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Fig. 1 · Structure
Cat. No.
A10961
CAS No.
77-52-1
Formula
C30H48O3
Mol. Weight
456.7

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Ursolic acid (Malol)

Cat. No. A10961 CAS 77-52-1
Ursolic acid(Malol) is a pentacyclic triterpene acid, used in cosmetics, that is also capable of inhibiting various types of cancer cells by inhibiting the STAT3 activation pathway and human fibrosarcoma cells by reducing the expression of matrix metalloproteinase-9 by acting through the glucocorticoid receptor.

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Publications for Ursolic acid

1 publication citing this product

  1. Abouzar Karimi, .et al. , Food Bioprod Process, 2020, 124: 329-341
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Biological Activity

Bioactivity / Mechanism

In differentiated 3T3-L1 adipocytes, ursolic acid increased glucose-analogue uptake and signaling-associated phosphorylation. Wortmannin reduced uptake with ursolic acid plus insulin but had only a weak effect without added insulin. The inhibitor controls do not isolate a ursolic-acid-specific effect, and these observations do not establish a selective direct molecular target. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Cellular Effect

Cell Line Activity Value Description Reference
4T1 IC50 44.08 μM Cytotoxicity activity against mouse 4T1 cells assessed as cell growth inhibition after 48 hrs by MTT assay [PMID: 30433783]
518A2 EC50 14.7 μM Cytotoxicity against human 518A2 cells after 96 hrs by SRB assay [PMID: 28033541]
518A2 EC50 14.7 μM Cytotoxicity against human 518A2 cells after 96 hrs by SRB assay [PMID: 26750249]
518A2 EC50 14.7 μM Cytotoxicity against human 518A2 cells assessed as cell survival after 96 hrs by SRB assay [PMID: 26177446]
518A2 EC50 14.7 μM Cytotoxicity against human 518A2 cells assessed as reduction in cell proliferation after 96 hrs by sulforhodamine B assay [PMID: 27149037]
8505C EC50 13.5 μM Cytotoxicity against human 8505C cells after 96 hrs by SRB assay [PMID: 28033541]
8505C EC50 13.5 μM Cytotoxicity against human 8505C cells assessed as cell survival after 96 hrs by SRB assay [PMID: 26177446]
A2780 EC50 11.7 μM Cytotoxicity against human A2780 cells assessed as reduction in cell viability incubated for 96 hrs by SRB assay [PMID: 31718946]
A2780 EC50 11.7 μM Cytotoxicity against human A2780 cells after 96 hrs by SRB assay [PMID: 28033541]
A2780 EC50 11.7 μM Cytotoxicity against human A2780 cells after 96 hrs by SRB assay [PMID: 26750249]
A2780 EC50 11.7 μM Cytotoxicity against human A2780 cells assessed as reduction in cell proliferation after 96 hrs by sulforhodamine B assay [PMID: 27149037]
A-375 IC50 30.88 μM Cytotoxicity activity against human A375 cells assessed as cell growth inhibition after 48 hrs by MTT assay [PMID: 30433783]
A549 IC50 11.4 μM Cytotoxicity against human A549 cells after 72 hrs by MTT assay [PMID: 22959527]
A549 EC50 15.5 μM Cytotoxicity against human A549 cells after 96 hrs by SRB assay [PMID: 28033541]
A549 EC50 15.5 μM Cytotoxicity against human A549 cells after 96 hrs by SRB assay [PMID: 26750249]
A549 EC50 15.5 μM Cytotoxicity against human A549 cells assessed as cell survival after 96 hrs by SRB assay [PMID: 26177446]
A549 EC50 15.5 μM Cytotoxicity against human A549 cells assessed as reduction in cell proliferation after 96 hrs by sulforhodamine B assay [PMID: 27149037]
A549 IC50 18.42 μM Cytotoxicity activity against human A549 cells assessed as cell growth inhibition after 48 hrs by MTT assay [PMID: 30433783]
A549 IC50 21.6 μM Antiinflammatory activity against human A549 cells assessed as inhibition of IL-1-alpha-induced ICAM1 expression treated after 1 hr before IL1alpha challenge [PMID: 15730243]
A549 IC50 33 μM Cytotoxicity against human A549 cells after 48 hrs by MTT assay [PMID: 26854375]

20 records · Scroll to view more

In Vitro Studies

After 2 h, ursolic acid at 2.5, 5 and 10 µM increased fluorescent glucose-analogue uptake by 17%, 29% and 35%, respectively, without added insulin. Insulin-containing arms showed a further increase. A separate 24 h immunoblot experiment reported increased GLUT4 protein without a change in GLUT1. [1]

Glucose uptake and wortmannin sensitivity in differentiated adipocytes

Cell-based study · Differentiated mouse 3T3-L1 adipocytes [1]

UA increased fluorescent glucose-analogue uptake without added insulin and further increased uptake with insulin. Wortmannin reduced uptake in the UA-plus-insulin condition but only weakly affected the UA response without insulin. A missing insulin-plus-wortmannin control without UA prevents isolating a UA-specific inhibitor effect.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Uptake without added insulin relative to 0 µM UAReported relative increase 17%, 29% and 35% at 2.5, 5 and 10 µM UA, respectively[1]
Uptake in UA-containing arms with versus without wortmannin, under basal or insulin-containing conditionsDirection Uptake reduced in UA-plus-insulin arms; uptake with UA but no added insulin only weakly affected[1]

Literature-Reported Treatment Conditions

Treatment concentration
UA 2.5, 5 or 10 µM; inhibitor experiment UA 10 µM with wortmannin 1 µM
Exposure duration
UA exposure 2 h; wortmannin pretreatment 30 min before the 2 h UA/wortmannin incubation
Method
Fluorescent NBD-glucose uptake assay after overnight starvation; no-UA and insulin-only comparisons.
Co-treatment
Parallel arms without or with insulin 1 µg/mL; mechanistic arms include wortmannin.
Reported limits
UA treatment solvent and matched solvent-control composition are not stated. n=3 is not defined as independent cultures or technical replicates. Figure 3 lacks a wortmannin-plus-insulin arm without UA and a wortmannin-only arm, limiting UA-specific pathway attribution.
Methods and source locations

Compound reported in the paper: Ursolic acid; Compound label in the paper: UA

Evidence concerns the authors’ reported ursolic acid material; it does not validate A10961 lots, formulations or clinical efficacy.

Results: UA increases glucose uptake; UA stimulates glucose uptake through the PI3K pathway; Figures 2–3; Methods: Measurement of glucose uptake

Uptake without added insulin relative to 0 µM UA: NBD-glucose fluorescence, 2 h; Figure 2 reports means ± SD (n=3), significance versus 0 µM UA. Values are from Results text, not graph digitization. — Results: UA increases glucose uptake; Figure 2 and caption

Uptake in UA-containing arms with versus without wortmannin, under basal or insulin-containing conditions: UA 10 µM ± insulin 1 µg/mL ± wortmannin 1 µM; means ± SD (n=3). Comparator arms and qualitative direction checked in Figure 3; no inhibition percentage inferred. — Results: UA stimulates glucose uptake through the PI3K pathway; Figure 3 and caption

Signaling-associated protein changes after 24 h in adipocytes

Cell-based study · Differentiated mouse 3T3-L1 adipocytes [1]

At 10 µM UA, the authors reported increased phosphorylation-associated signals for PDK, AKT, PKC and AS160 and increased GLUT4 protein, with no change in GLUT1. Wortmannin-sensitive changes support pathway involvement; the immunoblots do not demonstrate direct kinase activation or binding.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
PDK, AKT, PKC and AS160 phosphorylation-associated signalsReported direction Increased with UA; the authors describe inhibition by wortmannin[1]
Total GLUT4 and GLUT1 protein expressionReported direction GLUT4 increased; GLUT1 not altered[1]

Literature-Reported Treatment Conditions

Treatment concentration
UA 10 µM; wortmannin 1 µM in inhibitor arms
Exposure duration
24 h; wortmannin pretreatment 30 min
Method
Western blots of phosphorylated and total signaling proteins and GLUT1/GLUT4, with β-actin shown.
Co-treatment
Parallel arms without or with insulin 1 µg/mL and with or without wortmannin.
Reported limits
UA treatment vehicle is not stated. Figure 4 reports n=3, without defining the replicate type; no numerical densitometric values are provided in that figure.
Methods and source locations

Compound reported in the paper: Ursolic acid; Compound label in the paper: UA

Evidence concerns the authors’ reported ursolic acid material; it does not validate A10961 lots, formulations or clinical efficacy.

Results: UA stimulates glucose uptake through regulating protein activities in the PI3K pathway; Figure 4 and caption; Methods: Western blotting

PDK, AKT, PKC and AS160 phosphorylation-associated signals: Qualitative immunoblot assessment; Figure 4 states n=3. No fold-change or enzyme activity constant inferred. — Results: UA stimulates glucose uptake through regulating protein activities in the PI3K pathway; Figure 4

Total GLUT4 and GLUT1 protein expression: Total protein Western blot; Figure 4 viewed. No membrane-translocation result adopted. — Results: UA enhances GLUT4 expression and translocation (total-protein statement only); Figure 4

In Vivo Studies

In male C57BL/6 mice consuming a high-fat diet, 0.14% dietary ursolic acid for six weeks increased muscle phospho-Akt, muscle mass, grip strength and brown-fat mass, and lowered fasting glucose. With a separate 0.27% regimen, energy expenditure increased after six weeks but not after three days. These results do not isolate which tissue caused the metabolic changes. [2]

The signaling response was not uniform across mouse models: after two months of 0.27% dietary ursolic acid in aged male C57BL/6 mice, terminal quadriceps Akt and S6K phosphorylation were not significantly increased. Earlier transient activation was not excluded. [3]

Six-week high-fat diet study of muscle and metabolic responses

Animal study · Male C57BL/6 mice; Results specify 8 weeks old at treatment start; high-fat diet with 55% of calories from fat [2]

Compared with high-fat diet alone, dietary UA increased muscle phospho-Akt, grip strength and muscle mass, lowered fasting glucose and increased interscapular brown-fat mass. These correlated endpoints do not establish which tissue or direct molecular target mediates the systemic response.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Triceps phospho(Ser473)-Akt/total Akt relative to HFD controlReported fold difference More than two-fold increase[2]
Grip strength and bilateral quadriceps/triceps weightsDirection Increased versus HFD without UA[2]
Fasting blood glucose after 16 h fastMean ± SEM HFD: 109 ± 2 mg/dl; HFD + UA: 74 ± 5 mg/dl[2]
Interscapular brown-fat component weightDirection Increased versus HFD without UA[2]

Conditions shared by the study groups

Route
Oral, incorporated in diet
Frequency
Ad libitum access
Treatment course
6 weeks
Vehicle
High-fat diet (Harlan Teklad TD93075)
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
High-fat diet + 0.14% UA
0.14% UA in high-fat diet		Same high-fat diet without UAHigher muscle phospho-Akt, grip strength, muscle mass and brown-fat mass; lower fasting glucose.[2]
High-fat diet + 0.14% UA
Model: Male C57BL/6 mice; Results specify 8 weeks old at treatment start; high-fat diet with 55% of calories from fat
Reported limits: Dietary percentages are not converted to mg/kg; individual daily compound exposure is not specified for this endpoint.
Methods and source locations

Compound reported in the paper: Ursolic acid; Compound label in the paper: UA

Evidence concerns the authors’ reported ursolic acid material; it does not validate A10961 lots, formulations or clinical efficacy.

Results and Figures 1, 3 and 5; Materials and Methods: Animals and diets, Immunoblot analysis, Grip strength measurements, Glucose tolerance tests

Triceps phospho(Ser473)-Akt/total Akt relative to HFD control: Immunoblot densitometry; n=5 mice per diet; means ± SEM; *P<0.05 by t-test. Fold description from Results. — Results first subsection; Figure 1A and caption

Grip strength and bilateral quadriceps/triceps weights: Grip strength n=10 mice per diet; muscle weights n≥12 mice per diet; means ± SEM; *P<0.05 by t-test. No mass or force values digitized. — Figure 1C–D and caption

Fasting blood glucose after 16 h fast: Tail-vein glucose; n≥12 mice per diet; Figure 3 caption defines means ± SEM and *P<0.05 by t-test. — Results: Ursolic acid reduces diet-induced obesity, glucose intolerance and fatty liver disease; Figure 3C

Interscapular brown-fat component weight: Dissected fat-pad component weight; n=10 mice per diet; means ± SEM; *P<0.05 by t-test. No exact mass inferred. — Figure 5A and caption

High-fat diet + 0.14% UA · Figures 1, 3 and 5 captions; Animals and diets

Acute versus chronic dietary treatment and energy expenditure

Animal study · Male C57BL/6 mice fed high-fat diet [2]

UA increased measured energy expenditure after six weeks, whereas three-day treatment did not. Food intake was unchanged acutely and increased during the dark period with chronic treatment. The experiment does not isolate the causal contribution of muscle versus brown fat.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Whole-animal energy expenditure during dark and light periodsDirection by course 3 days: no effect; 6 weeks: increased during both dark and light periods[2]
Food intake during dark and light periodsDirection by course 3 days: no effect; 6 weeks: increased during the dark period[2]

Conditions shared by the study groups

Route
Oral, incorporated in diet
Frequency
Ad libitum access
Treatment course
3 days (acute) or 6 weeks (chronic)
Vehicle
High-fat diet (Harlan Teklad TD93075)
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
High-fat diet + 0.27% UA; acute/chronic comparison
0.27% UA in high-fat diet		HFD lacking UA for each corresponding courseNo acute increase in energy expenditure; increased chronic energy expenditure in light and dark periods. Chronic food intake increased in the dark period.[2]
High-fat diet + 0.27% UA; acute/chronic comparison
Model: Male C57BL/6 mice fed high-fat diet
Reported limits: Dietary percentages are not converted to mg/kg; individual daily compound exposure is not specified for this endpoint.
Methods and source locations

Compound reported in the paper: Ursolic acid; Compound label in the paper: UA

Evidence concerns the authors’ reported ursolic acid material; it does not validate A10961 lots, formulations or clinical efficacy.

Results: Ursolic acid increases energy expenditure; Figure 6; Materials and Methods: Animals and diets; Analysis of energy expenditure, food intake and activity

Whole-animal energy expenditure during dark and light periods: CLAMS indirect calorimetry; n=12 mice per diet; cumulative results means ± SEM; unpaired t-tests, *P<0.05. No kcal values digitized. — Results: Ursolic acid increases energy expenditure; Figure 6B and caption

Food intake during dark and light periods: CLAMS monitoring; n=12 mice per diet; cumulative means ± SEM; unpaired t-tests, *P<0.05. No g/h values digitized. — Results: Ursolic acid increases energy expenditure; Figure 6A and caption

High-fat diet + 0.27% UA; acute/chronic comparison · Figure 6 caption; Animals and diets

No sustained Akt/S6K phosphorylation increase in aged muscle

Animal study · Male C57BL/6 mice assigned to diets at 22 months of age; quadriceps analyzed after 2 months [3]

At the terminal measurement, dietary UA did not significantly increase Akt or S6K phosphorylation relative to control diet. This limits extrapolation of sustained Akt/mTORC1 activation across models; transient activation earlier in treatment was not ruled out.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Terminal quadriceps phospho-Akt/total Akt and phospho-S6K/total S6KSignificance/direction N.S. (p > 0.05) versus control for UA[3]

Conditions shared by the study groups

Route
Oral, incorporated in diet
Frequency
Ad libitum access
Treatment course
2 months
Vehicle
Standard chow (Harlan Teklad formula 7013)
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Aged mice: standard chow + UA
0.27% (w/w) UA in standard chow		Standard chow lacking UANo significant terminal increase in phospho-Akt/total Akt or phospho-S6K/total S6K.[3]
Aged mice: standard chow + UA
Model: Male C57BL/6 mice assigned to diets at 22 months of age; quadriceps analyzed after 2 months
Reported limits: Dietary percentages are not converted to mg/kg; individual daily compound exposure is not specified for this endpoint.
Methods and source locations

Compound reported in the paper: Ursolic acid; Compound label in the paper: Ursolic Acid

Evidence concerns the authors’ reported ursolic acid material; it does not validate A10961 lots, formulations or clinical efficacy.

Results paragraph immediately preceding Figure 4; Figure 4; Figure 2 cohort caption; Experimental Procedures: Chemicals and Antibodies, Mouse Protocols, Immunoblot Analyses

Terminal quadriceps phospho-Akt/total Akt and phospho-S6K/total S6K: Immunoblots; Ponceau S loading check; normalized ratios; means ± S.E.; one-way ANOVA with Dunnett’s multiple comparison test. Akt Ser-473 and S6K Thr-389 antibodies specified in Chemicals and Antibodies. — Figure 4A–B and caption; Chemicals and Antibodies; Immunoblot Analyses

Aged mice: standard chow + UA · Mouse Protocols; Figures 2 and 4 captions

Specifications

Manufacturer Adooq Bioscience
CAS Number 77-52-1
Formula C30H48O3
Molecular Weight 456.7
Synonyms Malol; Prunol; Urson; NSC 4060; NSC 167406; Maerotaine; Bungeolic Acid
SMILES
C[C@@H]1CC[C@@]2(CC[C@@]3(C(=CC[C@H]4[C@]3(CC[C@@H]5[C@@]4(CC[C@@H](C5(C)C)O)C)C)[C@@H]2[C@H]1C)C)C(=O)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 78 mg/mL (170.79 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Ursolic Acid Increases Glucose Uptake through the PI3K Signaling Pathway in Adipocytes PLoS ONE (2014). PMID: 25329874 DOI: 10.1371/journal.pone.0110711 Source material
  2. [2] Steven D. Kunkel, Christopher J. Elmore, Kale S. Bongers, et al. Ursolic Acid Increases Skeletal Muscle and Brown Fat and Decreases Diet-Induced Obesity, Glucose Intolerance and Fatty Liver Disease PLoS ONE (2012). PMID: 22745735 DOI: 10.1371/journal.pone.0039332 Source material
  3. [3] Identification and Small Molecule Inhibition of an Activating Transcription Factor 4 (ATF4)-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy The Journal of Biological Chemistry (2015). PMID: 26338703 DOI: 10.1074/jbc.M115.681445 Source material

Publications

1 publication citing this product

  1. Abouzar Karimi, .et al. , Food Bioprod Process, 2020, 124: 329-341

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