PROTAC PIN1 degrader-2
PROTAC PIN1 degrader-2 is a PROTAC PIN1 degrader. PROTAC PIN1 degrader-2 reduces PIN1-mediated oncogene expression, upregulates PIN1-inhibited tumor suppressor genes, and exerts killing effects on cancer cells. PROTAC PIN1 degrader-2 inhibits tumor growth in breast cancer mouse xenograft models. PROTAC PIN1 degrader-2 can be used for the research of breast cancer.
(Pink: PIN1 ligand (HY-186219); Blue: Cereblon ligand (HY-103596); Black: linker).
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 3083422-10-7
- Formel: C28H34ClN3O10S
- Molecular Weight:640.10
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
In Vitro
PROTAC PIN1 degrader-2 (compound A1) (2.2 μM-20 μM; 0-36 h) specifically degrades PIN1 protein in MCF-7 breast cancer cells with a DC50 of 269 nM, achieving 90% degradation at 2.2 μM and reaching maximum degradation at 12 hours post-treatment[1].
PROTAC PIN1 degrader-2 (2.2 μM-20 μM; 0-36 h) degrades PIN1 protein in PATU-8988t pancreatic cancer cells, with effective degradation at 2.2 μM and a Hook effect occurring at 20 μM[1].
PROTAC PIN1 degrader-2 (0.08 μM-20 μM; 72 h) inhibits the viability of MCF-7 breast cancer cells, and this inhibitory activity is enhanced in an additive manner when combined with RO3306[1].
PROTAC PIN1 degrader-2 (0.08 μM-20 μM; 72 h) inhibits the viability of PATU-8988t pancreatic cancer cells, and this inhibitory activity is enhanced in an additive manner when combined with RO3306[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:MCF-7 breast cancer cells
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Concentration:2.2; 6.7; 20 μM
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Incubation Time:0; 6; 12; 18; 24; 36 h
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Result:Significantly reduced PIN1 protein levels.
Achieved 90% degradation efficiency at 2.2 μM.
Exhibited a DC50 value of 269 nM for PIN1 degradation.
Reached peak PIN1 degradation at 12 hours, followed by protein recovery after 12 hours.
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Cell Line:MCF-7 breast cancer cells
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Concentration:0.08; 0.25; 0.74; 2.22; 6.66; 20 μM
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Incubation Time:72 h
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Result:Inhibited MCF-7 cell viability in a concentration-dependent manner when used alone.
Showed additive cell viability inhibition effect when combined with 1 μM or 5 μM RO3306, with significantly stronger inhibition than the degrader alone at equivalent concentrations.
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Cell Line:PATU-8988t pancreatic cancer cells
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Concentration:0.08; 0.25; 0.74; 2.22; 6.66; 20 μM
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Incubation Time:72 h
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Result:Inhibited PATU-8988t cell viability in a concentration-dependent manner when used alone.
Showed additive cell viability inhibition effect when combined with 1 μM or 5 μM RO3306, with significantly stronger inhibition than the degrader alone at equivalent concentrations.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c-Nude mice (female, 5 weeks old, MCF-7 cell xenograft model with estradiol pre-treatment)[1]
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Dosage:50 mg/kg
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Administration:i.p.; every other day; 20 days
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Result:Inhibited tumor growth significantly compared to vehicle control group after 20 days.
Maintained stable body weight and exhibited normal behavior with no observed toxicity.
Chemical Information
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CAS. Nr. 3083422-10-7
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Molecular Weight 640.10
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Formel C28H34ClN3O10S
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SMILES
O=C(CCCOC1=CC=CC(C(N2C3C(NC(CC3)=O)=O)=O)=C1C2=O)OCC(C)(CN(C4CCS(=O)(C4)=O)C(CCl)=O)C
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
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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.
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Calculators
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