2. Vitamin D Related/Nuclear Receptor Immunology/Inflammation NF-κB Metabolic Enzyme/Protease Cell Cycle/DNA Damage Neuronal Signaling Apoptosis
  3. Pregnane X Receptor (PXR) COX NF-κB Amylases β-glucuronidase DNA/RNA Synthesis Amyloid-β NOD-like Receptor (NLR) Pyroptosis
  4. Garcinoic acid

Garcinoic acid is an orally active anti-inflammatory agent that crosses the blood-brain barrier. Garcinoic acid also enhances efferocytosis and enzyme/receptor regulation, and selectively inhibits human COX-2, porcine α-amylase, Saccharomyces cerevisiae α-glucosidase and human DNA polymerase β (IC50=11 μM), as well as activates human PXR. Garcinoic acid enhances macrophage efferocytosis via receptors such as MerTK and LRP-1, and promotes the production of pro-resolving lipid mediators. Garcinoic acid inhibits NF-κB activation and pro-inflammatory cytokine secretion, interferes with Aβ aggregation, downregulates NLRP3 inflammasome activity, and binds to targets including CD44 and EGFR to inhibit leukemia cell proliferation. The pharmacological activities of Garcinoic acid, such as antioxidant, anti-inflammatory and lipid metabolism-regulating effects, are widely used in studies related to various diseases including atherosclerosis, Alzheimer's disease, type 2 diabetes, inflammatory bowel disease and viral pneumonia.

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Garcinoic acid

Garcinoic acid Chemical Structure

CAS No. : 91893-83-3

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Garcinoic acid Related Antibodies

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NLRP3 NLRP1 NOD1 NOD2

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Description

Garcinoic acid is an orally active anti-inflammatory agent that crosses the blood-brain barrier. Garcinoic acid also enhances efferocytosis and enzyme/receptor regulation, and selectively inhibits human COX-2, porcine α-amylase, Saccharomyces cerevisiae α-glucosidase and human DNA polymerase β (IC50=11 μM), as well as activates human PXR. Garcinoic acid enhances macrophage efferocytosis via receptors such as MerTK and LRP-1, and promotes the production of pro-resolving lipid mediators. Garcinoic acid inhibits NF-κB activation and pro-inflammatory cytokine secretion, interferes with Aβ aggregation, downregulates NLRP3 inflammasome activity, and binds to targets including CD44 and EGFR to inhibit leukemia cell proliferation. The pharmacological activities of Garcinoic acid, such as antioxidant, anti-inflammatory and lipid metabolism-regulating effects, are widely used in studies related to various diseases including atherosclerosis, Alzheimer's disease, type 2 diabetes, inflammatory bowel disease and viral pneumonia[1][2][3][4][5][6][7].

IC50 & Target

hCOX-2

 

In Vitro

Garcinoic acid (2.5 μM; 24 h, 14-24 h) inhibits LPS-induced Cox2 and iNos protein expression in murine RAW264.7 macrophages, reducing iNos levels to 17% of LPS control at 2.5 μM[1].
Garcinoic acid (0.02-100 μM; 72 h incubation with cells, following 24 h initial cell culture) inhibits proliferation of KASUMI-1, HL-60, THP-1, RS4;11, and MOLT-4 leukemia cell lines with IC50 values ranging from 18.04 μM to 49.01 μM, showing the strongest activity against HL-60 cells[2].
Garcinoic acid (0.25-5 μM; 24 h) does not reduce the viability of mouse bone marrow-derived macrophages[3].
Exogenous Lipoxin A4 (100 nM; 2 h) or Resolvin E1 (10 nM; 30 min) restores garcinoic acid (1 μM; 24 h)-enhanced efferocytosis in mouse bone marrow-derived macrophages with Nrf2 silenced or HO-1 inhibited[3].
Garcinoic acid (1-50 μM; 24 h) dose-dependently upregulates PXR, CYP3A4, and MDR1 expression in HepG2 cells, with the response dependent on functional PXR[5].
Garcinoic acid (25 μM; 24 h pre-incubation, 24 h incubation with Aβ(1-42)) restores and stimulates ApoE efflux in mouse cortical astrocytes via a PPARγ-independent mechanism, up-regulates PPARγ and PXR expression, and increases expression of the PXR-regulated genes CYP4F2 and MDR1 in these cells at 25 μM[6].
Garcinoic acid (5 μM; 6 h) suppresses cleavage of GSDMD into the pyroptosis-inducing NT-GSDMD fragment in LPS/ATP-stimulated murine J774A.1 macrophages after 6 hours of total incubation[8].

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

Garcinoic acid Related Antibodies

Western Blot Analysis[1]

Cell Line: murine RAW264.7 macrophages
Concentration: 2.5 μM
Incubation Time: 24 h (pre-incubated); 14 h (co-incubated with LPS for Cox2); 24 h (co-incubated with LPS for iNos)
Result: Did not detectably modulate basal Cox2 or iNos protein levels.
Reduced Cox2 protein expression to 67% relative to LPS-only controls.
Reduced iNos protein expression to 17% relative to LPS-only controls.

Cell Proliferation Assay[2]

Cell Line: KASUMI-1, HL-60, THP-1, RS4;11, MOLT-4
Concentration: 0.02-100 μM
Incubation Time: 72 h (incubation with cells, following 24 h initial cell culture)
Result: Inhibited proliferation of KASUMI-1 cells, with an IC50 value of 30.81 μM.
Inhibited proliferation of HL-60 cells, with an IC50 value of 18.04 μM.
Inhibited proliferation of THP-1 cells, with an IC50 value of 49.01 μM.
Inhibited proliferation of RS4;11 cells, with an IC50 value of 42.87 μM.
Inhibited proliferation of MOLT-4 cells, with an IC50 value of 26.73 μM.

Cell Viability Assay[3]

Cell Line: mouse bone marrow-derived macrophages (BMDMs)
Concentration: 0.25-5 μM
Incubation Time: 24 h
Result: Showed no cytotoxic effect on BMDMs, with cell viability remaining near 100% across all groups.
In Vivo

Garcinoic acid (1 mg/kg; i.p.; weekly; 8 weeks) significantly reduces intra-plaque nitrotyrosine levels and modulates select systemic and local immune cell populations in high fat diet-fed ApoE-/- mice without altering atherosclerotic plaque size or systemic inflammatory mediator levels[1].
Garcinoic acid (1 mg/kg; i.p.; daily; from 7 days pre-DSS exposure until study end) attenuates DSS (HY-116282C)-induced colitis in male C57BL/6 mice by restoring efferocytosis, increasing specialized pro-resolving lipid mediator levels, and activating Nrf2 signaling[3].
Garcinoic acid (5-100 mg; p.o.; single bolus) acts as a selective PXR agonist in mice, dose-dependently increasing PXR, CYP3A11, and MDR1 expression in liver and intestinal tissue at well-tolerated doses ≤25 mg, while higher doses cause mortality[5].
Garcinoic acid (5-25 mg; p.o.; single dose) dose-dependently up-regulates PPARγ, ApoE, and PXR expression in the brain of healthy C57Bl/6 mice, with significant effects observed at doses ≥5 mg[6].
Garcinoic acid (200 mg/kg; p.o.; daily; 10 days) significantly reduces amyloid β plaque number and deposition in the brain of TgCRND8 Alzheimer's disease model mice, while up-regulating ApoE and MDR1 expression[6].

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

Animal Model: C57Bl/6 background (8-week-old male, 25-28 g, apolipoprotein E knockout, high fat diet-fed for 8 weeks)[1]
Dosage: 1 mg/kg
Administration: i.p.; weekly; 8 weeks
Result: Decreased intra-plaque nitrotyrosine levels to 50% of control levels.
Downregulated blood CD4 positive T cells by 14.8%.
Increased blood natural killer (NK) cells from 3.2% to 5.6%.
Increased blood natural killer T (NKT) cells from 0.2% to 0.6%.
Upregulated spleen NK cells from 2.0% to 2.8%.
Showed no significant changes in body/organ weight, plasma lipid profile, total lesion size, necrotic core area, lipid content, collagen content, VCAM-1 levels, CD68 levels, MCP-1 levels, IL1β levels, plasma NO levels, or plasma prostanoid levels.
Animal Model: C57BL/6 (5-week-old male; DSS-induced colitis)[3]
Dosage: 1 mg/kg
Administration: i.p.; daily; from 7 days pre-DSS exposure until study end
Result: Prevented DSS-induced reduction in colon length.
Increased body weight compared to DSS-only mice.
Reduced Disease Activity Index (DAI) scores compared to DSS-only mice.
Restored colonic tissue architecture, reducing epithelial degeneration, inflammatory cell infiltration, and crypt loss compared to DSS-only mice.
Increased the ratio of macrophage-associated apoptotic cells to free apoptotic cells in colon tissue, restoring efferocytosis to control levels.
Increased plasma levels of Lipoxin A4, Resolvin D2, and Resolvin E1 compared to DSS-only mice.
Increased colon tissue levels of Lipoxin A4, Resolvin D2, and Resolvin E1 compared to DSS-only mice.
Increased colon tissue protein levels of Nrf2 and NAD(P)H:quinone oxidoreductase (NQO1) compared to control mice.
Animal Model: TgCRND8 transgenic (5-month-old, 14-15-month-old)[6]
Dosage: 200 mg/kg
Administration: p.o.; daily; 10 days
Result: Reduced 10-50 μm2 amyloid β plaques from ~400 to ~300, 50-200 μm2 plaques from ~100 to ~50, and 200-400 μm2 plaques from ~50 to ~10 (all significant vs. untreated Tg mice, p < 0.05 or p < 0.005) in 14-15-month-old Tg mice.
Confirmed decreased amyloid β deposition in both 5-month-old and 14-15-month-old Tg mice via Congo Red staining.
Increased ApoE and MDR1 expression in the hippocampus of Tg mice significantly.
Reached concentrations between 0.8 and 10.3 ppm (ng/mg of proteins) in the parietal cortex and hippocampus of treated Tg mice.
Molecular Weight

426.59

Formula

C27H38O4
CAS No.
SMILES

CC1=C2C(CC[C@](C)(O2)CC/C=C(C)/CC/C=C(C)/CC/C=C(C)/C(O)=O)=CC(O)=C1
Structure Classification
Initial Source
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Garcinoic acid Related Classifications

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Help & FAQs
  • 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:

Garcinoic acid91893-83-3Pregnane X Receptor (PXR)COXNF-κBAmylasesβ-glucuronidaseDNA/RNA SynthesisAmyloid-βNOD-like Receptor (NLR)PyroptosisPregnane X ReceptorCyclooxygenaseNuclear factor-κBNuclear factor-kappaBGUSBβ-amyloid peptideAβAbetaCOX-2α-glucosidaseDNA polymerase βLRP-1α-amylaseHL-60TIM4PXRMerTKRAW264.7 macrophagesInhibitorinhibitorinhibit

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