Pinusolide
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Pinusolide is an AMPK activator and PAF receptor antagonist. Pinusolide activates AMPK, phosphorylates ACC, enhances IRS-1 tyrosine phosphorylation, boosts glucose uptake, and modulates insulin signaling. Pinusolide inhibits caspase-3/7 activation, intracellular calcium elevation, reactive oxygen species overproduction, lipid peroxidation, and tumor cell proliferation. Pinusolide stabilizes superoxide dismutase activity, reduces apoptotic hallmarks, induces mitochondrial pathway apoptosis, and triggers DNA fragmentation. Pinusolide can be used for the research of type 2 diabetes, neurodegenerative diseases, acute lymphoblastic leukemia, acute myeloid leukemia, and Burkitt lymphoma.
For research use only. We do not sell to patients.
- Purity: 99.93%
- CAS No.: 31685-80-0
- Formula: C21H30O4
- Molecular Weight:346.46
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Storage:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Biological Activity
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Caspase 3 |
Caspase-7 |
AMPK |
Pinusolide (10-100 μM; 24 h) is non-cytotoxic to L6 myotubes at concentrations up to 100 μM[1].
Pinusolide (10-20 μM; 0.5-24 h) dose-dependently and time-dependently increases AMPK and ACC phosphorylation in L6 myotubes, with peak effects at 20 μM for 2 h and 10 μM at 2 h respectively[1].
Pinusolide (10-20 μM; 2 h) significantly increases glucose uptake in L6 myotubes, with 72% and 78% induction at 10 μM and 20 μM respectively after 2 h incubation[1].
Pinusolide (10 μM; 2 h) has its induced AMPK/ACC phosphorylation blocked and mediated glucose uptake reduced by Compound C (HY-13418A) in L6 myotubes, confirming AMPK dependence[1].
Pinusolide (10 μM; 2 h) requires LKB1 for induced AMPK activation and glucose uptake in L6 myotubes[1].
Pinusolide (10 μM; 2 h) improves high glucose-induced insulin resistance in L6 myotubes by restoring AMPK activation, reducing JNK phosphorylation, and reinstating insulin-stimulated IRS-1/Akt phosphorylation and glucose uptake[1].
Pinusolide (10 μM; 2 h) improves high glucose-induced insulin resistance in L6 myotubes via an AMPK-dependent mechanism, as AMPKα2 knockdown abolishes all beneficial effects[1].
Pinusolide (5.0 μM; 1 h pretreatment, 18 h STS exposure) protects primary mixed rat cortical cells from staurosporine-induced apoptotic morphological changes[2].
Pinusolide (1.0-5.0 μM; 1 h pretreatment, 18 h STS exposure) preserves superoxide dismutase activity reduced by staurosporine in primary rat cortical cells, with greater preservation at 5.0 μM[2].
Pinusolide (1.0-5.0 μM; 1 h pretreatment, 12 h STS exposure) reduces staurosporine-induced caspase-3/7 activation in primary rat cortical cells[2].
Pinusolide (5-100 μM; 24-48 h) inhibits the proliferation of Burkitt lymphoma BJAB cells in a concentration-dependent manner, with up to 44% inhibition after 24 h and up to 86% inhibition after 48 h of treatment[3].
Pinusolide (50-100 μM; 48 h) induces mitochondrial permeability transition in Burkitt lymphoma BJAB cells, with 86.36% of cells exhibiting low mitochondrial membrane potential after 48 h treatment with 100 μM pinusolide[3].
Pinusolide (50-100 μM; 72 h) induces apoptosis in Burkitt lymphoma BJAB cells, with 69.52% of cells showing DNA fragmentation after 72 h treatment with 100 μM pinusolide, accompanied by characteristic apoptotic morphological changes[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:L6 myotubes
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Concentration:10 μM; 20 μM
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Incubation Time:0.5 h; 1 h; 2 h; 4 h; 8 h; 24 h
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Result:Increased the phosphorylation of AMPK and ACC in a dose-dependent manner, with maximal increases observed at 20 μM after 2 h incubation.
Increased AMPK and ACC phosphorylation in a time-dependent manner, with peak phosphorylation observed at 2 h after treatment with 10 μM pinusolide, and elevated phosphorylation sustained up to 24 h.
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Cell Line:compound C-pretreated L6 myotubes
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Concentration:10 μM; 10 μM plus 10 μM Compound C
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Incubation Time:2 h
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Result:Induced phosphorylation of AMPK and ACC which was completely abrogated by compound C pretreatment.
Increased glucose uptake to 3.3 pmol/mg/min (1.7-fold induction, P < 0.05) versus untreated cells (1.9 pmol/mg/min), but compound C pretreatment reduced this uptake to 2.0 pmol/mg/min (40% of pinusolide-only levels, P < 0.05).
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Cell Line:LKB1 siRNA-transfected L6 myotubes
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Concentration:10 μM
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Incubation Time:2 h
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Result:Robustly increased AMPK and ACC phosphorylation and significantly increased glucose uptake in control siRNA-transfected cells.
Failed to increase AMPK and ACC phosphorylation and had no significant effect on glucose uptake in LKB1 siRNA-transfected cells.
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Cell Line:high glucose-exposed L6 myotubes
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Concentration:10 μM; 10 μM plus 30 mM glucose plus 100 nM
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Incubation Time:2 h
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Result:Increased AMPK and ACC phosphorylation in high glucose-exposed L6 myotubes.
Reduced high glucose-induced JNK phosphorylation.
Restored insulin-stimulated tyrosine phosphorylation of IRS-1 and Akt.
Improved insulin-stimulated glucose uptake.
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Cell Line:Burkitt lymphoma BJAB cells
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Concentration:5 μM; 10 μM; 20 μM; 30 μM; 50 μM; 100 μM
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Incubation Time:24 h; 48 h
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Result:Inhibited BJAB cell proliferation in a concentration-dependent manner.
Reduced cell count from 4.14 x105/mL (control) to 2.24 x105/mL at 50 μM and 2.46 x105/mL at 100 μM after 24 h, reaching 44% maximum proliferation inhibition.
Reduced cell count from 13.35 x105/mL (control) to 1.72 x105/mL at 100 μM after 48 h, reaching up to 86% proliferation inhibition.
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Cell Line:Burkitt lymphoma BJAB cells
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Concentration:50 μM; 100 μM
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Incubation Time:72 h
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Result:Induced apoptosis in BJAB cells in a concentration-dependent manner.
Caused 0.06% of cells to be apoptotic at 50 μM after 72 h.
Caused 69.52% of cells to be apoptotic at 100 μM after 72 h.
Triggered characteristic apoptotic morphological changes including cell shrinking, fragmentation, and formation of apoptotic bodies containing chromatin bits in nearly all cells treated with 100 μM for 72 h.
Chemical Information
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CAS No. 31685-80-0
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Appearance Solid
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Molecular Weight 346.46
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Formula C21H30O4
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Color White to off-white
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SMILES
C[C@@]1([C@H]2CCC3=CCOC3=O)[C@](CCC2=C)([H])[C@](C)(CCC1)C(OC)=O
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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, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Purity & Documentation
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Data Sheet (282 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1]. Hwang SL, et al. Pinusolide improves high glucose-induced insulin resistance via activation of AMP-activated protein kinase. Biochem Biophys Res Commun. 2013;437(3):374-379. [Content Brief]
[2]. Koo KA, et al. Pinusolide and 15-methoxypinusolidic acid attenuate the neurotoxic effect of staurosporine in primary cultures of rat cortical cells. Br J Pharmacol. 2007;150(1):65-71. [Content Brief]
[3]. Shults EE, et al. Gram-scale synthesis of pinusolide and evaluation of its antileukemic potential. Bioorg Med Chem Lett. 2006;16(16):4228-4232. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)