Asiatic Acid

Asiatic Acid at a Glance

Asiatic acid is a pentacyclic triterpene of the ursane type and one of the four “centelloside” markers that define gotu kola (Centella asiatica). Structurally and pharmacologically it is best understood as the free-acid aglycone of asiaticoside — the molecule left once that saponin glycoside sheds its sugars. It sits beside its oleanane-type analogues madecassic acid and the glycosides madecassoside and asiaticoside in every part of the story ^{1Reference 1Nagoor Meeran MF et al. · 2018Pharmacological Properties, Molecular Mechanisms, and Pharmaceutical Development of Asiatic Acid: A Pentacyclic Triterpenoid of Therapeutic PromiseView study →}.

The distinction from its glycoside is the point. Asiaticoside is poorly absorbed intact; in the gut it is hydrolysed to asiatic acid, which is the form that actually reaches the circulation and, in many assays, the more membrane-permeant and bioactive of the pair ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}. So most of gotu kola’s laboratory pharmacology — broad neuroprotection, anti-fibrotic effects in liver and skin, wound healing and anti-inflammatory activity — is either attributed to, or reproduced by, the free acid ^{1,2Reference 1Nagoor Meeran MF et al. · 2018Pharmacological Properties, Molecular Mechanisms, and Pharmaceutical Development of Asiatic Acid: A Pentacyclic Triterpenoid of Therapeutic PromiseView study →Reference 2Ding L et al. · 2023Neuroprotective mechanisms of Asiatic acidView study →}.

The honest posture: this is a preclinical molecule. The evidence is animal and cell-based; there are no clinical trials of isolated asiatic acid, and human gotu kola data belong to standardised whole extracts (TTFCA, TECA, ECa 233), not the isolate. Toxicity is low at exposures relevant to normal use, with a hepatic caution reserved for very high experimental doses.

Asiatic Acid vs. Asiaticoside (Aglycone vs. Glycoside)

The single most useful fact about this molecule is its relationship to its glycoside, and it is worth stating plainly because the two names are used almost interchangeably in the literature.

Asiaticoside is the glycoside; asiatic acid is its aglycone. Asiaticoside carries a trisaccharide chain that makes it large, polar and poorly absorbed as an intact molecule. After oral dosing it is hydrolysed by gut enzymes and microbiota to asiatic acid, which is smaller, more lipophilic, and the species that predominantly appears in plasma ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}. In a human pharmacokinetic study of the standardised extract ECa 233, the circulating exposure tracked the aglycones (asiatic and madecassic acid) rather than the parent glycosides ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}. For that reason, asiatic acid is frequently the more membrane-permeant and directly bioactive of the pair in cell assays — it does not need to cross a membrane as a bulky saponin first.

The distinction is not absolute, and it should not be overstated. At least one activity runs the other way: in a neuritogenicity assay, asiaticoside — but not asiatic acid — activated TrkA-mediated neurite outgrowth ^{24Reference 24Nalinratana N et al. · 2019Asiaticoside but not its aglycone exhibits neuritogenicity through TrkA receptor signaling: a bridge between ERK1/2-CREB and Akt-GSK3β/β-catenin pathwayView study →}, a reminder that the sugar chain is sometimes doing the pharmacology, not just gating absorption. The safe reading is that asiatic acid is the bioavailable circulating form that carries most of the systemic signal, while a handful of effects belong specifically to the intact glycoside.

What It's Used For

Asiatic acid’s research base is broad but shallow in the way that matters for humans: many rodent models across several organ systems, converging mechanisms (antioxidant, anti-inflammatory, anti-fibrotic, mitochondria-protective), and no human trials of the isolate. The evidence is strongest and most replicated in neuroprotection and anti-fibrotic contexts.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. There is no human isolate data, so scores stay modest and reflect preclinical depth/replication only.

01NeuroprotectionPromising46%Multiple rodent models — stroke, excitotoxicity, Parkinsonian ^{3,5,6,7,8Reference 3Lee MK et al. · 2000Asiatic acid derivatives protect cultured cortical neurons from glutamate-induced excitotoxicityView study →Reference 5Lee KY et al. · 2012Asiatic acid attenuates infarct volume, mitochondrial dysfunction, and matrix metalloproteinase-9 induction after focal cerebral ischemiaView study →Reference 6Xu MF et al. · 2012AnimalAsiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cellsView study →Reference 7Nataraj J et al. · 2017Neuroprotective effect of asiatic acid on rotenone-induced mitochondrial dysfunction and oxidative stress-mediated apoptosis in differentiated SH-SY5Y cellsView study →Reference 8Chen D et al. · 2019Asiatic Acid Protects Dopaminergic Neurons from Neuroinflammation by Suppressing Mitochondrial ROS ProductionView study →}

02Anti-Fibrotic (Liver)Shaky38%Several rat liver-fibrosis models, TGF-β/Smad + PI3K/AKT ^{9,10,11Reference 9Tang LX et al. · 2012In vitroAsiatic acid inhibits liver fibrosis by blocking TGF-beta/Smad signaling in vivo and in vitroView study →Reference 10Wei L et al. · 2018AnimalAsiatic acid attenuates CCl₄-induced liver fibrosis in rats by regulating the PI3K/AKT/mTOR and Bcl-2/Bax signaling pathwaysView study →Reference 11Li Y et al. · 2022Asiatic acid alleviates liver fibrosis via multiple signaling pathways based on integrated network pharmacology and lipidomicsView study →}

03Wound Healing & Anti-Scarring (Skin)Shaky34%Keloid-fibroblast in-vitro + review of Centella wound data ^{13,14,15Reference 13Diniz LRL et al. · 2023Centella asiatica and Its Metabolite Asiatic Acid: Wound Healing Effects and Therapeutic PotentialView study →Reference 14Bian D et al. · 2013Asiatic acid isolated from Centella asiatica inhibits TGF-β1-induced collagen expression in human keloid fibroblasts via PPAR-γ activationView study →Reference 15Wu J et al. · 2025Asiatic acid inhibits keloid fibroblast migration and collagen deposition via suppression of STAT3 activationView study →}

04Anti-InflammatoryShaky30%NF-κB suppression in macrophage/colitis models ^{16,17Reference 16Yun KJ et al. · 2008Inhibition of LPS-induced NO and PGE2 production by asiatic acid via NF-κB inactivation in RAW 264.7 macrophages: possible involvement of the IKK and MAPK pathwaysView study →Reference 17Park S et al. · 2025AnimalAsiatic acid inhibits NF-κB signaling and ameliorates experimental acute and chronic colitis in miceView study →}

05Anticancer (Preclinical)Shaky24%In-vitro apoptosis + a few xenograft-adjacent models ^{18,19Reference 18Tang XL et al. · 2009Asiatic acid induces colon cancer cell growth inhibition and apoptosis through mitochondrial death cascadeView study →Reference 19Gou XJ et al. · 2020Asiatic Acid Interferes with Invasion and Proliferation of Breast Cancer Cells by Inhibiting WAVE3 Activation through PI3K/AKT Signaling PathwayView study →}

06Metabolic (Glycaemic / Vascular)Shaky22%Streptozotocin-diabetic and hypertensive rat models ^{20,21Reference 20Liu J et al. · 2010AnimalAsiatic acid preserves beta cell mass and mitigates hyperglycemia in streptozocin-induced diabetic ratsView study →Reference 21Bunbupha S et al. · 2014AnimalAsiatic acid reduces blood pressure by enhancing nitric oxide bioavailability with modulation of eNOS and p47phox expression in L-NAME-induced hypertensive ratsView study →}

Mechanisms

The unifying thread is mitochondrial protection + antioxidant/anti-inflammatory signalling, with TGF-β/Smad suppression carrying the anti-fibrotic story. The same stellate-cell apoptosis that treats liver fibrosis is why very high doses raise a hepatic-caution flag.

Pharmacokinetics

Asiatic acid is a lipophilic pentacyclic triterpene acid (C₃₀H₄₈O₅), and its pharmacokinetics are dominated by the aglycone–glycoside relationship. Orally administered asiaticoside is poorly absorbed intact and is hydrolysed to asiatic acid in the gut, so the free acid is the principal circulating centelloside after dosing of gotu kola extracts ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}. Even so, asiatic acid itself has limited aqueous solubility and modest oral bioavailability — the reason much of the delivery literature pursues nanostructured lipid carriers, albumin nanoparticles and other formulation rescues to raise brain and liver exposure. A human study of the standardised extract ECa 233 characterised the aglycone-dominated plasma profile and found the capsules well tolerated ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}. On the interaction side, a Centella asiatica water extract showed low potential for cytochrome-P450-mediated drug interactions in vitro ^{23Reference 23Wright KM et al. · 2020Centella asiatica Water Extract Shows Low Potential for Cytochrome P450-Mediated Drug InteractionsView study →}, suggesting the free acid is not a strong CYP perturber at realistic exposures. No dedicated human PK study of the isolated molecule exists.

Clinical Trials

There are no human trials of isolated asiatic acid. All human Centella asiatica evidence uses standardised whole extracts or topicals (TTFCA/TECA, ECa 233) whose effects cannot be attributed to this single triterpene; the one human study touching the molecule directly is a pharmacokinetic/safety study of the ECa 233 extract, not an efficacy trial of the isolate ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}.

Last checked: July 2026.

Isolate vs. Plant Studies

This molecule shows the usual triterpene split, with an extra twist from its glycoside. Most of the mechanistic pharmacology above used the isolated asiatic acid — cortical-neuron, stroke, liver-fibrosis and keloid-fibroblast studies all dose the pure compound ^{3,5,9,14Reference 3Lee MK et al. · 2000Asiatic acid derivatives protect cultured cortical neurons from glutamate-induced excitotoxicityView study →Reference 5Lee KY et al. · 2012Asiatic acid attenuates infarct volume, mitochondrial dysfunction, and matrix metalloproteinase-9 induction after focal cerebral ischemiaView study →Reference 9Tang LX et al. · 2012In vitroAsiatic acid inhibits liver fibrosis by blocking TGF-beta/Smad signaling in vivo and in vitroView study →Reference 14Bian D et al. · 2013Asiatic acid isolated from Centella asiatica inhibits TGF-β1-induced collagen expression in human keloid fibroblasts via PPAR-γ activationView study →}, which is a genuine strength for mechanism. But every human result belongs to whole Centella asiatica extracts (TTFCA, TECA, ECa 233) standardised to the centelloside mixture, not to asiatic acid alone ^{1,22Reference 1Nagoor Meeran MF et al. · 2018Pharmacological Properties, Molecular Mechanisms, and Pharmaceutical Development of Asiatic Acid: A Pentacyclic Triterpenoid of Therapeutic PromiseView study →Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}. Complicating the picture, asiatic acid is partly an in-vivo metabolite — much of what a person is exposed to arrives via hydrolysis of ingested asiaticoside/madecassoside rather than as pre-formed acid ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}. And the aglycone-vs-glycoside boundary is not clean: asiaticoside, not asiatic acid, carried the neuritogenic TrkA signal in one assay ^{24Reference 24Nalinratana N et al. · 2019Asiaticoside but not its aglycone exhibits neuritogenicity through TrkA receptor signaling: a bridge between ERK1/2-CREB and Akt-GSK3β/β-catenin pathwayView study →}. The transferability caveat is therefore double: from isolate to whole extract, and from the free acid to the glycoside that generates it.

Prevalence in Nature

Asiatic acid is characteristic of, but not abundant in, gotu kola (Centella asiatica). Of the herb’s four centelloside markers — asiaticoside, madecassoside, asiatic acid and madecassic acid — the two free acids are the minor pair, with asiatic acid typically the least abundant, roughly 0–0.3% of dry aerial parts, far below the glycosides that dominate the raw herb ^{25Reference 25Shen Q et al. · 2014Shen Q, et al. (2014). [Simultaneous determination of madecassoside, asiaticoside and their aglycones in Centella asiatica extracts by RP-HPLC]. Journal of Zhejiang University (Medical Sciences). https://pubmed.ncbi.nlm.nih.gov/24782366/View study →}. Concentrations vary enormously with accession, growing conditions, plant part and season, and commercial extracts are standardised far higher than raw herb, so the free acid a consumer is exposed to comes substantially from hydrolysis of the glycosides rather than from pre-formed acid in the leaf.

Beyond Centella, asiatic acid occurs in scattered unrelated taxa as a triterpene constituent: it has been isolated from the leaves of tropical almond (Terminalia catappa) ^{1Reference 1Nagoor Meeran MF et al. · 2018Pharmacological Properties, Molecular Mechanisms, and Pharmaceutical Development of Asiatic Acid: A Pentacyclic Triterpenoid of Therapeutic PromiseView study →}, among other plants. As a ubiquitous ursane skeleton it is biosynthetically kin to ursolic acid; the closely related oleanane acids oleanolic acid and madecassic acid travel with it in Centella, and beta-sitosterol is a common co-occurring phytosterol in the same extracts.

Discovery & Synthesis

Asiatic acid entered the literature not on its own but as the triterpene aglycone of asiaticoside, the wound-healing saponin isolated from Centella asiatica in the study of the herb’s “centelloside” triterpenes in the mid-twentieth century; its name records the botanical source (Centella asiatica, “the Asiatic” pennywort). It is formally 2α,3β,23-trihydroxyurs-12-en-28-oic acid — an ursane-type pentacyclic triterpene carboxylic acid, the free-acid counterpart of the sugar-bearing asiaticoside.

A total synthesis is not well documented; the molecule’s complex pentacyclic skeleton makes de-novo synthesis impractical against extraction. Manufacture today is by extraction and hydrolysis: asiatic acid is obtained from Centella asiatica biomass, most efficiently by isolating the far-more-abundant glycoside asiaticoside and hydrolysing it to the aglycone, rather than purifying the scarce pre-formed acid directly. Standardised centelloside fractions (TTFCA/TECA) remain the commercial workhorse from which the individual triterpenes are separated.

Patents: not yet researched.

Toxicity & Safety

Asiatic acid carries a low flag: it is a constituent (and metabolite) of gotu kola, a plant with a long record of food and medicinal use, and its safety at exposures relevant to normal supplementation is unremarkable. The one caveat worth naming is dose-dependent and specific to this molecule.

Safety at a Glance

✅ Low / no toxicity

• Low toxicity at realistic exposures. A minor triterpene of an edible, long-used herb; human extract studies report good tolerability ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}.
• Low CYP-interaction potential. Centella water extract showed weak cytochrome-P450 inhibition in vitro, arguing against strong pharmacokinetic drug interactions ^{23Reference 23Wright KM et al. · 2020Centella asiatica Water Extract Shows Low Potential for Cytochrome P450-Mediated Drug InteractionsView study →}.
• High-dose hepatic caution. Its anti-fibrotic action works partly by inducing apoptosis in activated hepatic stellate cells; at very high experimental doses this same pro-apoptotic activity is the basis for a hepatotoxicity signal, distinct from its hepatoprotection at lower doses ^{10,12Reference 10Wei L et al. · 2018AnimalAsiatic acid attenuates CCl₄-induced liver fibrosis in rats by regulating the PI3K/AKT/mTOR and Bcl-2/Bax signaling pathwaysView study →Reference 12Ma K et al. · 2009Protective effects of asiatic acid against D-galactosamine/lipopolysaccharide-induced hepatotoxicity in hepatocytes and Kupffer cells co-cultured systemView study →}.
• Preclinical safety only. No dedicated human safety dataset for the isolate; whole-herb cautions (rare idiosyncratic hepatotoxicity reports for Centella products) govern real-world use.

Full Safety & Interactions Detail

At the low levels supplied by normal gotu kola use, asiatic acid is regarded as low in toxicity, and standardised Centella extract capsules were well tolerated in a human pharmacokinetic study ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}.

The molecule’s own safety literature is otherwise preclinical, and the notable feature is a biphasic, dose-dependent relationship with the liver: at lower doses asiatic acid is hepatoprotective and anti-fibrotic, protecting hepatocytes against toxin injury ^{12Reference 12Ma K et al. · 2009Protective effects of asiatic acid against D-galactosamine/lipopolysaccharide-induced hepatotoxicity in hepatocytes and Kupffer cells co-cultured systemView study →} and reversing fibrosis by driving apoptosis of activated hepatic stellate cells ^{10Reference 10Wei L et al. · 2018AnimalAsiatic acid attenuates CCl₄-induced liver fibrosis in rats by regulating the PI3K/AKT/mTOR and Bcl-2/Bax signaling pathwaysView study →}.

That pro-apoptotic mechanism is therapeutic against fibrosis but is also the plausible basis for a hepatotoxicity signal at very high experimental doses — a caution rather than a documented human harm.

Drug interactions: a Centella asiatica water extract showed low potential for CYP-mediated interactions in vitro ^{23Reference 23Wright KM et al. · 2020Centella asiatica Water Extract Shows Low Potential for Cytochrome P450-Mediated Drug InteractionsView study →}, so clinically meaningful pharmacokinetic interactions from the free acid appear unlikely at realistic exposures, though this has not been tested for the pure isolate in humans.

Reproductive note (prose only): no dedicated reproductive- or developmental-toxicity dataset exists for isolated asiatic acid. Pregnancy and lactation decisions belong to the gotu kola herb page and any product page, where intake is actually decided, not to this molecule-level page. Interactions and repeat-dose toxicology for the pure compound in humans remain uncharacterised — do not read safety from silence.

Dosage

There is no established human dose for isolated asiatic acid — it has never been given as an isolate in a human trial. Preclinical studies use roughly 5–75 mg/kg in rodents (oral or intraperitoneal), figures that do not translate to a human dose. Real-world human exposure is indirect: as the in-vivo hydrolysis product of asiaticoside and madecassoside in standardised gotu kola preparations (TTFCA/TECA typically dosed at 60–120 mg/day of total triterpene fraction; ECa 233 in the human PK study) ^{22Reference 22Songvut P et al. · 2019Clinical trialSafety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical StudyView study →}. These are research figures and standardised-extract doses, not a personal recommendation.

References

1. Nagoor Meeran MF, et al. (2018). Pharmacological Properties, Molecular Mechanisms, and Pharmaceutical Development of Asiatic Acid: A Pentacyclic Triterpenoid of Therapeutic Promise. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/30233358/
2. Ding L, et al. (2023). Neuroprotective mechanisms of Asiatic acid. Heliyon. https://pubmed.ncbi.nlm.nih.gov/37180926/
3. Lee MK, et al. (2000). Asiatic acid derivatives protect cultured cortical neurons from glutamate-induced excitotoxicity. Research Communications in Molecular Pathology and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/11758977/
4. Krishnamurthy RG, et al. (2009). Asiatic acid, a pentacyclic triterpene from Centella asiatica, is neuroprotective in a mouse model of focal cerebral ischemia. Journal of Neuroscience Research. https://pubmed.ncbi.nlm.nih.gov/19382233/
5. Lee KY, et al. (2012). Asiatic acid attenuates infarct volume, mitochondrial dysfunction, and matrix metalloproteinase-9 induction after focal cerebral ischemia. Stroke. https://pubmed.ncbi.nlm.nih.gov/22511009/
6. Xu MF, et al. (2012). Asiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells. Acta Pharmacologica Sinica. https://pubmed.ncbi.nlm.nih.gov/22447225/
7. Nataraj J, et al. (2017). Neuroprotective effect of asiatic acid on rotenone-induced mitochondrial dysfunction and oxidative stress-mediated apoptosis in differentiated SH-SY5Y cells. Nutritional Neuroscience. https://pubmed.ncbi.nlm.nih.gov/26856988/
8. Chen D, et al. (2019). Asiatic Acid Protects Dopaminergic Neurons from Neuroinflammation by Suppressing Mitochondrial ROS Production. Biomolecules & Therapeutics (Seoul). https://pubmed.ncbi.nlm.nih.gov/30971058/
9. Tang LX, et al. (2012). Asiatic acid inhibits liver fibrosis by blocking TGF-beta/Smad signaling in vivo and in vitro. PLoS One. https://pubmed.ncbi.nlm.nih.gov/22363627/
10. Wei L, et al. (2018). Asiatic acid attenuates CCl₄-induced liver fibrosis in rats by regulating the PI3K/AKT/mTOR and Bcl-2/Bax signaling pathways. International Immunopharmacology. https://pubmed.ncbi.nlm.nih.gov/29702278/
11. Li Y, et al. (2022). Asiatic acid alleviates liver fibrosis via multiple signaling pathways based on integrated network pharmacology and lipidomics. European Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/35963324/
12. Ma K, et al. (2009). Protective effects of asiatic acid against D-galactosamine/lipopolysaccharide-induced hepatotoxicity in hepatocytes and Kupffer cells co-cultured system. European Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/19087874/
13. Diniz LRL, et al. (2023). Centella asiatica and Its Metabolite Asiatic Acid: Wound Healing Effects and Therapeutic Potential. Metabolites. https://pubmed.ncbi.nlm.nih.gov/36837896/
14. Bian D, et al. (2013). Asiatic acid isolated from Centella asiatica inhibits TGF-β1-induced collagen expression in human keloid fibroblasts via PPAR-γ activation. International Journal of Biological Sciences. https://pubmed.ncbi.nlm.nih.gov/24250248/
15. Wu J, et al. (2025). Asiatic acid inhibits keloid fibroblast migration and collagen deposition via suppression of STAT3 activation. Burns. https://pubmed.ncbi.nlm.nih.gov/40700781/
16. Yun KJ, et al. (2008). Inhibition of LPS-induced NO and PGE2 production by asiatic acid via NF-κB inactivation in RAW 264.7 macrophages: possible involvement of the IKK and MAPK pathways. International Immunopharmacology. https://pubmed.ncbi.nlm.nih.gov/18279797/
17. Park S, et al. (2025). Asiatic acid inhibits NF-κB signaling and ameliorates experimental acute and chronic colitis in mice. International Journal of Immunopathology and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/41368736/
18. Tang XL, et al. (2009). Asiatic acid induces colon cancer cell growth inhibition and apoptosis through mitochondrial death cascade. Biological & Pharmaceutical Bulletin. https://pubmed.ncbi.nlm.nih.gov/19652380/
19. Gou XJ, et al. (2020). Asiatic Acid Interferes with Invasion and Proliferation of Breast Cancer Cells by Inhibiting WAVE3 Activation through PI3K/AKT Signaling Pathway. BioMed Research International. https://pubmed.ncbi.nlm.nih.gov/32104680/
20. Liu J, et al. (2010). Asiatic acid preserves beta cell mass and mitigates hyperglycemia in streptozocin-induced diabetic rats. Diabetes/Metabolism Research and Reviews. https://pubmed.ncbi.nlm.nih.gov/20809533/
21. Bunbupha S, et al. (2014). Asiatic acid reduces blood pressure by enhancing nitric oxide bioavailability with modulation of eNOS and p47phox expression in L-NAME-induced hypertensive rats. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/24723332/
22. Songvut P, et al. (2019). Safety and Pharmacokinetics of Standardized Extract of Centella asiatica (ECa 233) Capsules in Healthy Thai Volunteers: A Phase 1 Clinical Study. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/30699457/
23. Wright KM, et al. (2020). Centella asiatica Water Extract Shows Low Potential for Cytochrome P450-Mediated Drug Interactions. Drug Metabolism and Disposition. https://pubmed.ncbi.nlm.nih.gov/32581050/
24. Nalinratana N, et al. (2019). Asiaticoside but not its aglycone exhibits neuritogenicity through TrkA receptor signaling: a bridge between ERK1/2-CREB and Akt-GSK3β/β-catenin pathway. Neuroreport. https://pubmed.ncbi.nlm.nih.gov/31651704/
25. Shen Q, et al. (2014). [Simultaneous determination of madecassoside, asiaticoside and their aglycones in Centella asiatica extracts by RP-HPLC]. Journal of Zhejiang University (Medical Sciences). https://pubmed.ncbi.nlm.nih.gov/24782366/

View all 25 references▾