Petunidin-3-O-glucoside chloride
Based on 1 publication(s) in Google Scholar
Petunidin-3-O-glucoside chloride is a blood-brain barrier-penetrating tyrosinase inhibitor with an IC50 of 10.3 μM and a Ki of 9.0 μM. Petunidin-3-O-glucoside also acts as an α-glucosidase inhibitor with an IC50 of 218.2 µM. Petunidin-3-O-glucoside chloride inhibits the SIRT3/p53-mediated mitochondrial pathway and the PI3K/Akt-ERK pathway, suppresses glycolysis, and induces cell apoptosis. Petunidin-3-O-glucoside chloride scavenges ROS to exert antioxidant activity. It can be used in research related to glioblastoma multiforme, skin anti-aging and whitening, as well as obesity.
For research use only. We do not sell to patients.
- Purity : 98.11%
- CAS No.: 6988-81-4
- Formula: C22H23ClO12
- Molecular Weight:514.86
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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)
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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HY-W040045
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Pelargonidin 3,5-diglucoside chlorideNatural Pigment -
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Petunidin-3-O-glucoside chloride (Standard)Reference Standard -
HY-N2409R
Delphinidin chloride (Standard)Anthocyanidin -
HY-W040045R
Callistephin chloride (Standard)Stanard of Callistephin chloride -
HY-129138R
Cyanidin 3,5-diglucoside chloride (Standard)Standard Of Cyanidin 3,5-diglucoside chloride
Publications Citing Use of MedChemExpress (MCE) Petunidin-3-O-glucoside chloride
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Biological Activity
Description
In Vitro
Petunidin-3-O-glucoside (10-40 μM; 12-48 h) chloride induces dose- and time-dependent killing of human glioblastoma DBTRG-05MG cells[1].
Petunidin-3-O-glucoside (20-40 μM; 48 h) chloride downregulates the protein levels of c-Myc, PDK1, PKM2, p53 and MDM2, and upregulates the protein level of SIRT3 in DBTRG-05MG cells[1].
Petunidin-3-O-glucoside (20-40 μM; 24 h) chloride increases ROS levels in DBTRG-05MG cells[1].
Petunidin-3-O-glucoside (20-40 μM; 24-48 h) chloride induces apoptosis in DBTRG-05MG cells[1].
Petunidin-3-O-glucoside (20-40 μM; 48 h) chloride inhibits glucose uptake and lactate production in DBTRG-05MG cells, and the effect is stronger when combined with LY294002 (HY-10108)[1].
Petunidin-3-O-glucoside (30 min) scavenges DPPH free radicals in a cell-free system, with an EC50 value of 62.11 μM[4].
Petunidin-3-O-glucoside (6 min) scavenges ABTS+ free radicals in a cell-free system, with an EC50 value of 39.26 μM[4].
Petunidin-3-O-glucoside (25-100 μM; 12 h) chloride exerts no significant cytotoxicity on HepG2 cells[4].
Petunidin-3-O-glucoside (100 μM; 12 h) chloride significantly restores the glucose uptake capacity of HepG2 cells treated with high glucose (Glucose) (HY-B0389)/oleic acid (HY-N1446) after 12 h of incubation[4].
Petunidin-3-O-glucoside (50-100 μM; 12 h) chloride significantly reduces intracellular total cholesterol and triglyceride levels in HepG2 cells treated with high glucose/oleic acid after 12 h of incubation[4].
Petunidin-3-O-glucoside (50-100 μM; 12 h) chloride significantly reduces intracellular lipid droplet accumulation in HepG2 cells treated with high glucose/oleic acid after 12 h of incubation[4].
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:DBTRG-05MG cells
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Concentration:10, 20 and 40 μM
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Incubation Time:12, 36 and 48 h
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Result:Induced dose- and time-dependent killing of human glioblastoma DBTRG-05MG cells.
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Cell Line:DBTRG-05MG cells
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Concentration:20 and 40 μM
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Incubation Time:48 h
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Result:Downregulatec the protein levels of c-Myc, PDK1, PKM2, p53 and MDM2, and upregulated the protein level of SIRT3.
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Cell Line:DBTRG-05MG cells
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Concentration:20 and 40 μM
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Incubation Time:24 h (Annexin V/PI) and
48 h (WB) -
Result:Increased Bax and decrease the activated forms of Bcl-2 and caspase-3.
Increased the levels of early and late apoptosis in cells.
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Cell Line:HepG2 human hepatocellular carcinoma cells
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Concentration:25, 50 and 100 μM
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Incubation Time:12 h
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Result:Showed no significant cytotoxicity relative to the control group at all tested concentrations.
Chemical Information
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CAS No. 6988-81-4
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Appearance Solid
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Molecular Weight 514.86
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Formula C22H23ClO12
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Color Purple to black
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SMILES
OC1=CC2=[O+]C(C3=CC(OC)=C(O)C(O)=C3)=C(O[C@H]4[C@@H]([C@H]([C@@H]([C@@H](CO)O4)O)O)O)C=C2C(O)=C1.[Cl-]
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Structure Classification
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Initial Source
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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)
Publications (1)
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Journal Impact Factor
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Most Recent
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Food Chem
Flavonoid-mediated metabolic underpinning quality variation in red bud-sport pear mutants. [Abstract]2025 Oct 15:489:144992. PMID: 40466530
Solvent & Solubility
In Vitro:
Ethanol : 0.5 mg/mL (0.97 mM; ultrasonic and warming and heat to 60°C)
Protocols
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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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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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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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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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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
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Data Sheet (284 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
References
[1]. Wang G, et al. Inhibition of glycolytic metabolism in glioblastoma cells by Pt3glc combinated with PI3K inhibitor via SIRT3-mediated mitochondrial and PI3K/Akt-MAPK pathway. Journal of cellular physiology. 2019 May;234(5):5888-5903. [Content Brief]
[2]. Yang SY, et al. The Luteolinidin and Petunidin 3--Glucoside: A Competitive Inhibitor of Tyrosinase. Molecules (Basel, Switzerland). 2022 Sep 04;27(17):5703. [Content Brief]
[3]. Kim SM, et al. Neuroprotective effects of black soybean anthocyanins via inactivation of ASK1-JNK/p38 pathways and mobilization of cellular sialic acids. Life sciences. 2012 Jun 06;90(21-22):874-82. [Content Brief]
[4]. Zhu CW, et al. Five blueberry anthocyanins and their antioxidant, hypoglycemic, and hypolipidemic effects . Frontiers in nutrition. 2023;10:1172982. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Petunidin-3-O-glucoside chloride Related Classifications
HY-N7832 Related Classifications
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Keywords
- Petunidin-3-O-glucoside
- 6988-81-4
- Tyrosinase
- Glycosidase
- Apoptosis
- PI3K
- Akt
- ERK
- Reactive Oxygen Species (ROS)
- MDM-2/p53
- SIRT3/p53-mediated mitochondrial pathway
- HepG2 cells
- Saccharomyces cerevisiae
- blood-brain barrier
- DBTRG-05MG glioblastoma cells
- tyrosinase
- PI3K/Akt-ERK pathway
- neuroblastoma cells
- hepatic cells
- glioblastoma cells
- Inhibitor
- inhibitor
- inhibit