2. PI3K/Akt/mTOR Stem Cell/Wnt NF-κB Apoptosis
  3. Akt GSK-3 Keap1-Nrf2 NF-κB Apoptosis
  4. Tovophyllin A

Tovophyllin A is an orally active xanthonoid compound. Tovophyllin A exerts neuroprotective effects against Parkinson's disease by activating the Akt/GSK3β signaling pathway. Tovophyllin A protects mouse models of liver injury by activating Nrf2. Tovophyllin A exhibits protective anti-inflammatory activity in mouse models of acute lung injury. Tovophyllin A inhibits the activation of NF-κB and subsequent release of pro-inflammatory cytokines. Tovophyllin A reduces apoptotic cell death (Apoptosis). Tovophyllin A has antiplasmodial activity. Tovophyllin A shows cytotoxic activity against lung epithelial cancer cells and breast cancer cells. Tovophyllin A can be used in research related to Parkinson's disease, liver injury, acute lung injury, lung epithelial cancer, and breast cancer.

For research use only. We do not sell to patients.

Tovophyllin A

Tovophyllin A Chemical Structure

CAS No. : 40738-44-1

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Tovophyllin A Related Antibodies

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Description

Tovophyllin A is an orally active xanthonoid compound. Tovophyllin A exerts neuroprotective effects against Parkinson's disease by activating the Akt/GSK3β signaling pathway. Tovophyllin A protects mouse models of liver injury by activating Nrf2. Tovophyllin A exhibits protective anti-inflammatory activity in mouse models of acute lung injury. Tovophyllin A inhibits the activation of NF-κB and subsequent release of pro-inflammatory cytokines. Tovophyllin A reduces apoptotic cell death (Apoptosis). Tovophyllin A has antiplasmodial activity. Tovophyllin A shows cytotoxic activity against lung epithelial cancer cells and breast cancer cells. Tovophyllin A can be used in research related to Parkinson's disease, liver injury, acute lung injury, lung epithelial cancer, and breast cancer[1][2][3].

In Vitro

Tovophyllin A (0.01-20 μM; 24 h) protects primary cortical neurons against MPP+- and paraquat (PQ)-induced neurotoxicity. After 24 h of co-treatment, it significantly increases cell viability in the MPP+ model at concentrations ≥0.1 μM and in the PQ model at concentrations ≥1 μM[1].
Tovophyllin A (serial twofold dilutions starting at 200 μM; 48 h) inhibits the proliferation of A549 human lung adenocarcinoma cells and MCF7 breast cancer cells, with IC50 values of 2.2 μM and 6.1 μM, respectively[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Tovophyllin A Related Antibodies

Cell Cytotoxicity Assay[3]

Cell Line: A549 (epithelial lung carcinoma), MCF7 (breast carcinoma)
Concentration: Serial twofold dilutions starting at 200 μM
Incubation Time: 48 h
Result: Exhibited cytotoxic activity against A549 cells with an IC50 of 2.2 μM.
Exhibited cytotoxic activity against MCF7 cells with an IC50 of 6.1 μM.
In Vivo

Tovophyllin A (5 mg/kg; single pre-treatment dose) alleviates MPTP (HY-W114750)-induced Parkinson's disease in male C57BL/6 mice by restoring motor function, preserving dopaminergic neurons in the substantia nigra pars compacta (SNc), and activating the Akt/GSK3β pro-survival signaling pathway[1].
Tovophyllin A (50-100 mg/kg; p.o.; once daily; 5 days) dose-dependently protects male BALB/c mice against Acetaminophen (HY-66005)-induced acute liver injury. At the dose of 100 mg/kg, it almost completely reverses hepatic necrosis, oxidative stress and the elevation of inflammatory mediators, and potently activates the Nrf2 cytoprotective pathway[2].
Tovophyllin A (50-100 mg/kg; p.o.; daily; 5 days prior to LPS challenge) improves LPS (HY-D1056)-induced acute lung injury in male BALB/c mice in a dose-dependent manner[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (male, 8-10 weeks old, 25-28 g, MPTP-induced Parkinson's disease)[1]
Dosage: 5 mg/kg
Administration: single pre-treatment dose
Result: Increased total distance traveled in the open field test to levels comparable to control mice.
Increased latency to fall in the rotarod test to levels comparable to control mice.
Alleviated MPTP-induced reductions in tyrosine hydroxylase (TH) protein levels in the midbrain, and striatum.
Increased the number of TH-positive dopaminergic neurons in the substantia nigra pars compacta (SNc).
Reversed MPTP-induced decreases in the ratio of phosphorylated Akt (Ser473) to total Akt in the midbrain, and striatum.
Reversed MPTP-induced decreases in phosphorylated GSK3β (Ser9) levels in the midbrain, and striatum.
Animal Model: BALB/c (male, 20-30 g, acetaminophen-induced acute liver injury)[2]
Dosage: 50 mg/kg; 100 mg/kg
Administration: p.o.; once daily; 5 days
Result: Reduced the elevated serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase levels induced by acetaminophen.
Reduced the elevated liver necrosis score and myeloperoxidase activity induced by acetaminophen.
Reduced the elevated liver malondialdehyde, 4-hydroxynonenal, and nitrite/nitrate levels induced by acetaminophen, while increasing the levels of superoxide dismutase, catalase, reduced glutathione, and total antioxidant capacity in the liver.
Increased the relative mRNA expression levels of Nrf2, NQO1, GCLm, GCLc, and HO-1 in the liver.
Increased the proportion of Nrf2-immunopositive and HO-1-immunopositive cells in the liver.
Reduced the elevated liver NF-κB levels induced by acetaminophen and decreases the proportion of NF-κB-immunopositive cells.
Reduced the elevated liver TNF-α, IL-1β, and IL-6 levels induced by acetaminophen.
Animal Model: BALB/c albino mice (male, 20-25 g, LPS-induced acute lung injury)[3]
Dosage: 50 mg/kg; 100 mg/kg
Administration: p.o.; daily; 5 days prior to LPS challenge
Result: Significantly reduced LPS-induced lung wet/dry ratio (W/D), total protein content in bronchoalveolar lavage fluid (BALF), and BALF lactate dehydrogenase (LDH) activity.
Inhibited LPS-induced total inflammatory cell count and differential inflammatory cell count (neutrophils, macrophages, lymphocytes) in BALF.
Decreased malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) levels in lung tissue, and increased superoxide dismutase (SOD) and reduced glutathione (GSH) levels in lung tissue.
Attenuated LPS-induced increases in lung tissue NF-κB levels and percentage of immunopositive cells, as well as decreases in lung tissue TNF-α and IL-6 levels and percentage of immunopositive cells, and decreases in lung tissue IL-1β levels.
Improved LPS-induced pathological damage in lung tissue.
Molecular Weight

462.53

Formula

C28H30O6
CAS No.
SMILES

O=C1C2=C(C(C/C=C(C)\C)=C(C=C2OC3=C(C/C=C(C)\C)C(O)=C4OC(C)(C)C=CC4=C31)O)O
Structure Classification
Initial Source
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Room temperature in continental US; may vary elsewhere.
Storage

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Purity & Documentation
References
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Tovophyllin A Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Tovophyllin A40738-44-1AktGSK-3Keap1-Nrf2NF-κBApoptosisPKBProtein kinase BGlycogen synthase kinase-3Glycogen synthase kinase 3Nuclear factor-κBNuclear factor-kappaBxanthonoid compoundParkinson's diseaseliver injuryacute lung injurylung epithelial cancerbreast cancerprimary cortical neuronsC57BL/6 miceBALB/c mice
Inhibitorinhibitorinhibit

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