(-)-β-Peltatin
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(-)-β-Peltatin is an aryltetrahydronaphthalene lignan. (-)-β-Peltatin exhibits antitumor activity and cytotoxicity against pancreatic cancer cells. (-)-β-Peltatin induces G2/M cell cycle arrest and apoptosis in pancreatic cancer cells. (-)-β-Peltatin inhibits the growth of subcutaneous xenografts of pancreatic cancer cells in nude mice. (-)-β-Peltatin can be used in pancreatic cancer-related research.
For research use only. We do not sell to patients.
- Purity : 99.45%
- CAS No.: 518-29-6
- Formula: C22H22O8
- Molecular Weight:414.41
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Storage:
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
All Caspase Isoforms
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| BXPC-3 | GI50 |
0.0012 μg/mL
Compound: 3
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Growth inhibition of human BxPC3 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human BxPC3 cells measured after 48 hrs by sulforhodamine B assay
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[PMID: 26938998] |
| DU-145 | GI50 |
0.0021 μg/mL
Compound: 3
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Growth inhibition of human DU145 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human DU145 cells measured after 48 hrs by sulforhodamine B assay
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[PMID: 26938998] |
| HL-60 | IC50 |
0.0052 μg/mL
Compound: 11
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Cytotoxicity against human HL-60 cells after 72 hrs by MTT assay
Cytotoxicity against human HL-60 cells after 72 hrs by MTT assay
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[PMID: 10514313] |
| HT-29 | IC50 |
2.5 ng/mL
Compound: beta-peltatin A
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Growth inhibition of human HT29 cells
Growth inhibition of human HT29 cells
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[PMID: 15332833] |
| KM-20L2 | GI50 |
0.0076 μg/mL
Compound: 3
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Growth inhibition of human KM20L2 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human KM20L2 cells measured after 48 hrs by sulforhodamine B assay
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[PMID: 26938998] |
| MCF7 | GI50 |
0.00055 μg/mL
Compound: 3
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Growth inhibition of human MCF7 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human MCF7 cells measured after 48 hrs by sulforhodamine B assay
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[PMID: 26938998] |
| MCF7 | GI50 |
0.55 ng/mL
Compound: 3
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Growth inhibition of human MCF7 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human MCF7 cells measured after 48 hrs by sulforhodamine B assay
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[PMID: 26938998] |
| NCI-H460 | GI50 |
0.00077 μg/mL
Compound: 3
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Growth inhibition of human NCI-H460 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human NCI-H460 cells measured after 48 hrs by sulforhodamine B assay
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[PMID: 26938998] |
| NCI-H460 | GI50 |
0.77 ng/mL
Compound: 3
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Growth inhibition of human NCI-H460 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human NCI-H460 cells measured after 48 hrs by sulforhodamine B assay
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[PMID: 26938998] |
| P388 | IC50 |
2.5 ng/mL
Compound: beta-peltatin A
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Growth inhibition of mouse P388 cells
Growth inhibition of mouse P388 cells
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[PMID: 15332833] |
| P388 | ED50 |
0.0031 μg/mL
Compound: 3
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Growth inhibition of mouse P388 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of mouse P388 cells measured after 48 hrs by sulforhodamine B assay
|
[PMID: 26938998] |
| SF-268 | GI50 |
0.0004 μg/mL
Compound: 3
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Growth inhibition of human SF268 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human SF268 cells measured after 48 hrs by sulforhodamine B assay
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[PMID: 26938998] |
| SF-268 | GI50 |
0.4 ng/mL
Compound: 3
|
Growth inhibition of human SF268 cells measured after 48 hrs by sulforhodamine B assay
Growth inhibition of human SF268 cells measured after 48 hrs by sulforhodamine B assay
|
[PMID: 26938998] |
In Vitro
(-)-β-Peltatin (0-8 nM, 24-72 h) inhibits the viability of MIA PaCa-2 and BxPC-3 cells, with IC50 values of 2.09 nM and 1.49 nM, respectively[2].
(-)-β-Peltatin (0-4 nM, 12 h) induces G2/M phase arrest and apoptosis in PAC cells[2].
(-)-β-Peltatin (0-4 nM, 12 h) downregulates the expression levels of CDC25C, phosphorylated CDC25C (Ser216) and phosphorylated CDK1 (Tyr15), upregulates the protein expression level of cyclin B1, downregulates the expression of the anti-apoptotic protein Bcl-2, and activates caspase 3, caspase 9 and PARP[2] in MIA PaCa-2 and BxPC-3 cells.
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:PaCa-2, BxPC-3 cells
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Concentration:0, 1, 2, 4, 8 nM
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Incubation Time:24, 48, 72 h
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Result:Inhibited the viability of MIA PaCa-2 and BxPC-3 cells, with IC50 values of 2.09 nM and 1.49 nM, respectively.
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 (female, 6 weeks of age)[2]
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Dosage:15 mg/kg
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Administration:i.p.; once weekly
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Result:Significantly suppressed subcutaneous tumor growth relative to vehicle control.
Prolonged mouse survival time by 65.85% (34 days) compared to control mice (21 days).
Showed no notable alterations in mouse body weight or gross anatomy of primary organs relative to control.
Reduced Ki-67 positive cell percentage from ~100% relative in control to ~30% relative in treated tumors.
Increased cleaved caspase 3 positive cell percentage from ~0% in control to ~50% in treated tumors.
Increased p-Histone H3 (Ser10) positive cell percentage from ~1% in control to ~4% in treated tumors.
Chemical Information
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CAS No. 518-29-6
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Appearance Solid
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Molecular Weight 414.41
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Formula C22H22O8
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Color White to off-white
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SMILES
O=C1[C@]2([H])[C@H](C3=CC(OC)=C(C(OC)=C3)OC)C4=CC(OCO5)=C5C(O)=C4C[C@@]2([H])CO1
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Synonyms
β-Peltatin
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Structure Classification
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Protocols
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How to Select the Route of Administration for Mammals
Route-of-administration selection in mammals is a pharmacokinetic, pharmacodynamic, formulation, animal-welfare, and translational decision, not a default technical choice. The selected route should match the study goal: intravenous dosing is most useful when complete systemic exposure and rapid onset are required, oral dosing is most translational for orally intended medicines but is affected by absorption and first-pass metabolism, subcutaneous or intramuscular dosing can provide slower systemic exposure, and intraperitoneal dosing can be useful in rodent proof-of-concept studies but may have limited clinical translation. Published route-comparison studies show that the same compound can produce different exposure, onset, bioavailability, tissue distribution, and tolerability depending on route; therefore, route choice should be supported by pilot pharmacokinetic or pharmacodynamic evidence when the literature is insufficient. Unresolved questions include how to standardize route sel
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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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.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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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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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
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Data Sheet (281 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)