OXPHOS-IN-3
OXPHOS-IN-3 is a mitochondria-targeted dual OXPHOS/glycolysis inhibitor. OXPHOS-IN-3 exhibits potent antiproliferative activity against pancreatic cancer cells. OXPHOS-IN-3 induces mitochondrial dysfunction, ferroptosis, and immunogenic cell death (ICD). OXPHOS-IN-3 shows potent antitumor activity in pancreatic ductal adenocarcinoma (PDAC) models.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- Formule: C49H55BrClF3N3O5PS
- Masse moléculaire:1001.37
-
Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Activité biologique
-
Chemical Information
- Pureté et documentation
- Références
-
Help & FAQs
Activité biologique
|
SIRT3 |
GPX4 |
OXPHOS-IN-3 (Compound 14c) (0.1-0.8 μM; 24-72 h) exhibits potent antiproliferative activity in hypoxic MIAPaCa-2 cells (IC50 = 0.27 μM) with good selectivity over normal HS-5 and L02 cells (IC50 > 20 μM)[1].
OXPHOS-IN-3 (0.1-0.8 μM; 24-72 h) dose-dependently inhibits colony formation, migration, and invasion while downregulating epithelial-mesenchymal transition (EMT) markers in hypoxic MIAPaCa-2 cells[1].
OXPHOS-IN-3 (0.1-2.0 μM; 12-72 h) inhibits PDKs (IC50 = 97.8 nM), reduces PDH phosphorylation (EC50 = 14.3 nM), decreases lactate production, and suppresses glycolytic parameters under hypoxic conditions[1].
OXPHOS-IN-3 (0.2-2.0 μM; 12-48 h) downregulates SDHB and SIRT3, induces mitochondrial dysfunction and triggers ferroptosis with low apoptosis level in hypoxic MIAPaCa-2 cells[1].
OXPHOS-IN-3 (0.2-2.0 μM; 12-48 h) induces mitochondrial ROS accumulation, MMP collapse, mPTP opening, and cytochrome c release in MIAPaCa-2 cells[1].
OXPHOS-IN-3 (0.2-2.0 μM; 12-24 h) induces immunogenic cell death hallmarks in human MIAPaCa-2 cells, including CRT surface exposure, HMGB1 translocation/release, and intracellular ATP depletion[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:MIAPaCa-2, PANC-1, BxPC-3 (normoxic and hypoxic), HS-5, L02 cells
-
Concentration:0.1, 0.4, 0.8 μM (and broader range for IC50 determination)
-
Incubation Time:24-72 h
-
Result:Inhibited cell viability in PDAC cells, showing IC50 values of 0.27 μM, 6.25 μM, and 3.15 μM against MIAPaCa-2 , PANC-1 , and BxPC-3 cells under hypoxic conditions, respectively.
Exhibited IC50 values of 3.36 μM, 2.07 μM, and 2.06 μM against MIAPaCa-2 , PANC-1 , and BxPC-3 cells under normoxic conditions, respectively.
Showed markedly reduced cytotoxicity to normal HS-5 and L02 cells (IC50 > 20 μM).
-
Cell Line:MIAPaCa-2 cells (hypoxic)
-
Concentration:0.1, 0.4, 0.8 μM
-
Incubation Time:72 h (followed by 10-14 days culture)
-
Result:Dose-dependently suppressed clonogenic capacity, while Gemcitabine (HY-17026) showed weakened effect under hypoxia.
-
Cell Line:MIAPaCa-2 cells (hypoxic)
-
Concentration:0.1, 0.4, 0.8 μM
-
Incubation Time:24 h
-
Result:Significantly inhibited wound healing and transwell migration.
-
Cell Line:MIAPaCa-2 cells (hypoxic, Matrigel-coated)
-
Concentration:0.1, 0.4, 0.8 μM
-
Incubation Time:48 h
-
Result:Effectively inhibited the invasive potential of MIAPaCa-2 cells under hypoxic conditions
-
Cell Line:MIAPaCa-2 (hypoxic), PANC-1, BxPC-3 cells
-
Concentration:0.2, 1.0, 2.0 μM
-
Incubation Time:12-72 h
-
Result:Reduced expression of p-PDH, SDHB, SIRT3, EMT markers (ZEB1, Slug, Vimentin, Snail, N-cadherin), xCT and GPX4.
Increased HIF-1α and PDK1 expression under hypoxic validation.
-
Cell Line:MIAPaCa-2 cells (hypoxic)
-
Concentration:0.2, 1.0, 2.0 μM
-
Incubation Time:12-24 h
-
Result:Promoted CRT surface exposure and HMGB1 nuclear-to-cytoplasmic translocation, visualized by confocal microscopy.
-
Cell Line:MIAPaCa-2 cells (hypoxic)
-
Concentration:0.2, 1.0, 2.0 μM
-
Incubation Time:24-48 h
-
Result:Induced only low-level apoptosis (≤15%), which was not the primary mode of cell death.
OXPHOS-IN-3 (5 and 10 mg/kg; i.p.; every 2 days for 6 doses) dose-dependently inhibits tumor growth in the syngeneic PANC02-EGFP subcutaneous model in C57BL/6 mice, accompanied by downregulation of p-PDH, SDHB, SIRT3, and EMT markers in tumor tissues[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:Syngeneic bilateral PANC02 model (Male C57BL/6 mice, 6-8 weeks old)[1]
-
Dosage:5 mg/kg
-
Administration:Intratumoral injection (i.t.), every 2 days for 3 doses
-
Result:Reduced primary and contralateral tumor volume/weight compared with control and Gemcitabine (HY-17026) groups.
Decreased Arg-1 and MRC-1 expression in tumor tissues (M1-like TAM reprogramming).
Enhanced HMGB1 release and CRT exposure in tumor sections (IHC/IF).
No significant body weight loss.
-
Animal Model:Syngeneic PANC02-EGFP subcutaneous model (Male C57BL/6 mice, 6-8 weeks old)[1]
-
Dosage:5 and 10 mg/kg
-
Administration:Intraperitoneal injection (i.p.), every 2 days for 6 doses
-
Result:Dose-dependently inhibited tumor growth as shown by reduced EGFP fluorescence, caliper measurement, and tumor weight.
Decreased p-PDH, SDHB, SIRT3, and EMT markers in tumor tissues.
Showed pronounced tumor cell damage with normal histology in major organs (heart, liver, spleen, lung, kidney).
Exhibited good tolerability with stable body weight throughout the treatment period.
Chemical Information
-
Masse moléculaire 1001.37
-
Formule C49H55BrClF3N3O5PS
-
SMILES
ClC1=C(C=CC(S(C2=CC=C(C=C2)C(N3CCN(CC3)CCCCCCCCCC[P+](C4=CC=CC=C4)(C5=CC=CC=C5)C6=CC=CC=C6)=O)(=O)=O)=C1)NC([C@@](C(F)(F)F)(C)O)=O.[Br-]
-
Livraison
Room temperature in continental US; may vary elsewhere.
-
Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
OXPHOS-IN-3 Related Classifications
HY-184173 Related Classifications
Powered by Bioz
- OXPHOS-IN-3
- Oxidative Phosphorylation
- PDK-1
- Ferroptosis
- Mitochondrial Metabolism
- Sirtuin
- Glutathione Peroxidase
- OXPHOS
- Glycolysis
- Cancer Metabolism
- Metabolic Reprogramming
- Mitochondria
- Mitochondrial Dysfunction
- Immunogenic Cell Death
- Pancreatic Cancer
- Pancreatic Ductal Adenocarcinoma
- PDAC
- Orthotopic Pancreatic Cancer Model
- Syngeneic Tumor Model
- Tumor Immune Microenvironment
- ROS
- Inhibitor
- inhibitor
- inhibit