Bakkenolide IIa
Bakkenolide IIa is a bakkenolide-type sesquiterpene with antioxidant and neuroprotective activities. It scavenges DPPH (HY-112053) free radicals, inhibits lipid peroxidation, and protects primary cortical neurons from oxygen-glucose deprivation and oxidative damage. Bakkenolide IIa can be used in neuroprotection-related research.
For research use only. We do not sell to patients.
- CAS No.: 915289-59-7
- Formula: C25H34O6
- Molecular Weight:430.54
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
Bakkenolide IIa (25-100 μg/mL; 1 h pre-incubation, 2 h anoxia, 24 h re-oxygenation) protects primary cultured rat cerebral cortical neurons against oxygen-glucose deprivation-induced injury, increasing cell viability to 73.4% at 100 μg/mL and reducing LDH release in a concentration-dependent manner[1].
Bakkenolide IIa (25-100 μg/mL; co-incubated during oxidative insult, 24 h recovery) protects primary cultured rat cerebral cortical neurons against multiple oxidative insults, with the highest efficacy against Fe2+/ascorbic acid-induced damage, reaching 85.3% cell viability at 100 μg/mL[1].
Bakkenolide IIa (25-100 μg/mL; 30 min) exhibits concentration-dependent DPPH radical scavenging activity, reaching 80.1% at 100 μg/mL[1].
Bakkenolide IIa (25-100 μg/mL; 1 h) potently inhibits lipid peroxidation in rat forebrain homogenates, with 93.1% inhibition at 100 μg/mL[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 915289-59-7
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Molecular Weight 430.54
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Formula C25H34O6
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SMILES
O(C(C=C(C)C)=O)[C@H]1[C@@]2(C[C@@]3(C)[C@@]1([C@@H](OC(C=C(C)C)=O)CC[C@@H]3C)[H])C(=C)COC2=O
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Structure Classification
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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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Primary Embryonic Cortical Neuron Culture
Primary embryonic cortical neuron culture isolates cortical tissue from prenatal rodents, dissociates it into single cells, and maintains neurons in vitro so that neurite extension, neuronal marker expression, synapse formation, survival, and treatment responses can be examined outside the intact brain.
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Bakkenolide IIa Related Classifications
HY-N21782 Related Classifications
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Keywords
- Bakkenolide IIa
- 915289-59-7
- Biochemical Assay Reagents
- neuroprotective
- Petasites tricholobus
- rat forebrain homogenates
- oxygen-glucose deprivation
- DPPH free radicals
- antioxidant
- lipid peroxidation
- bakkenolide-type sesquiterpene
- primary cultured cortical neurons
- spirolactone-containing natural product
- Inhibitor
- inhibitor
- inhibit