Hydroxycitric acid tripotassium

Name: Hydroxycitric acid tripotassium
Brand: MedChemExpress
SKU: HY-W338584
Rating: 4.5 (1 reviews)

Cat. No.: HY-W338584 Purity: 98.0%: Data Sheet
COA

SDS
Handling Instructions
FAQs
Technical Support

Tripotassium hydroxycitrate is an orally active, multi-target, multi-bioactive organic acid. Tripotassium hydroxycitrate activates Nrf2 and its downstream molecule GPX4, increases glutathione levels, and thereby inhibits ferroptosis. Tripotassium hydroxycitrate activates the Nrf2/Keap1 and ACLY/NF-κB signaling pathways, upregulates the activities of antioxidant enzymes such as superoxide dismutase, reduces MDA content, thereby alleviating oxidative stress and renal tubular epithelial cell apoptosis, and improves pulmonary vascular and right ventricular remodeling. Tripotassium hydroxycitrate activates both the AMPK and mTORC1/S6K pathways, triggers the unfolded protein response, arrests the cancer cell cycle, and induces DNA fragmentation.

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

Hydroxycitric acid tripotassium Chemical Structure

CAS No. : 232281-44-6

Size	Stock	Quantity
Solid + Solvent (Highly Recommended)
10 mM * 1 mL in Water ready for reconstitution	In-stock	Estimated Time of Arrival: December 31
Solution
10 mM * 1 mL in Water	In-stock	Estimated Time of Arrival: December 31
Solid
25 mg	In-stock	Estimated Time of Arrival: December 31
50 mg	In-stock	Estimated Time of Arrival: December 31
100 mg	In-stock	Estimated Time of Arrival: December 31
200 mg	Get quote
500 mg	Get quote

or Bulk Inquiry

* Please select Quantity before adding items.

This product is a controlled substance and not for sale in your territory.

Customer Review

Based on 1 publication(s) in Google Scholar

Other Forms of Hydroxycitric acid tripotassium:

Hydroxycitric acid In-stock

1 Publications Citing Use of MCE Hydroxycitric acid tripotassium

•Polymers. 2025 Jun 18;17(12):1697. [Abstract]

Featured Recommendations

•Related Screening Libraries:

•Related Small Molecules:

•Related Proteins:

View All mTOR Isoform Specific Products:

View All Isoforms

mTOR mTORC1 mTORC2

View All NF-κB Isoform Specific Products:

View All Isoforms

NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

View All AMPK Isoform Specific Products:

View All Isoforms

NUAK1 NUAK2 AMPK AMPK α1β1γ1 AMPK α2β1γ1 AMPK α1β2γ1 AMPK α2β2γ1 BRSK1 BRSK2 HUNK AMPKα

View All Ribosomal S6 Kinase (RSK) Isoform Specific Products:

View All Isoforms

p70S6K RSK2 RSK3 RSK4

View All DNA/RNA Synthesis Isoform Specific Products:

View All Isoforms

RNASE L DNA Polymerases RNA Polymerases Helicases DNA Ligase

Biological Activity
Purity & Documentation
References
Customer Review

Description

In Vitro

Hydroxycitric acid (1-100 mM; 72 h) tripotassium potently inhibits the proliferation of K562, MEG-01, CML-T1, KYO-1 and SKH-1 chronic myeloid leukemia (CML) cell lines, with IC₅₀ values ranging from 3.73 to 11.34 mM; in contrast, it exerts no effect on normal mouse embryonic fibroblasts even at concentrations as high as 100 mM^[1].
Hydroxycitric acid (0.5-5 mM) tripotassium induces DNA fragmentation in K562 chronic myeloid leukemia (CML) cells^[1].
Hydroxycitric acid (0.5-10 mM; 48-72 h) tripotassium induces G₂/M cell cycle arrest in K562 chronic myeloid leukemia (CML) cells^[1].
Hydroxycitric acid (0.5-5 mM, 24-48 h) tripotassium activates AMPK by increasing the phosphorylation level of T172 in K562, MEG-01, KYO-1 and SKH-1 chronic myeloid leukemia (CML) cells, without altering the total protein level of AMPK^[1].
Hydroxycitric acid (0.5-1 mM; 24-48 h) tripotassium activates both the AMPK and mTORC1 pathways, and triggers the unfolded protein response in K562 chronic myeloid leukemia (CML) cells by upregulating the phosphorylation level of eIF2α and the expression level of ATF4^[1].
Hydroxycitric acid tripotassium (5-10 mM) significantly inhibits hypoxia-induced proliferation of human pulmonary artery smooth muscle cells at concentrations of 5 mM and 10 mM^[3].
Hydroxycitric acid tripotassium (matched to hypoxic/normoxic exposure conditions) inhibits the proliferation of human pulmonary artery smooth muscle cells under both normoxic and hypoxic conditions, with a stronger inhibitory effect on cells in a hypoxic environment^[3].
Hydroxycitric acid tripotassium (24 h) significantly inhibits hypoxia-induced migration of human pulmonary artery smooth muscle cells^[3].
Hydroxycitric acid tripotassium (overnight) significantly reduces hypoxia-induced reactive oxygen species production in human pulmonary artery smooth muscle cells^[3].
Hydroxycitric acid tripotassium (combined with hypoxic exposure) significantly reduces the expression of hypoxia-inducible factor-1 (HIF-1) mRNA in hypoxia-induced human pulmonary artery smooth muscle cells^[3].

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

Cell Cycle Analysis^[1]

Cell Line:	K562 CML cells
Concentration:	0.5, 5 and 10 mM
Incubation Time:	48 h; 72 h
Result:	Caused a significant accumulation of K562 cells in the G2/M phase of the cell cycle after 48 h treatment with 10 mM. Caused significant accumulation of cells in the G2/M phase after 72 h treatment with 5 mM and 10 mM.

Western Blot Analysis^[1]

Cell Line:	CML cell lines K562, MEG-01, KYO-1, SKH-1
Concentration:	0.5 and 1 mM (K562); 0.5 mM, 1 mM, and 5 mM (MEG-01, KYO-1, SKH-1)
Incubation Time:	24 h
Result:	Significantly increased phosphorylation of AMPKα at T172 in all tested CML cell lines without altering total AMPKα protein levels. Increased p-AMPKα levels by ~2-, ~6-, and ~4-fold in MEG-01 cells at 0.5 mM, 1 mM, and 5 mM doses, respectively. Increased p-AMPKα levels by ~1.5-, ~1.2-, and ~1-fold in KYO-1 cells at 0.5 mM, 1 mM, and 5 mM doses, respectively. Increased p-AMPKα levels by ~30-fold in SKH-1 cells at 5 mM dose.

Western Blot Analysis^[1]

Cell Line:	K562 CML cells
Concentration:	0.5 and 1 mM
Incubation Time:	24 and 48 h
Result:	Increased phosphorylation of AMPKα, ACC, p70 S6 kinase, S6 ribosomal protein, and eIF2α, and increased ATF4 protein levels. Indicated concurrent activation of the AMPK and mTORC1 pathways, plus activation of the unfolded protein response.\nShowed AMPK and ACLY interacted in K562 cells via co-immunoprecipitation. Reduced the total level of immunoprecipitated AMPK-ACLY complex, but the ratio of immunoprecipitated ACLY to AMPK remained unchanged compared to untreated controls, indicating no effect on the interaction between the two proteins.

Western Blot Analysis^[1]

Cell Line:	K562 CML cells
Concentration:	1 mM
Incubation Time:	24 and 48 h
Result:	Confirmed a fraction of AMPK co-eluted with ACLY, showing they are part of a common protein complex. Had no major effect on the migration of this protein complex.

In Vivo

Hydroxycitric acid (3 mg/kg; p.o.; daily; 25 days) tripotassium reduces the final tumor volume to 1/3 of the original level and significantly decreases tumor weight in a chronic myeloid leukemia xenograft mouse model^[1].
Hydroxycitric acid tripotassium (250 mg/kg; i.p.; administered daily for 4 consecutive weeks) significantly reduces monocrotaline-induced pulmonary arterial hypertension in rats, decreases RVSP by 28.97% via anti-inflammatory and anti-fibrotic effects, and ameliorates right ventricular and pulmonary vascular remodeling^[3].
Tripotassium hydroxycitrate (250 mg/kg; i.p.; administered daily for 4 consecutive weeks) significantly alleviates hypoxia-induced pulmonary arterial hypertension in rats, reduces RVSP by 17.5% via anti-inflammatory and antioxidant effects, and improves right ventricular and pulmonary vascular remodeling^[3].

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

Animal Model:	NOD.Cg-PrkdcscidIl2rgtm1WjI/SzJ (NSG) (male, 8-10 weeks old)^[1]
Dosage:	3 mg/kg
Administration:	p.o.; daily; 25 days
Result:	Reduced final average tumor volume.

Animal Model:	Sprague-Dawley (male, 8-10 weeks old, monocrotaline-induced model)^[3]
Dosage:	250 mg/kg/day
Administration:	i.p.; daily; 4 weeks
Result:	Reduced right ventricular systolic pressure (RVSP) from 47.60 mmHg to 33.81 mmHg . Decreased right ventricular index from 39.7% to 26.48%. Decreased right ventricular weight/body weight ratio from 0.87 mg/g to 0.63 mg/g. Reduced right ventricular fibrotic area from 15.40% to 8.82%. Attenuated upregulated mRNA levels of α-SMA, collagen-1, and collagen-3. Reduced pulmonary arteriole medium film layer thickness from 30.14 μm to 21.86 μm. Decreased vascular wall area ratio from 0.65% to 0.51%. Reduced serum levels of IL-6 from 121.20 pg/mL to 59.73 pg/mL, and TNF-α from 19.13 pg/mL to 11.82 pg/mL. Suppressed elevated p-IκBα and p65 protein expressions in lung tissue.

Animal Model:	Sprague-Dawley (male, 8-10 weeks old, hypobaric hypoxia-induced model)^[3]
Dosage:	250 mg/kg/day
Administration:	i.p.; daily; 4 weeks
Result:	Reduced RVSP from 42.30 mmHg to 34.9 mmHg. Decreased right ventricular index from 32.62% to 26.11%. Reduced right ventricular fibrotic area from 8.94% to 5.80%. Attenuated upregulated collagen-1 mRNA levels. Reduced pulmonary arteriole medium film layer thickness from 33.57 μm to 22.29 μm. Decreased vascular wall area ratio from 0.71% to 0.45%. Reduced serum IL-1β levels from 66.50 pg/mL to 55.80 pg/mL. Increased cardiac SOD concentration from 7.31 U/mg to levels significantly higher than hypoxia-only controls. Reduced cardiac H₂O₂ concentration from 8.76 mM to levels significantly lower than hypoxia-only controls.

Molecular Weight

322.39

Formula

C₆H₅K₃O₈

CAS No.

232281-44-6

Appearance

Solid

Color

White to off-white

SMILES

O=C(CC(C(O)=O)(C(C(O[K])=O)O)O[K])O[K]

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Solvent & Solubility

In Vitro:

H₂O : 125 mg/mL (387.73 mM; Need ultrasonic)

Preparing
Stock Solutions

Concentration Solvent Mass	1 mg	5 mg	10 mg

1 mM	3.1018 mL	15.5092 mL	31.0183 mL
5 mM	0.6204 mL	3.1018 mL	6.2037 mL
10 mM	0.3102 mL	1.5509 mL	3.1018 mL

View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

Molarity Calculator
Dilution Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

This equation is commonly abbreviated as: C₁V₁ = C₂V₂

Concentration _(start)

Volume _(start)

Concentration _(final)

Volume _(final)

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage

mg/kg

Animal weight
(per animal)

Dosing volume
(per animal)

μL

Number of animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Calculation results:

Working solution concentration: mg/mL

This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.

The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact MedChemExpress (MCE).

Purity & Documentation

Purity: 98.0%

Select Batch:

Data Sheet (289 KB) SDS (393 KB)

COA (252 KB) HNMR (251 KB) MS (75 KB)

Handling Instructions (2659 KB)

References

[1]. Verrelli D, et al. Hydroxycitric Acid Inhibits Chronic Myelogenous Leukemia Growth through Activation of AMPK and mTOR Pathway. Nutrients. 2022;14(13):2669. Published 2022 Jun 27. [Content Brief]

[2]. Yang D, et al. Hydroxycitric acid inhibits ferroptosis and ameliorates benign prostatic hyperplasia by upregulating the Nrf2/GPX4 pathway. World J Urol. 2025;43(1):318. Published 2025 May 20. [Content Brief]

[3]. Wang S, et al. Hydroxycitric Acid Tripotassium Hydrate Attenuates Monocrotaline and Hypoxia-Induced Pulmonary Hypertension in Rats. Int Heart J. 2024;65(2):318-328. [Content Brief]

[4]. Yang B, et al. Hydroxycitric acid prevents hyperoxaluric-induced nephrolithiasis and oxidative stress via activation of the Nrf2/Keap1 signaling pathway. Cell Cycle. 2023;22(17):1884-1899. [Content Brief]

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg

H₂O	1 mM	3.1018 mL	15.5092 mL	31.0183 mL	77.5458 mL
	5 mM	0.6204 mL	3.1018 mL	6.2037 mL	15.5092 mL
	10 mM	0.3102 mL	1.5509 mL	3.1018 mL	7.7546 mL
	15 mM	0.2068 mL	1.0339 mL	2.0679 mL	5.1697 mL
	20 mM	0.1551 mL	0.7755 mL	1.5509 mL	3.8773 mL
	25 mM	0.1241 mL	0.6204 mL	1.2407 mL	3.1018 mL
	30 mM	0.1034 mL	0.5170 mL	1.0339 mL	2.5849 mL
	40 mM	0.0775 mL	0.3877 mL	0.7755 mL	1.9386 mL
	50 mM	0.0620 mL	0.3102 mL	0.6204 mL	1.5509 mL
	60 mM	0.0517 mL	0.2585 mL	0.5170 mL	1.2924 mL
	80 mM	0.0388 mL	0.1939 mL	0.3877 mL	0.9693 mL
	100 mM	0.0310 mL	0.1551 mL	0.3102 mL	0.7755 mL

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.