CYP1B1-IN-14 TFA
CYP1B1-IN-14 TFA is a metabolically stable hCYP1B1 competitive inhibitor with an IC50 of 1.32 nM and a Ki of 0.72 μM. CYP1B1-IN-14 TFA reverses the resistance of cancer cells to Paclitaxel (HY-B0015). CYP1B1-IN-14 TFA acts synergistically with Paclitaxel (HY-B0015) to inhibit tumor growth in xenograft models without obvious toxicity. CYP1B1-IN-14 TFA can be used for the research of cancers such as paclitaxel-resistant lung cancer.
For research use only. We do not sell to patients.
- Formula: C23H26Br2F3N3O5
- Molecular Weight:641.27
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
CYP1B1 1.32 nM (IC50) |
CYP1B1 0.72 μM (Ki) |
In Vitro
CYP1B1-IN-14 (compound 26a) (0-32 μM; 8 h) TFA inhibits cellular hCYP1B1 activity in CHO-1B1 cells with an IC50 of 2.21 μM[1].
CYP1B1-IN-14 (5 μM; 48 h) TFA reverses Paclitaxel (HY-B0015) resistance in H460/PTX and A549/PTX cells[1].
CYP1B1-IN-14 (1-10 μM; 2.75 h) TFA dose-dependently inhibits the function of P-gp transporter in MDR1-MDCK cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:Paclitaxel-resistant lung cancer cell lines (H460/PTX and A549/PTX)
-
Concentration:5 μM (co-administered with PTX)
-
Incubation Time:48 h
-
Result:Enhanced PTX's anticancer activity 26.5-fold in H460/PTX cells and 22.9-fold in A549/PTX cells, respectively.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:BALB/c nude treated A549/
PTX xenograft tumors (female, 4-6 weeks old)[1] -
Dosage:45 mg/kg
-
Administration:i.p.; once daily; 16 days
-
Result:Showed no influence on tumor growth when administered alone.
Produced a synergistic antitumor effect with a 41.1% tumor growth inhibition rate when co-administered with Paclitaxel.
Caused no animal death or notable body weight loss.
Chemical Information
-
Molecular Weight 641.27
-
Formula C23H26Br2F3N3O5
-
SMILES
FC(F)(F)C(O)=O.CO/N=C(CC1=CC=CC=C1)/C(NCCC2=CC(Br)=C(C(Br)=C2)OCCCN)=O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
-
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.
-
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.
-
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.
-
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.
-
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
-
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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)