Pipoxolan
Pipoxolan is an orally active smooth muscle relaxant, anti-inflammatory agent and anticancer agent. Pipoxolan modulates PI3K/AKT signaling pathways, and reduces the levels of Ras/MEK/p-ERK, MMP-2 and MMP-9. Pipoxolan inhibits pro-inflammatory transcription factor pathways, activates Nrf2/HO-1, and suppresses the production of pro-inflammatory mediators. Pipoxolan induces ROS generation, endogenous mitochondrial Apoptosis, and G0/G1 cell cycle arrest. Pipoxolan reduces cerebral infarction size and inhibits intimal hyperplasia. Pipoxolan can be used in research related to cerebral ischemia, intimal hyperplasia, oral squamous cell carcinoma, leukemia and lung cancer.
연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.
- CAS No.: 23744-24-3
- 화학식: C22H25NO3
- 분자량:351.45
-
보관:
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]
-
Biological Activity
-
Chemical Information
- 순도&문서
- References
-
Help & FAQs
All MEK Isoforms
More
Biological Activity
|
MMP-9 |
MMP-2 |
HO-1 |
Pipoxolan (5-15 µM; 24, 48, 72 hr) potently inhibits PDGF-BB-stimulated migration of A7r5 vascular smooth muscle cells in a dose-dependent manner over 24, 48, and 72 hours[1].
Pipoxolan (5-15 µM; 48 hr pre-treatment; 8 hr migration period) inhibits PDGF-BB-stimulated migration of A7r5 vascular smooth muscle cells in a transwell assay, with 76.5% inhibition at the highest concentration[1].
Pipoxolan (5-15 µM; 48 hr) downregulates Ras, MEK, p-ERK, MMP-2, and MMP-9 protein levels in PDGF-BB-stimulated A7r5 vascular smooth muscle cells, with the greatest reduction in p-ERK (75%) at 15 µM[1].
Pipoxolan (1.6-100 μg/mL; 24 h) is cytotoxic to human TW206, HSC-3, and Cal-27 cells in vitro, with IC50 values of 13.13 μg/mL, 42.28 μg/mL, and 52.69 μg/mL respectively, and TW206 and HSC-3 cells are more sensitive than Cal-27 cells[2].
Pipoxolan (20 μg/mL; 2-6 h) induces apoptosis in human TW206 OSCC cells in a time-dependent manner, with detectable apoptosis at 2 h and maximal levels at 6 h of treatment with 20 μg/mL pipoxolan[2].
Pipoxolan (4-32 μM; 1 h pretreatment; 24 h LPS incubation) exhibits no significant cytotoxicity in LPS-stimulated RAW 264.7 murine macrophage cells[3].
Pipoxolan (4-32 μM; 1 h pretreatment; 24 h LPS incubation) dose-dependently inhibits LPS-induced nitrite production in RAW 264.7 murine macrophage cells, with 68.24% inhibition at 32 μM[3].
Pipoxolan (4-32 μM; 1 h pretreatment; 24 h LPS incubation) dose-dependently inhibits LPS-induced production of PGE2, TNF-α, and IL-6 in RAW 264.7 murine macrophage cells, with maximum inhibition of 90.73% (PGE2), 90% (TNF-α), and 95.27% (IL-6) at 32 μM[3].
Pipoxolan (1.6-50 μg/mL; 24 h) potently inhibits proliferation of human leukaemia HL-60 cells with an IC50 of 6.25 μg/mL, U937 cells with an IC50 of 12.5 μg/mL, and K562 cells with an IC50 of 25 μg/mL after 24 h, while showing no cytotoxicity against normal human PBMC at concentrations up to 50 μg/mL[4].
Pipoxolan (1.6-25 μg/mL; 2-48 h) arrests human leukaemia HL-60 cells in the G0/G1 phase in a time-dependent manner, reaching 62.0% at 48 h with 6.25 μg/mL, and induces dose-dependent sub-G1 apoptotic cell accumulation after 24 h[4].
Pipoxolan (3.2-25 μg/mL; 15 min-24 h) induces rapid, time- and concentration-dependent intracellular ROS generation in human leukaemia HL-60 cells, which is critical for its apoptotic activity, as NAC pretreatment blocks both ROS production and apoptosis[4].
Pipoxolan (2-10 μg/mL; 24 h) significantly inhibits proliferation of CL1-5 lung adenocarcinoma cells at 5 and 10 μg/mL after 24 h of incubation[5].
Pipoxolan (2-10 μg/mL; 24 h) does not induce apoptosis in CL1-5 or CL1-0 lung adenocarcinoma cells at concentrations of 2, 5, or 10 μg/mL after 24 h of incubation[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:A7r5 vascular smooth muscle cells (VSMCs)
-
Concentration:5-15 µM
-
Incubation Time:24, 48, 72 hr
-
Result:Attenuated PDGF-BB-stimulated A7r5 cell migration in a dose-dependent manner at all time points tested.
Significantly reduced relative migration compared to PDGF-BB-only controls.
Exhibited the highest inhibition at the 15 µM concentration across all time points.
-
Cell Line:A7r5 vascular smooth muscle cells (VSMCs)
-
Concentration:5-15 µM
-
Incubation Time:48 hr pre-treatment; 8 hr migration period
-
Result:Significantly reduced the number of PDGF-BB-stimulated A7r5 cells migrating across the membrane.
Achieved percent inhibition of 46.2% at 5 µM, 62.2% at 10 µM, and 76.5% at 15 µM compared to PDGF-BB-only controls.
-
Cell Line:A7r5 vascular smooth muscle cells (VSMCs)
-
Concentration:5-15 µM
-
Incubation Time:48 h
-
Result:Reduced Ras protein levels by 21% at 5 µM, 24.75% at 10 µM, and 24% at 15 µM compared to PDGF-BB-only controls.
Reduced MEK protein levels by 21.67% at 5 µM, 21% at 10 µM, and 26.67% at 15 µM compared to PDGF-BB-only controls.
Reduced p-ERK protein levels by 50.33% at 5 µM, 51.67% at 10 µM, and 75% at 15 µM compared to PDGF-BB-only controls.
Reduced MMP-2 protein levels by 12.4% at 10 µM and 24.4% at 15 µM compared to PDGF-BB-only controls.
Reduced MMP-9 protein levels by 39.4% at 5 µM, 45.4% at 10 µM, and 36.6% at 15 µM compared to PDGF-BB-only controls.
-
Cell Line:human oral squamous cell carcinoma (OSCC) TW206, HSC-3 cells; human head and neck squamous cell carcinoma (HNSCC) Cal-27 cells
-
Concentration:1.6, 3.2, 6.25, 12.5, 25, 50, 100 μg/mL
-
Incubation Time:24 h
-
Result:Dose-dependently reduced cell viability in all three cell lines.
Reached IC50 values of 13.13 μg/mL for TW206 cells, 42.28 μg/mL for HSC-3 cells, and 52.69 μg/mL for Cal-27 cells.
Showed greater cytotoxicity to TW206 and HSC-3 cells than Cal-27 cells.
-
Cell Line:human OSCC TW206 and HSC-3 cells
-
Concentration:20 μg/mL (TW206 cells); 50 μg/mL (HSC-3 cells)
-
Incubation Time:2, 4, 8, 12, 24, 48 h
-
Result:Caused time-dependent increases in cytosolic cytochrome c, active caspase-9, active caspase-3, and cleaved PARP in HSC-3 cells, and did not alter caspase-8 expression.
Increased pro-apoptotic BAX protein expression and decreased anti-apoptotic BCL2 protein expression in both TW206 and HSC-3 cells after 24 h.
Caused time-dependent decreases in PI3K and phosphorylated AKT (pAKT) levels in both cell lines, with significant suppression after 24 h.
-
Cell Line:RAW 264.7 murine macrophage cells
-
Concentration:4-32 μM
-
Incubation Time:1 h pretreatment; 24 h LPS incubation
-
Result:Dose-dependently inhibited LPS-induced production of PGE2, TNF-α, and IL-6.
Inhibited PGE2 production by 90.73%, TNF-α production by 90%, and IL-6 production by 95.27% at 32 μM compared to LPS-only treated cells.
Showed statistically significant inhibition at all tested concentrations for each cytokine.
-
Cell Line:RAW 264.7 murine macrophage cells
-
Concentration:32 μM
-
Incubation Time:1 h pretreatment; 6 h LPS incubation
-
Result:Promoted LPS-induced translocation of Nrf2 from the cytoplasm to the nucleus, as visualized by increased nuclear Nrf2 fluorescence compared to LPS-only treated cells.
-
Cell Line:human leukaemia HL-60 cells
-
Concentration:1.6, 3.2, 6.25, 12.5, 25 μg/mL (24 h incubation); 6.25 μg/mL (2-48 h incubation)
-
Incubation Time:2, 6, 12, 24, 48 h
-
Result:Induced significant apoptosis (sub-G1 hypodiploid cells) with 6.25 μg/mL for 24 h.
Caused dose-dependent increases in sub-G1 cells at 12.5, 25 μg/mL after 24 h.
Caused time-dependent accumulation of cells in the G0/G1 phase: 48.7% at 12 h, 58.1% at 24 h, and 62.0% at 48 h, all statistically significant compared to controls.
Pipoxolan (10-30 mg/kg; p.o.; daily; 28 days starting on the day of ligation) dose-dependently reduces carotid artery ligation-induced intimal hyperplasia in male ICR mice, with 30 mg/kg (p.o., daily for 28 days) achieving a 47.20% reduction in the I/M ratio and 62.40% inhibition of PCNA-positive cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:Sprague-Dawley (male, 225-275 g, transient focal cerebral ischemia-reperfusion model)[1]
-
Dosage:10 mg/kg; 30 mg/kg
-
Administration:p.o.; single dose 1 hour pre-ischemia
-
Result:Reduced cerebral infarction area by 43.18%, neurological deficit score by 31.25%, TUNEL-positive cells by 31.25%, and cleaved caspase-3-positive cells by 37.18%.
Reduced cerebral infarction area by 73.43%, neurological deficit score by 46.88%, TUNEL-positive cells by 46.88%, and cleaved caspase-3-positive cells by 63.44%.
Did not alter mean arterial pressure or cerebral blood flow compared to controls.
-
Animal Model:ICR (male, 20-25 g, left common carotid artery ligation-induced model)[1]
-
Dosage:10 mg/kg; 30 mg/kg
-
Administration:p.o.; daily; 28 days starting on the day of ligation
-
Result:Reduced the intima/media (I/M) ratio by 24.21% and inhibited PCNA-positive cells by 42.11%.
Reduced the intima/media (I/M) ratio by 47.20% and inhibited PCNA-positive cells by 62.40%.
Chemical Information
-
CAS No. 23744-24-3
-
분자량 351.45
-
화학식 C22H25NO3
-
SMILES
O=C1OC(OC1(C=2C=CC=CC2)C=3C=CC=CC3)CCN4CCCCC4
-
선적
Room temperature in continental US; may vary elsewhere.
-
보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
References
[1]. Chen YF, et al. Pipoxolan ameliorates cerebral ischemia via inhibition of neuronal apoptosis and intimal hyperplasia through attenuation of VSMC migration and modulation of matrix metalloproteinase-2/9 and Ras/MEK/ERK signaling pathways. PLoS One. 2013;8(9):e75654. Published 2013 Sep 24. [Content Brief]
[2]. Chou PY, et al. Pipoxolan Exhibits Antitumor Activity Toward Oral Squamous Cell Carcinoma Through Reactive Oxygen Species-mediated Apoptosis. Anticancer Res. 2017;37(11):6391-6400. [Content Brief]
[3]. Lin YH, et al. Pipoxolan suppresses the inflammatory factors of NF-κB, AP-1, and STATs, but activates the antioxidative factor Nrf2 in LPS-stimulated RAW 264.7 murine macrophage cells. Environ Toxicol. 2020;35(12):1352-1363. [Content Brief]
[4]. Sheu MJ, et al. Pipoxolan inhibits proliferation of HL-60 human leukaemia cancer cells by arresting the cell cycle at the G0/G1 phase. Clin Exp Pharmacol Physiol. 2010;37(5-6):605-612. [Content Brief]
[5]. Lee MM, et al. Pipoxolan inhibits CL1-5 lung cancer cells migration and invasion through inhibition of MMP-9 and MMP-2. Chem Biol Interact. 2015;236:19-30. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Pipoxolan Related Classifications
HY-105854A Related Classifications
Powered by Bioz
- Pipoxolan
- 23744-24-3
- Ras
- MEK
- ERK
- PI3K
- Akt
- MMP
- Keap1-Nrf2
- Heme Oxygenase (HO)
- Reactive Oxygen Species (ROS)
- Apoptosis
- vascular smooth muscle cells
- RAW 264.7 murine macrophage cells
- lung cancer
- CL1-5 lung adenocarcinoma cells
- A7r5 vascular smooth muscle cells
- PI3K/AKT signaling pathways
- HL-60 cells
- leukaemia
- Ras/MEK/ERK signaling pathways
- oral squamous cell carcinoma
- Inhibitor
- inhibitor
- inhibit