Arjunolic Acid

Arjunolic Acid at a Glance

Arjunolic acid is a pentacyclic oleanane-type triterpenoid acid (2,3,23-trihydroxyolean-12-en-28-oic acid) and the best-studied single molecule of arjuna (Terminalia arjuna) bark — the tree Ayurveda has used as a cardiac tonic for centuries. Together with its close relatives arjunic acid and arjungenin, it is one of the triterpenes usually credited with arjuna’s cardioactive reputation, though it makes up only a minor fraction of the bark ^{1,13Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →}.

Its scientific profile is large but almost entirely preclinical. In rodent and cell studies the isolated molecule is a potent antioxidant and metal chelator that protects the heart, liver and kidney against a wide range of injuries — ischaemic and toxin-induced — largely by preserving mitochondrial function and blunting oxidative-stress and apoptotic signalling ^{1,2Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 2Hemalatha T et al. · 2010Arjunolic acid: a novel phytomedicine with multifunctional therapeutic applicationsView study →}. This breadth is why reviews describe it as a “multifunctional” phytomedicine ^{1,2Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 2Hemalatha T et al. · 2010Arjunolic acid: a novel phytomedicine with multifunctional therapeutic applicationsView study →}.

Two honesty caveats run through the whole page. First, there are no human trials of isolated arjunolic acid — arjuna’s clinical evidence belongs to whole bark extract, not this molecule. Second, arjunolic acid is a large, lipophilic triterpene acid with poor water solubility, so its oral bioavailability is expected to be low, which tempers how far the in-vitro potency translates to a swallowed dose.

Arjunolic Acid & Cardioprotection

Cardioprotection is the defining thread of the arjunolic-acid literature, and it is unusually mechanistically coherent for a plant isolate — even though it remains rodent and cell work.

The earliest signal is antioxidant and haemostatic. In rats with isoproterenol-induced myocardial necrosis, arjunolic acid pre-treatment reduced platelet aggregation and coagulation abnormalities, limited the rise in cardiac marker enzymes, and preserved antioxidant status — with the authors framing it as a triterpene cardioprotectant comparable in some respects to acetylsalicylic acid ^{3Reference 3Sumitra M et al. · 2001AnimalExperimental myocardial necrosis in rats: role of arjunolic acid on platelet aggregation, coagulation and antioxidant statusView study →}. Later work sharpened the picture: against oral sodium-nitrite cardiotoxicity, arjunolic acid rebalanced pro- and anti-inflammatory cytokines and shifted the tissue away from apoptosis ^{5Reference 5Al-Gayyar MMH et al. · 2014Protective effects of arjunolic acid against cardiac toxicity induced by oral sodium nitrite: effects on cytokine balance and apoptosisView study →}; and in LPS-induced septic myocardial injury, it lowered circulating troponin I, lactate dehydrogenase and creatine kinase and reduced oxidative damage in vivo ^{6Reference 6Elsawy H et al. · 2022AnimalIn vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injuryView study →}, with companion cell work tracing the anti-inflammatory effect to suppression of the MyD88-dependent TLR4 signalling pathway in H9C2 cardiomyocytes and C2C12 myotubes ^{7Reference 7Hasan MM et al. · 2023Cardioprotective effects of arjunolic acid in LPS-stimulated H9C2 and C2C12 myotubes via the MyD88-dependent TLR4 signaling pathwayView study →}.

The most molecularly detailed study reframes arjunolic acid as a PPAR-α agonist that regresses established cardiac fibrosis by inhibiting non-canonical (SMAD-independent) TGF-β signalling — a genuine anti-remodelling mechanism rather than a generic antioxidant effect ^{4Reference 4Bansal T et al. · 2017Arjunolic acid, a peroxisome proliferator-activated receptor α agonist, regresses cardiac fibrosis by inhibiting non-canonical TGF-β signalingView study →}. A separate line found it to be a carbonic anhydrase II inhibitor that lowers intracellular calcium and prevents mitochondrial-membrane depolarisation in cardiomyocytes, offering yet another route to cardioprotection ^{8Reference 8Kalyanavenkataraman S et al. · 2016Discovery of arjunolic acid as a novel non-zinc binding carbonic anhydrase II inhibitorView study →}.

The same antioxidant/mitochondrial machinery extends beyond the heart. Arjunolic acid protects the liver against acetaminophen (paracetamol) injury — partly by inhibiting the cytochrome-P450 bioactivation of the drug and partly by blocking JNK-mediated mitochondrial permeabilisation, cytochrome-c release and downstream apoptosis ^{9Reference 9Ghosh J et al. · 2010Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protectionView study →} — and the kidney against the same drug’s oxidative, TNF-α-driven nephrotoxicity ^{10Reference 10Ghosh J et al. · 2010Acetaminophen induced renal injury via oxidative stress and TNF-alpha production: therapeutic potential of arjunolic acidView study →}. It is therefore best read not as a narrow “heart compound” but as a broad cytoprotective antioxidant whose most-developed application happens to be cardiac.

The Arjuna Triterpenes

Arjunolic acid does not act alone in the plant. Terminalia arjuna bark carries a small suite of oleanane-type triterpenes and their saponin glycosides — chiefly arjunolic acid and the closely related arjunic acid, the sapogenin arjungenin, and glycosides such as arjunetin and arjunin — alongside tannins, proanthocyanidins and flavonoids ^{1Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →}. These triterpenes and saponins are the constituents most often nominated as the source of arjuna’s traditional cardiac activity, credited in phytochemical reviews with effects on myocardial contractility, coronary flow and lipids ^{1Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →}.

Quantitatively, though, the triterpene fraction is minor: careful compositional analysis of the stem bark puts total triterpenoids under ~1%, with arjunolic acid around 0.5% w/w and arjungenin near 0.3% ^{13Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →}. This matters for interpretation — the whole-bark preparations used in human cardiology deliver only small amounts of any one triterpene, so arjuna’s clinical effects cannot be attributed to arjunolic acid specifically. (The sibling molecules arjunic acid, arjungenin, arjunetin and arjunin do not yet have their own reference pages here.)

Arjunolic acid is also a member of the wider oleanane triterpene-acid family and shares its structural template and antioxidant/cytoprotective leanings with oleanolic acid, the isomeric ursolic acid and betulinic acid. Its distinguishing feature within that family is an extra hydroxyl at C-23 (and at C-2), giving the 2,3,23-trihydroxy pattern that underlies its metal-chelating and carbonic-anhydrase activity ^{8Reference 8Kalyanavenkataraman S et al. · 2016Discovery of arjunolic acid as a novel non-zinc binding carbonic anhydrase II inhibitorView study →}.

What It's Used For

Arjunolic acid’s preclinical record is broad and internally consistent, but the compound-page discipline is the load-bearing caveat: almost every finding is rodent or cell work on the isolated molecule, and none of it has been tested in a human trial ^{1,2Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 2Hemalatha T et al. · 2010Arjunolic acid: a novel phytomedicine with multifunctional therapeutic applicationsView study →}.

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. Every score here is capped by the same fact: the evidence is preclinical isolate work, with no human isolate trials, so nothing rises into “clinically supported” territory.

01CardioprotectionPromising48%Multiple rodent/cell isolate models; PPAR-α, anti-fibrotic, carbonic-anhydrase, mitochondrial mechanisms ^{3,4,5,6,7,8Reference 3Sumitra M et al. · 2001AnimalExperimental myocardial necrosis in rats: role of arjunolic acid on platelet aggregation, coagulation and antioxidant statusView study →Reference 4Bansal T et al. · 2017Arjunolic acid, a peroxisome proliferator-activated receptor α agonist, regresses cardiac fibrosis by inhibiting non-canonical TGF-β signalingView study →Reference 5Al-Gayyar MMH et al. · 2014Protective effects of arjunolic acid against cardiac toxicity induced by oral sodium nitrite: effects on cytokine balance and apoptosisView study →Reference 6Elsawy H et al. · 2022AnimalIn vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injuryView study →Reference 7Hasan MM et al. · 2023Cardioprotective effects of arjunolic acid in LPS-stimulated H9C2 and C2C12 myotubes via the MyD88-dependent TLR4 signaling pathwayView study →Reference 8Kalyanavenkataraman S et al. · 2016Discovery of arjunolic acid as a novel non-zinc binding carbonic anhydrase II inhibitorView study →}

02HepatoprotectionShaky40%Rat/hepatocyte isolate; acetaminophen + arsenic injury; CYP-inhibition + JNK/mitochondrial protection ^{9,11Reference 9Ghosh J et al. · 2010Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protectionView study →Reference 11Manna P et al. · 2007Arjunolic acid, a triterpenoid saponin, ameliorates arsenic-induced cyto-toxicity in hepatocytesView study →}

03Nephroprotection & antidiabeticShaky34%Rat isolate; acetaminophen renal injury and streptozotocin diabetic nephropathy ^{10,12Reference 10Ghosh J et al. · 2010Acetaminophen induced renal injury via oxidative stress and TNF-alpha production: therapeutic potential of arjunolic acidView study →Reference 12Manna P et al. · 2009Prophylactic role of arjunolic acid in response to streptozotocin mediated diabetic renal injury: activation of polyol pathway and oxidative stress responsive signaling cascadesView study →}

04Metal / xenobiotic detoxificationShaky30%Hepatocyte/animal isolate vs. arsenic; antioxidant + metal-chelation ^{11Reference 11Manna P et al. · 2007Arjunolic acid, a triterpenoid saponin, ameliorates arsenic-induced cyto-toxicity in hepatocytesView study →}

05Enzyme inhibition & otherShaky24%In-vitro carbonic-anhydrase-II inhibition; miscellaneous antioxidant/antimicrobial assays ^{1,8Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 8Kalyanavenkataraman S et al. · 2016Discovery of arjunolic acid as a novel non-zinc binding carbonic anhydrase II inhibitorView study →}

Mechanisms

The unifying read is a single upstream theme — preserved redox balance and mitochondrial integrity — expressed in whichever organ is injured, with the PPAR-α/TGF-β and TLR4 mechanisms layered on top for the specifically cardiac effects.

Pharmacokinetics

Formal human ADME for arjunolic acid is not established, and even rodent pharmacokinetics are sparse; the isolate is used at fixed research doses (commonly ~20 mg/kg in rats and mice) rather than characterised for Cmax, half-life or oral bioavailability ^{1Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →}. Structurally, though, the expectation is clear: arjunolic acid is a large (MW ≈ 489), highly lipophilic pentacyclic triterpene acid with poor aqueous solubility, the same physicochemical profile that gives its oleanane relative oleanolic acid an oral bioavailability under ~1%. Low absorption is therefore the likely rule, and it undercuts any read-across from micromolar in-vitro potencies (e.g. the 9 µM carbonic-anhydrase IC50 ^{8Reference 8Kalyanavenkataraman S et al. · 2016Discovery of arjunolic acid as a novel non-zinc binding carbonic anhydrase II inhibitorView study →}) to a swallowed human dose. This poor-solubility problem is exactly why formulation and delivery strategies are of interest for triterpene acids of this class. Its metal-chelating capacity is a genuine molecular property that travels with it regardless of systemic exposure ^{11Reference 11Manna P et al. · 2007Arjunolic acid, a triterpenoid saponin, ameliorates arsenic-induced cyto-toxicity in hepatocytesView study →}.

Clinical Trials

There are no clinical trials of isolated arjunolic acid — completed, ongoing or terminated. The human evidence associated with this molecule is really the evidence for whole Terminalia arjuna bark (chronic stable angina, heart-failure and lipid endpoints), where arjunolic acid is only one minor constituent of a complex tannin/triterpene/flavonoid matrix ^{1,13Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →}; those trials belong to the arjuna herb monograph, not here.

Last checked: July 2026.

Isolate vs. Plant Studies

This molecule sits firmly on the isolate-mechanism-but-no-isolate-clinic side of the ledger, and the split is stark. The mechanistic and protective work is overwhelmingly the purified molecule in rodents and cell lines — the Sumitra myocardial-necrosis study ^{3Reference 3Sumitra M et al. · 2001AnimalExperimental myocardial necrosis in rats: role of arjunolic acid on platelet aggregation, coagulation and antioxidant statusView study →}, the Ghosh/Manna/Sil acetaminophen liver and kidney series ^{9,10Reference 9Ghosh J et al. · 2010Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protectionView study →Reference 10Ghosh J et al. · 2010Acetaminophen induced renal injury via oxidative stress and TNF-alpha production: therapeutic potential of arjunolic acidView study →}, the arsenic-hepatocyte work ^{11Reference 11Manna P et al. · 2007Arjunolic acid, a triterpenoid saponin, ameliorates arsenic-induced cyto-toxicity in hepatocytesView study →}, the streptozotocin diabetic-nephropathy study ^{12Reference 12Manna P et al. · 2009Prophylactic role of arjunolic acid in response to streptozotocin mediated diabetic renal injury: activation of polyol pathway and oxidative stress responsive signaling cascadesView study →}, the Bansal PPAR-α/TGF-β fibrosis study ^{4Reference 4Bansal T et al. · 2017Arjunolic acid, a peroxisome proliferator-activated receptor α agonist, regresses cardiac fibrosis by inhibiting non-canonical TGF-β signalingView study →} and the carbonic-anhydrase discovery ^{8Reference 8Kalyanavenkataraman S et al. · 2016Discovery of arjunolic acid as a novel non-zinc binding carbonic anhydrase II inhibitorView study →} all test arjunolic acid directly. As a preclinical mechanism base for the isolate, that is a real strength.

The human evidence, by contrast, is entirely whole-plant: arjuna’s cardiology trials use stem-bark powder or standardised water/alcohol extract, not the isolated triterpene, and the bark delivers only ~0.5% arjunolic acid ^{13Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →}. So the correct framing is: strong isolate mechanism + meaningful whole-bark clinical tradition + zero isolate clinical data — and the two must not be conflated. A rat responding to 20 mg/kg of pure arjunolic acid is not the same as a person taking 500 mg of arjuna bark three times a day.

Prevalence in Nature

Arjunolic acid is characteristically a Terminalia triterpene, most associated with the bark (and heartwood) of Terminalia arjuna, where it occurs at roughly 0.5% w/w of the stem bark within a total-triterpenoid fraction under ~1% ^{13Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →}. It is not confined to arjuna, however: it has been reported from other Terminalia species (including T. bellirica and T. catappa) and, notably, from several Combretaceae and beyond — Combretum leprosum root and Leandra chaeton among the sources reviewers list for the isolated molecule ^{1,2Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 2Hemalatha T et al. · 2010Arjunolic acid: a novel phytomedicine with multifunctional therapeutic applicationsView study →}. Across these plants it co-occurs with its structural relatives arjunic acid and arjungenin and with the wider antioxidant matrix of tannins, gallic acid, ellagic acid, β-sitosterol and flavonoids ^{1Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →}.

Its natural role is best understood as part of the plant’s triterpene/saponin defence and cuticular chemistry, the same functional niche occupied by oleanolic acid and ursolic acid in other species; a dedicated ecological-function literature for arjunolic acid specifically is thin.

Major Natural Sources

Source	Plant part	Reported arjunolic-acid content
Arjuna (Terminalia arjuna)	stem bark	~0.5% w/w 13Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →
Bahera (Terminalia bellirica)	bark	reported, not quantified here 1Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →
Terminalia catappa	root bark	reported, not quantified here 1Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →
Combretum leprosum	root	reported, not quantified here 1,2Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 2Hemalatha T et al. · 2010Arjunolic acid: a novel phytomedicine with multifunctional therapeutic applicationsView study →

Only the arjuna stem-bark figure rests on a quantified analytical determination ^{13Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →}; the other occurrences are reported qualitatively in reviews. The concentration holes are logged in this compound’s gaps tracker for a later pass.

Discovery & Synthesis

Arjunolic acid was first isolated from the bark of Terminalia arjuna by King and co-workers in the mid-twentieth century, among the earliest of the arjuna triterpenes to be characterised; its structure was established as 2,3,23-trihydroxyolean-12-en-28-oic acid (C₃₀H₄₈O₅), a pentacyclic oleanane bearing three hydroxyls and a C-28 carboxylic acid ^{1,2Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 2Hemalatha T et al. · 2010Arjunolic acid: a novel phytomedicine with multifunctional therapeutic applicationsView study →}. Its name records its botanical origin — the arjun tree, itself long used as a cardiac tonic in Ayurveda — and the compound’s early study was motivated by that traditional cardioactive reputation ^{1Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →}.

Manufacture today is by extraction from plant material rather than synthesis: arjunolic acid is obtained from arjuna bark or heartwood by solvent extraction and chromatographic separation (analytical methods deliberately separate the triterpenoid acids from the co-extracted tannins) ^{13Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →}. A practical, scalable total synthesis of arjunolic acid is not well documented, so the isolate remains a plant-derived material; its poor aqueous solubility is the main obstacle to developing it further.

Patents: not yet researched.

Toxicity & Safety

Arjunolic acid carries a low toxicity flag. Nothing in its preclinical record points to intrinsic toxicity at the doses studied — on the contrary, it is repeatedly protective, and in animal models it defends the heart, liver and kidney against toxins and drugs rather than damaging them ^{1,3,9,10Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 3Sumitra M et al. · 2001AnimalExperimental myocardial necrosis in rats: role of arjunolic acid on platelet aggregation, coagulation and antioxidant statusView study →Reference 9Ghosh J et al. · 2010Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protectionView study →Reference 10Ghosh J et al. · 2010Acetaminophen induced renal injury via oxidative stress and TNF-alpha production: therapeutic potential of arjunolic acidView study →}. Its parent plant, arjuna bark, also has a long record of traditional use with generally good tolerability. The honest safety statement here is therefore mostly about absence of data, not evidence of harm.

Safety at a Glance

✅ Low / no toxicity

• No intrinsic-toxicity signal in preclinical work. The isolate is cytoprotective across cardiac, hepatic and renal injury models at the doses tested (~20 mg/kg in rodents) ^{1,3,9,10Reference 1Ghosh J · 2013Arjunolic acid: a new multifunctional therapeutic promise of alternative medicineView study →Reference 3Sumitra M et al. · 2001AnimalExperimental myocardial necrosis in rats: role of arjunolic acid on platelet aggregation, coagulation and antioxidant statusView study →Reference 9Ghosh J et al. · 2010Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protectionView study →Reference 10Ghosh J et al. · 2010Acetaminophen induced renal injury via oxidative stress and TNF-alpha production: therapeutic potential of arjunolic acidView study →}.
• Traditional parent-plant tolerability. Arjuna bark has centuries of Ayurvedic cardiac use, though that is the whole plant, not the isolate.
• No human isolate safety data. There are no clinical trials of purified arjunolic acid, so its human tolerability, dosing ceiling and drug interactions are simply uncharacterised.
• Poor oral bioavailability. As a large lipophilic triterpene acid it is likely poorly absorbed by mouth, which limits both efficacy and any systemic-toxicity read-across from in-vitro concentrations.
• Interaction potential is unstudied. Given its reported inhibition of cytochrome-P450-mediated drug bioactivation ^{9Reference 9Ghosh J et al. · 2010Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protectionView study →}, a theoretical potential to alter the metabolism of co-administered drugs cannot be excluded or confirmed from current data.

Reproductive and developmental safety for isolated arjunolic acid has not been characterised, and no dedicated genotoxicity or repeat-dose package exists for the pure compound. Pregnancy and lactation decisions belong to the arjuna herb monograph — where intake is actually decided — not to this molecule-level page; no isolate-specific verdict is issued here.

Dosage

There is no established or recommended human dose for isolated arjunolic acid, and no human trial has used the isolate. The figures that appear in the literature are preclinical rodent research doses — most protective studies dose rats and mice at around 20 mg/kg by mouth or injection ^{9,11Reference 9Ghosh J et al. · 2010Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protectionView study →Reference 11Manna P et al. · 2007Arjunolic acid, a triterpenoid saponin, ameliorates arsenic-induced cyto-toxicity in hepatocytesView study →} — and these are not convertible to human self-dosing.

The nearest thing to a human “dose” is really a dose of the whole plant: arjuna bark is studied as powder (commonly ~500 mg three times daily) or as a standardised water extract (e.g. 750 mg twice daily), preparations in which arjunolic acid is only a ~0.5% constituent ^{13Reference 13Kalola J · 2006Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tanninsView study →}. Those are arjuna doses, not arjunolic-acid doses. These are research and traditional figures, not a personal recommendation.

References

1. Ghosh J, Sil PC (2013). Arjunolic acid: a new multifunctional therapeutic promise of alternative medicine. Biochimie. https://pubmed.ncbi.nlm.nih.gov/23402784/
2. Hemalatha T, et al. (2010). Arjunolic acid: a novel phytomedicine with multifunctional therapeutic applications. Indian Journal of Experimental Biology. https://pubmed.ncbi.nlm.nih.gov/21046976/
3. Sumitra M, et al. (2001). Experimental myocardial necrosis in rats: role of arjunolic acid on platelet aggregation, coagulation and antioxidant status. Molecular and Cellular Biochemistry. https://pubmed.ncbi.nlm.nih.gov/11693190/
4. Bansal T, et al. (2017). Arjunolic acid, a peroxisome proliferator-activated receptor α agonist, regresses cardiac fibrosis by inhibiting non-canonical TGF-β signaling. The Journal of Biological Chemistry. https://pubmed.ncbi.nlm.nih.gov/28821620/
5. Al-Gayyar MMH, et al. (2014). Protective effects of arjunolic acid against cardiac toxicity induced by oral sodium nitrite: effects on cytokine balance and apoptosis. Life Sciences. https://pubmed.ncbi.nlm.nih.gov/25064822/
6. Elsawy H, et al. (2022). In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury. PeerJ. https://pubmed.ncbi.nlm.nih.gov/35190789/
7. Hasan MM, et al. (2023). Cardioprotective effects of arjunolic acid in LPS-stimulated H9C2 and C2C12 myotubes via the MyD88-dependent TLR4 signaling pathway. Pharmaceutical Biology. https://pubmed.ncbi.nlm.nih.gov/37497554/
8. Kalyanavenkataraman S, et al. (2016). Discovery of arjunolic acid as a novel non-zinc binding carbonic anhydrase II inhibitor. Bioorganic Chemistry. https://pubmed.ncbi.nlm.nih.gov/27038848/
9. Ghosh J, Das J, Manna P, Sil PC (2010). Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protection. Free Radical Biology and Medicine. https://pubmed.ncbi.nlm.nih.gov/19969075/
10. Ghosh J, Das J, Manna P, Sil PC (2010). Acetaminophen induced renal injury via oxidative stress and TNF-alpha production: therapeutic potential of arjunolic acid. Toxicology. https://pubmed.ncbi.nlm.nih.gov/19922764/
11. Manna P, Sinha M, Pal P, Sil PC (2007). Arjunolic acid, a triterpenoid saponin, ameliorates arsenic-induced cyto-toxicity in hepatocytes. Chemico-Biological Interactions. https://pubmed.ncbi.nlm.nih.gov/17854788/
12. Manna P, Sinha M, Sil PC (2009). Prophylactic role of arjunolic acid in response to streptozotocin mediated diabetic renal injury: activation of polyol pathway and oxidative stress responsive signaling cascades. Chemico-Biological Interactions. https://pubmed.ncbi.nlm.nih.gov/19682444/
13. Kalola J, Rajani M (2006). Extraction and TLC densitometric determination of triterpenoid acids (arjungenin, arjunolic acid) from Terminalia arjuna stem bark without interference of tannins. Chromatographia. https://doi.org/10.1365/s10337-006-0772-3

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