells[1].
UBX-382 (0.1-10 μM, 24 h) effectively degrades wild-type and various BTK mutants (E41K, C481S/R/T/Y/F, L528W) in HEK293 cells and strongly suppresses their phosphorylation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:U2932 cells
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Concentration:100 nM
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Incubation Time:6, 24 h
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Result:Showed far more effective inhibition of BTK Y223 phosphorylation than Ibrutinib (HY-10997), Acalabrutinib (HY-17600), and Nemtabrutinib (ARQ-531) (HY-112215) in U2932 cells.
Inhibited the phosphorylation of SYK, MEK, and ERK.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:TMD-8 cells (1 × 107 in Matrigel) were subcutaneously injected into the flanks of 6-week-old CB17/severe combined immunodeficient mice[1]
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Dosage:3, 10, 30 mg/kg
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Administration:p.o. once daily for 21 days
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Result:Achieved complete tumor regression in TMD-8 xenograft models.
Showed no significant changes in body weight and no other clinical toxicity signs during the experiment.
Reduced BTK levels in tumors of TMD-8 xenograft models.
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Animal Model:TMD-8 BTK C481S cells were subcutaneously inoculated into the right flank of male CB17/severe combined immunodeficient mice[1]
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Dosage:3, 10, 30 mg/kg
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Administration:p.o. once daily for 21 days
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Result:Induced remarkable dose-dependent tumor regression in TMD-8 BTK C481S xenograft models, while Ibrutinib failed to inhibit tumor growth.
Chemical Information
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CAS No. 2884554-45-2
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Appearance Solid
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Molecular Weight 752.86
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Formula C42H44N10O4
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Color Light yellow to green yellow
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SMILES
O=C1C2=CC=C(N3CCC(CC3)CN4CC5=CC(NC6=NC7=C(C(NC8=C(C)C=CC=C8C)=NN7C)C=N6)=CC=C5CC4)C=C2C(N1C9C(NC(CC9)=O)=O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Protocols
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
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Splenic/Portal-Vein Liver Metastasis Xenograft
Splenic and portal-vein liver metastasis xenograft models deliver tumor cells into the portal circulation so that cells reach the liver first and form hepatic metastatic lesions; splenic injection uses the spleen as an access route to the portal system, while direct portal-vein injection introduces cells into the portal vein without requiring splenectomy. The assay detects liver colonization, intrahepatic tumor growth, tumor distribution, treatment response, survival, and liver-metastasis microenvironment changes; readouts include bioluminescence or fluorescence imaging, gross liver nodule counts, liver weight or tumor burden, histology, and survival.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
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Intraperitoneal/Peritoneal Dissemination Xenograft
Intraperitoneal (IP) or peritoneal dissemination xenograft models are based on the introduction of human cancer cells into the peritoneal cavity of immunodeficient mice, where they attach to peritoneal surfaces, form multicellular aggregates or spheroids, and progressively generate disseminated tumor nodules that mimic advanced peritoneal metastatic disease. These models are widely used to study ovarian cancer progression, tumor-microenvironment interactions, and intraperitoneal therapeutic responses, often incorporating bioluminescence or fluorescence imaging to longitudinally monitor tumor burden in vivo. The biological principle relies on the capacity of tumor cells such as SKOV3 or related ovarian carcinoma lines to survive in suspension, aggregate within ascites-like fluid, adhere to mesothelial surfaces, and invade peritoneal organs, thereby recapitulating human peritoneal carcinomatosis patterns observed in advanced disease.
Purity & Documentation
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Data Sheet (271 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)