Histone acetyltransferases (HATs), specifically p300/CBP and PCAF. Garcinol is a cell-permeable natural HAT inhibitor that also modulates multiple signaling pathways including NF-κB, STAT3, PI3K/AKT, MAPK, and Wnt/β-catenin. It also regulates microRNA expression and reverses epithelial-mesenchymal transition (EMT). [1, 2]
In leishmanicidal assays, garcinol (as guttiferone A) showed an IC₅₀ of 0.16 μM against L. donovani amastigotes. [1]
For anticholinesterase activity, garcinol (as garcinol) showed an IC₅₀ of 0.66 μM against AChE and 7.39 μM against BChE. [1]

Garcinol (as guttiferone A and guttiferone F) exhibited prominent leishmanicidal activity against Leishmania donovani axenic amastigotes, with IC₅₀ values of 0.16 μM (guttiferone A) and 0.20 μM (guttiferone F), which were more potent than the reference compound miltefosine (0.47 μM). [1]
Garcinol (as garcinol) showed potent acetylcholinesterase (AChE) inhibitory activity with an IC₅₀ of 0.66 μM, comparable to galanthamine (0.50 μM). It also showed butyrylcholinesterase (BChE) inhibitory activity with an IC₅₀ of 7.39 μM. Guttiferone A and guttiferone F were more active than galanthamine against BChE (IC₅₀ 2.77 and 3.50 μM, respectively). [1]
As a HAT inhibitor, garcinol suppresses the expression of more than 70% of evaluated genes in HeLa cells, many of which govern cell division, programmed death, and oncogenic processes. [2]
Garcinol induces cell cycle arrest at the S-phase and promotes apoptosis across multiple cancer cell lines, including ovarian, gastric, colon, oral squamous, glioblastoma, hepatocellular, melanoma, breast, pancreatic, and endometrial cancers. [2]
Garcinol downregulates cyclin D1 and cyclin D3, inhibits CDK2 and CDK4, and suppresses PI3K/AKT signaling. It activates p53 and thioredoxin reductase, leading to increased ROS accumulation, JNK activation, and DNA damage signaling. In MCF-7 breast cancer cells, it activates mitochondrial apoptosis through the ROS/JNK/ATF-2/Bcl-2 axis. [2]
Garcinol inhibits NF-κB signaling by interfering with IκBα phosphorylation and p65 nuclear translocation, reducing expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), anti-apoptotic factors (Bcl-2, Bcl-xL, survivin), and cell cycle regulators (cyclin D1). [2]
Garcinol upregulates tumor-suppressive miRNAs (miR-200 family, let-7 family, miR-218, miR-181) and downregulates oncogenic miRNAs (miR-196a, miR-495, miR-605, miR-638, miR-453, miR-21). [2]
Garcinol reverses epithelial-mesenchymal transition (EMT) by increasing E-cadherin and decreasing vimentin, ZEB1/2, and Snail expression. [2]
Garcinol inhibits VEGF expression and angiogenesis by suppressing NF-κB, STAT3, and HIF-1α pathways. [2]

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Two HNSCC cell lines (CAL27 and UMSCC1) are evaluated, and the growth of these lines is inhibited by garcinol (10-50 μM; 24-72 hours) in a time- and dose-dependent way [3]. In HNSCC cells, garcinol (10–50 μM; 24-72 hours) causes apoptosis [3]. In a time-dependent manner, garcinol (50 μM; 1-6 hours) suppresses the phosphorylation and degradation of constitutive IκBα [3].

In a primary effusion lymphoma (PEL) model using NOD/SCID mice engrafted with BCBL1-Luc cells, intraperitoneal administration of garcinol at 2.5 and 25 mg/kg every other day for three weeks suppressed tumor growth in a dose-dependent manner. [2]
In a prostate cancer xenograft model (PC-3 cells in nude mice), intraperitoneal or oral garcinol (50 mg/kg/day, 5 days/week) reduced tumor mass by >80%, increased NK cell activity, increased caspase-3 and -9 activity, decreased Bcl-2 and Bcl-xL, and increased Bax and Bad. [2]
In a breast cancer xenograft model (MDA-MB-231 cells in SCID mice), oral garcinol (5 mg/animal/day, 6 days/week for 4 weeks) inhibited NF-κB, vimentin, nuclear β-catenin, and EMT markers, while upregulating miR-200 and let-7 families. In a 4T1 breast cancer model, garcinol (1 mg/kg) combined with low-dose Taxol (5 mg/kg) enhanced therapeutic efficacy. [2]
In a pancreatic cancer KPC transgenic mouse model, dietary garcinol (0.05% in diet) delayed pancreatic intraepithelial neoplasia progression, enhanced NK cell activity, and improved survival when combined with gemcitabine. [2]
In colon carcinogenesis models (AOM/DSS), dietary garcinol (250 or 500 ppm) decreased tumor size and incidence, reduced COX-2, cyclin D1, and VEGF via inhibition of ERK1/2, PI3K/Akt, and Wnt/β-catenin pathways. [2]
In head and neck squamous cell carcinoma xenografts, garcinol (dose not specified) decreased tumor growth, reduced NF-κB, STAT3, MAPKs, p65, Ki-67, and CD31, and induced apoptosis without toxicity. Garcinol combined with cisplatin showed enhanced efficacy. [2]
In glioblastoma xenografts (U87MG cells in NOD/SCID mice), garcinol (1 mg/kg i.p.) reduced tumor size, resulted in 100% survival (vs. 60% in controls), reduced STAT3, pSTAT3, STAT5A, pSTAT5A, Ki-67, and Bcl-xL, and increased Bax and miR-181d expression. [2]
In skin cancer models (TPA-induced), topical or oral garcinol reduced ear inflammation, inhibited TPA-induced skin tumor development, reduced iNOS and COX-2 expression, and blocked NF-κB nuclear translocation. [2]
In lung cancer xenografts (A549 cells in NMRI nu/nu mice), garcinol (15 mg/kg i.p. for 40 days) reduced tumor size by approximately 50% and downregulated ALDH1A1 through DDIT3 activation. [2]
In leishmanicidal assays in vitro, guttiferone A and F showed IC₅₀ values of 0.16 and 0.20 μM against L. donovani, more potent than miltefosine (0.47 μM). However, these compounds showed cytotoxicity to L6 cells (IC₅₀ 7.34 and 5.4 μM, respectively), with selectivity indices of 46 and 27. [1]

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Garcinol (intraperitoneal injection; 1 and 2 mg/kg; 5 times per week for 4 weeks) effectively slows tumor development [3].

Acetylcholinesterase and Butyrylcholinesterase Inhibition Assay: The assay was performed using a slightly modified spectrophotometric method. Acetylthiocholine iodide and butyrylthiocholine chloride were used as substrates for AChE and BChE, respectively. DTNB (5,5′-dithiobis[2-nitrobenzoic acid]) was used to measure cholinesterase activity. A 100 mM sodium phosphate buffer (pH 8.0, 140 μL), DTNB (10 μL), test compound solution (20 μL), and enzyme solution (20 μL) were mixed and incubated for 15 minutes at 25°C. The reaction was initiated by adding 10 μL of substrate. Hydrolysis was monitored by formation of the yellow 5-thio-2-nitrobenzoate anion at 412 nm for 15 minutes. All reactions were performed in triplicate in 96-well plates. IC₅₀ values were calculated using EZ-Fit Enzyme Kinetics software. [1]

Leishmanicidal Activity Assay: Leishmania donovani axenic amastigotes (strain MHOM/ET/67/L82) were cultured in a 1:1 mixture of SM and SDM-79 medium (pH 5.4) with 10% heat-inactivated FBS. Compounds were serially diluted (30 to 0.041 μg/mL) in 96-well plates. Then 10⁵ amastigotes in 50 μL medium were added per well and incubated at 37°C under 5% CO₂ for 72 hours. Resazurin solution (12.5 mg in 100 mL distilled water, 10 μL) was added and incubated for 2-4 hours. Fluorescence was measured at 536 nm excitation and 588 nm emission. Miltefosine was used as a positive control. IC₅₀ values were calculated from sigmoidal inhibition curves. [1]
Cytotoxicity Assay (L6 cells): Rat skeletal muscle myoblasts (L6 cells) were seeded in 96-well plates at 2 × 10³ cells/100 μL in MEM with 10% heat-inactivated FBS. Three-fold serial dilutions of extracts (90 to 0.13 μg/mL) were added. Plates were incubated at 37°C with 5% CO₂ for 72 hours. Resazurin was added as a viability indicator, and fluorescence was measured at 536 nm excitation and 588 nm emission. Podophyllotoxin was used as a positive control. IC₅₀ values were calculated using Softmax Pro software. [1]
General Cell-Based Assays: Garcinol has been tested in numerous cancer cell lines including HeLa, MCF-7, MDA-MB-231, PC-3, A549, U87MG, CAL27, PANC-1, and others. Assays included MTT for viability, flow cytometry for cell cycle and apoptosis, Western blotting for protein expression, qPCR for gene expression, and miRNA arrays. Garcinol treatment typically induced S-phase arrest, increased ROS, activated caspases, altered Bcl-2 family protein expression, and modulated signaling pathways (NF-κB, STAT3, PI3K/AKT). [2]

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Cell proliferation assay[3]
Cell Types: CAL27 and UMSCC1 Cell
Tested Concentrations: 10, 25, 50 µM
Incubation Duration: 24, 48 and 72 hrs (hours)
Experimental Results: Inhibition of proliferation of both HNSCC cell lines in a time- and dose-dependent manner.

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Apoptosis analysis[3]
Cell Types: CAL27 and UMSCC1 Cell
Tested Concentrations: 10, 25, 50 µM
Incubation Duration: 24, 48 and 72 hrs (hours)
Experimental Results: Induction of apoptosis in HNSCC cells.

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Western Blot Analysis[3]
Cell Types: CAL27 Cell
Tested Concentrations: 50 µM
Incubation Duration: 1, 2, 4, 6 hrs (hours)
Experimental Results: Inhibition of constitutive IκBα phosphorylation and degradation in a time-dependent manner.

Animal/Disease Models: Fiveweeks old athymic nu/nu male mice bearing subcutaneousCAL27 tumors [3]
Doses: 1 and 2 mg/kg
Route of Administration: intraperitoneal (ip) injection; five times per week for 4 weeks
Experimental Results: Significant Inhibit tumor growth.

In silico ADMET analysis (using tools like SwissADME, pkCSM, or ADMETlab) predicts that garcinol has drug-like properties and is orally bioavailable. However, native garcinol suffers from poor aqueous solubility, rapid metabolism, and limited bioavailability. [2]
Nanoparticle formulations (liposomes, PLGA nanoparticles, BSA nanoparticles) have been developed to improve solubility, stability, and tumor targeting. In B16F10 melanoma tumor-bearing mice, ⁹⁹ᵐTc-labeled garcinol-loaded PLGA nanoparticles showed moderate accumulation in the tumor region. [2]

In leishmanicidal studies, garcinol (as guttiferone A) showed cytotoxicity to rat skeletal myoblast L6 cells with an IC₅₀ of 7.34 μM, giving a selectivity index of 46. Guttiferone F showed IC₅₀ of 5.4 μM (SI 27). [1]
In animal studies, garcinol was well-tolerated with no significant toxic effects, including no histological or pathological changes to liver, kidneys, lungs, heart, or esophagus at the doses used. [2]
In an acute safety study using Wistar rats, 40% garcinol formulation did not produce any adverse effects at a high single dose of 2000 mg/kg and can be classified as GHS Category 5 (unclassified). No treatment-related changes were observed at the highest tested dose of 100 mg/kg/day in 28-day and 90-day repeated-dose oral toxicity studies, as well as in reproductive and developmental toxicity assessments. [2]
In a clinical trial with human patients with non-alcoholic steatohepatitis, a combination of garcinol, curcuminoids, and piperine (GCP) showed no adverse toxicity effects over a 90-day period, with no significant changes in hematological and clinical laboratory parameters. [2]

[1]. Leishmanicidal and cholinesterase inhibiting activities of phenolic compounds from Allanblackia monticola and Symphonia globulifera. Molecules. 2007 Jul 20;12(8):1548-57.

[2]. Garcinol as an Epigenetic Modulator: Mechanisms of Anti-Cancer Activity and Therapeutic Potential. Int J Mol Sci. 2025 Nov 11;26(22):10917.

[3]. Garcinol, a polyisoprenylated benzophenone modulates multiple proinflammatory signalingcascades leading to the suppression of growth and survival of head and neck carcinoma. Cancer Prev Res (Phila). 2013 Aug;6(8):843-54.

Garcinol is a polyisoprenylated benzophenone derived primarily from the rind and leaves of Garcinia indica and Garcinia cambogia. It constitutes approximately 2-3% of the fruit rind content. [2]
Garcinol was first identified as a cell-permeable histone acetyltransferase (HAT) inhibitor in 2004, targeting p300/CBP and PCAF. This discovery provided a molecular explanation for its anti-cancer activity. [2]
Garcinol shares structural and functional similarities with curcumin, including the C3 ketonic group, hydroxylated phenolic rings, and an α,β-unsaturated ketone moiety that facilitates apoptosis induction. [2]
Garcinol has demonstrated anti-cancer effects across multiple malignancies, including ovarian, gastric, colon, oral squamous, glioblastoma, hepatocellular, melanoma, breast, pancreatic, endometrial, lymphoma, prostate, lung, head and neck, and skin cancers. [2]
Garcinol exhibits anti-inflammatory properties by inhibiting NF-κB and STAT3 signaling, reducing pro-inflammatory cytokine production (TNF-α, IL-6, IL-1β), and downregulating COX-2 and iNOS. [2]
Garcinol targets cancer stem cells (CSCs) by inhibiting STAT3 signaling, reducing NOTCH1 and Wnt/β-catenin signaling, and inducing mesenchymal-to-epithelial transition (MET). [2]
Nanoparticle formulations of garcinol (PLGA, liposomal, BSA-based) have been developed to overcome poor solubility and bioavailability issues, showing improved tumor accumulation and therapeutic efficacy in preclinical models. [2]
Garcinol analogs, including isogarcinol, epigarcinol, and cambogin, have also shown anti-cancer activities. [2]

C38H50O6

602.8

602.36

C, 75.71; H, 8.36; O, 15.92

78824-30-3

5490884

Light yellow to yellow solid powder

1.1±0.1 g/cm3

710.8±60.0 °C at 760 mmHg

235-236ºC

397.6±29.4 °C

0.0±2.4 mmHg at 25°C

1.563

11.26

3

6

10

44

1300

4

CC(=CC[C@@H]1C[C@@]2(C(=O)/C(=C(/C3=CC(=C(C=C3)O)O)\O)/C(=O)[C@@](C2=O)(C1(C)C)CC=C(C)C)C[C@H](CC=C(C)C)C(=C)C)C

DTTONLKLWRTCAB-UDFURZHRSA-N

InChI=1S/C38H50O6/c1-22(2)11-13-27(25(7)8)20-37-21-28(15-12-23(3)4)36(9,10)38(35(37)44,18-17-24(5)6)34(43)31(33(37)42)32(41)26-14-16-29(39)30(40)19-26/h11-12,14,16-17,19,27-28,39-41H,7,13,15,18,20-21H2,1-6,8-10H3/b32-31+/t27-,28+,37+,38-/m0/s1

(1S,3E,5R,7R)-3-[(3,4-dihydroxyphenyl)-hydroxymethylidene]-6,6-dimethyl-5,7-bis(3-methylbut-2-enyl)-1-[(2S)-5-methyl-2-prop-1-en-2-ylhex-4-enyl]bicyclo[3.3.1]nonane-2,4,9-trione

Garcinol; Camboginol; SCHEMBL19565392; 78824-30-3; CID 5281560

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~82.95 mM)
Ethanol : ~20 mg/mL (~33.18 mM)

Solubility in Formulation 1: 2.5 mg/mL (4.15 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)