Bakkenolide Iva
Bakkenolide Iva is a bakkenolide-type sesquiterpene. Bakkenolide Iva is isolated from the rhizomes of Petasites tricholobus. Bakkenolide Iva inhibits lipid peroxidation in rat brain homogenates and scavenges DPPH free radicals. Bakkenolide Iva protects cortical neurons against oxygen-glucose deprivation-induced injury and oxidative stress-induced neuronal injury. Bakkenolide Iva can be used in research on paralysis and allergic rhinitis.
For research use only. We do not sell to patients.
- CAS No.: 915289-61-1
- Formula: C24H32O6S
- Molecular Weight:448.57
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Storage:
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]
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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 IVa (25-100 μg/mL; 1 h) exerts dose-dependent neuroprotective effects against oxygen-glucose deprivation-induced damage in primary cultured rat cortical neurons, improving viability to 72.6% at 100 μg/mL[1].
Bakkenolide IVa (25-100 μg/mL) significantly protects primary cultured rat cortical neurons against oxidative damage, providing near-complete protection (84.6% viability) against Fe2+/ascorbic acid at 100 μg/mL[1].
Bakkenolide IVa (25-100 μg/mL; 1 h) potently inhibits Fe2+/ascorbic acid-induced lipid peroxidation in rat brain homogenates with a maximal inhibition of 92.5% at 100 μg/mL[1].
Bakkenolide IVa (25-100 μg/mL; 30 min) is an effective DPPH free radical scavenger, reaching 82.7% scavenging activity 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. 915289-61-1
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Molecular Weight 448.57
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Formula C24H32O6S
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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=CSC)=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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Neurotoxicity Study
This protocol assesses in vitro neurotoxicity by combining neuronal viability, mitochondrial/metabolic activity, neurite outgrowth, and optional neuronal network function readouts. Calcein-AM or resazurin/PrestoBlue readouts estimate viable or metabolically active cells; βIII-tubulin immunofluorescence detects neuronal morphology and neurite networks; TMRE detects mitochondrial membrane potential; and MEA recordings detect functional changes in neuronal network activity.
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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
[1]. Wang YL, et al. Bakkenolides from Petasites tricholobus and their neuroprotective effects related to antioxidant activities. Planta medica. 2009 Feb;75(3):230-5. [Content Brief]
[2]. van der Meer JW, et al. Abstract!. The Netherlands journal of medicine. 2002 Dec;60(11):418. [Content Brief]
[3]. Zhang FJ, et al. Anti-allergic effects of total bakkenolides from Petasites tricholobus in ovalbumin-sensitized rats. Phytotherapy research : PTR. 2011 Jan;25(1):116-21. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Bakkenolide Iva Related Classifications
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