IngredientsArjunic acid — also known by its systematic IUPAC name (2α,3β,19α)-2,3,19-trihydroxyolean-12-en-28-oic acid and by the synonym arjuntriterpenic acid — is a naturally occurring pentacyclic triterpenoid. Its empirical molecular formula is C₃₀H₄₈O₅, it carries CAS registry number 31298-06-3, and has a molecular weight of 488.70. It belongs to the oleanane class of triterpenoids and exists in nature primarily as a free acid or as the aglycone (sugar-free component) of larger triterpenoid glycoside molecules.
It is important not to conflate arjunic acid with the closely related and more extensively studied arjunolic acid (CAS 465-00-9; IUPAC: 2α,3β,23α-trihydroxyolean-12-en-28-oic acid), which differs from arjunic acid in the position of one hydroxyl substituent (C-19 in arjunic acid versus C-23 in arjunolic acid). Arjunolic acid is a pentacyclic triterpene acid, a major constituent of T. arjuna, with the IUPAC name 2α,3β,23α-trihydroxy-olean-12-en-28-oic acid. Both compounds share the same molecular formula and are frequently found together in the same plant tissues, a situation that historically created analytical challenges in their separation and identification. The two names are sometimes used loosely in older literature, but modern spectroscopic identification clearly distinguishes them.
Arjunic acid (2α,3β,19α-trihydroxy-olea-12-en-28-oic acid) is a triterpenoid compound that exists widely in natural plants in the form of a free acid or as the aglycone for triterpenoid saponins, and it has been isolated and identified from various plant species.
The primary and most historically recognized botanical source of arjunic acid is Terminalia arjuna (Roxb.) Wight & Arn. Terminalia arjuna is a species in the genus Terminalia of the family Combretaceae, which includes approximately 20 genera and 600 species. T. arjuna is found throughout the sub-Himalayan regions of Bihar, Delhi, Madhya Pradesh, Uttar Pradesh, and the Deccan Plateau in India, as well as in the forests of Sri Lanka, Bangladesh, Mauritius, and Myanmar, and is a deciduous tree with buttressed roots, a sturdy trunk, and horizontally spreading branches that can reach heights of 60–70 feet.
Arjunic acid, an aglycone, is one of the main bioactive components of Terminalia arjuna stem bark known to have a diverse range of therapeutic applications, including cardio-protection, neuro-protection, and hepato-protection.
Beyond T. arjuna, arjunic acid has been identified in additional plant species. Bioassay-guided fractionation of ethyl acetate root extracts of Terminalia sericea yielded the known compound arjunic acid. The compound has also been isolated from Sanguisorba officinalis L., where arjunic acid (arjuntriterpenic acid) is described as a triterpenoid compound isolated from Sanguisorba officinalis L., with identification of new ursane-type triterpenoids from the roots of this species reported in Phytochemistry Letters, 2019.
Within T. arjuna, arjunic acid is found in greatest concentration in the stem bark. The bark of Terminalia arjuna is reported to contain many bioactive compounds, including arjunic acid, arjunolic acid, arjungenin, arjunetin, arjunoglucoside-I, arjunoglucoside-II, asiatic acid, catechin, and gallocatechin, which can be isolated from the cambium. As a glycoside aglycone, arjunic acid constitutes the core structural unit of the bark glycosides arjunoside III and arjunoside IV. The structure of arjunoside III was established as the 28-β-D-(+)-glucuronopyranoside of arjunic acid, while arjunoside IV was shown to be the 3-O-α-L-(−)-rhamnoside of arjunic acid.
Isolation of arjunolic/arjunic acid in its pure form is very difficult because of the presence of asiatic acid along with it in almost all sources. Solvent extraction methods, including methanolic, ethanolic, and aqueous extraction followed by column chromatography, have been employed at research scale. The antioxidant activity, free radical scavenging capacity, and antibacterial activity of this triterpenoid compound have been investigated.
In commercial and traditional settings, arjunic acid is not typically sold as an isolated purified compound for human consumption. Rather, it is consumed as a component of the whole bark or standardized bark extracts of T. arjuna. Common preparations include:
Arjuna bark has been used in the traditional Ayurvedic medical system for at least 3,000 years as a remedy for heart ailments. The tree and its bark hold a prominent place in the three major South Asian systems of indigenous medicine: Ayurveda, Siddha, and Unani. T. arjuna is one of the most used plants in the Siddha, Ayurveda, and Unani systems of treatment.
It was Vagabhatta who, for the first time, advocated the use of stem bark powder in heart ailments. The bark has been described as an astringent, demulcent, expectorant, cardiotonic, styptic, antidysenteric, and urinary astringent, and has been shown to be useful in fracture, ulcers, leukorrhea, diabetes, anemia, cardiopathy, and cirrhosis. The physician Vagbhatta's advocacy for its use in cardiac disease is estimated to date to approximately 1,200 years ago. Vagbhatta mentioned the use of Terminalia arjuna for treating heart diseases about 1200 years ago.
The ancient physician Chakradatta recommended that it be given as a decoction of bark with milk, or as a ghrita (a preparation with ghee or butter). A decoction of its bark with cane sugar and boiled cow's milk is highly recommended in classical texts for endocarditis, pericarditis, and angina.
Various parts of this tree have been used to treat numerous ailments such as cancer, diabetes, inflammation, and microbial infections, as mentioned in ancient medicinal texts such as Ayurveda and Charaka Samhita. Ancient Indian practitioners utilized the powdered tree bark of arjuna for the treatment of "hritshool" (angina) and other cardiovascular problems.
Decoction of the bark has been used as an ulcer wash, while bark ashes have been prescribed for snakebite and scorpion sting. The bark is also prescribed in biliousness and sores and as an antidote to poison, and is believed to have an ability to cure hepatic, congenital, venereal, and viral diseases.
In the Unani system, the plant — where it is known under synonyms including Anjan and Anjani — is classified with the primary traditional indication of cardiotonic and aphrodisiac action. The compound arjunic acid itself, as an isolated entity, was not known to classical practitioners; the bark as a whole — containing arjunic acid alongside arjunolic acid, flavonoids, tannins, and other phytochemicals — was the medicinal agent.
Arjunic acid occurs within a complex matrix of phytochemicals. Terminalia's active constituents include tannins, cardenolides, triterpenoid saponins (arjunic acid, arjunolic acid, arjungenin, arjunoglycosides), flavonoids (arjunone, arjunolone, luteolin), gallic acid, ellagic acid, phytosterols, calcium, magnesium, zinc, and copper.
Arjunic acid, arjunolic acid, arjungenin, arjunone, arjunolone, and luteolin, gallic acid, ellagic acid, oligomeric proanthocyanidins (OPCs), and phytosterols are the major phytoconstituents of Terminalia arjuna that possess many useful biological properties such as anti-microbial, anti-inflammatory, antioxidant, antifeedant, and cardioprotective activities.
Arjunic acid is considered a minor constituent relative to arjunolic acid, the latter being recognized as the dominant and more thoroughly investigated triterpenoid of the bark. Along with arjunolic acid, other known reported minor constituents of T. arjuna include arjunic acid, arjuntenin, baicalein, and quercetin. Despite being described as a minor constituent in comparative phytochemical terms, arjunic acid has been independently investigated for its own biological properties and has been found to contribute meaningfully to the pharmacological profile of the bark.
Arjunic acid and arjunoglycoside (I, II, III and IV) undergo a drug-metabolizing cascade, produce some active molecules, and are responsible for lipid-lowering activity.
The most extensively documented mechanism for arjunic acid is its direct antioxidant capacity. In a study designed to investigate the antioxidant and free radical scavenging capacities of arjunic acid (obtained as an aglycone from the fruit of Terminalia), liver microsomes, mitochondria, and red blood cells (RBCs) were prepared from Wistar rats, and antioxidant capacity was determined by inhibitory effect on lipid peroxidation, hydrogen peroxide-induced RBC hemolysis, and RBC autoxidative hemolysis, with free radical scavenging activity tested by the DPPH method and the DCFHâ‚‚-DA assay. Results showed that arjunic acid was a strong antioxidant and a free radical scavenger, more potent than ascorbic acid, in microsomes lipid peroxidation, DPPH, hydrogen peroxide-induced RBC hemolysis, and DCFHâ‚‚-DA assay (p < 0.05).
The structural basis for this activity is its multiple hydroxyl groups. Its antioxidant property coupled with metal-chelating property (via its hydroxyl groups) protects different organs from metal- and drug-induced organ pathophysiology. The mechanism of cytoprotection of arjunolic acid, at least in part, results from the detoxification of reactive oxygen species (ROS) produced in the respective pathophysiology.
The plant's oleanane triterpenoids, such as arjunic acid, arjunoglycosides, arjunone and arjunolic acid, are primarily responsible for the cardioprotective effects of T. arjuna. Studies using the closely related arjunolic acid (which share structural features with arjunic acid) have elucidated several molecular mechanisms of cardiac protection.
Arjunolic acid binds to and stabilizes the ligand-binding domain of peroxisome proliferator-activated receptor α (PPARα) and increases its expression during cardiac hypertrophy. Arjunolic acid significantly represses collagen expression and improves cardiac function during hypertrophy.
The protective role of arjunolic acid (2:3:23-trihydroxyolean-12-en-28-oic acid) has been studied in the modulation of neutrophil functions in vitro by measuring ROS generation; neutrophils were isolated from normal and acute MI mice to find out the efficacy of arjunolic acid in reducing oxidative stress. Arjunolic acid can inhibit ROS activation through phosphorylation of p47phox and extracellular regulated kinase (ERK) in activated neutrophils.
In AA-pretreated mice exposed to lipopolysaccharide (LPS), C-reactive protein and proinflammatory cytokines (interleukin-1 and tumor necrosis factor-alpha) were significantly reduced, and anti-inflammatory cytokines (interleukin-4 and -10) were significantly increased in cardiac tissues. Furthermore, prior administration of AA to LPS-exposed mice led to a significant decrease in heart caspase-3, -8, and -9 as compared to the LPS group.
The scientific basis behind the therapeutic application of arjunolic acid as a cardioprotective agent in traditional medicine is justified by its ability to prevent myocardial necrosis and apoptosis, platelet aggregation, coagulation, and lowering of blood pressure, heart rate, as well as cholesterol levels.
A study investigated the agonistic property of arjungenin and arjunic acid towards farnesoid X receptor protein (FXR), with pharmacokinetic properties including molecular interactions, absorption, distribution, metabolism, elimination, and toxicity (ADMET) of the ligands checked through in-silico studies. Molecular docking analysis confirmed strong binding energy and interaction of arjungenin and arjunic acid with the target protein, and the ADMET profiles identified for both compounds were promising. Treatment with arjungenin and arjunic acid confirmed increased differentiation of 3T3-L1 cells with a significant (P < 0.05) increase in adiponectin (118.07% and 132.92%) and leptin (133.52% and 149.74%) protein levels compared to the negative control group. FXR is a nuclear receptor involved in bile acid metabolism, cholesterol homeostasis, and glucose regulation; this finding suggests a potential mechanism by which arjunic acid may influence lipid and glucose metabolism.
In cyclooxygenase assays, arjunic acid showed weak inhibitory activity with IC₅₀ values of 36 μM (COX-1) and 253 μM (COX-2). This finding, from research on arjunic acid isolated from Terminalia sericea roots, indicates some capacity to modulate prostaglandin synthesis, though the selectivity and potency at these concentrations is modest.
Bioassay-guided fractionation of ethyl acetate root extracts of Terminalia sericea yielded arjunic acid; both arjunic acid and termilignan B showed activity against Gram-positive and Gram-negative bacteria with MIC values ranging between 1.9 and 15.6 μg/mL. No potential mutagenic effects were observed with these compounds in the Salmonella microsome assay (TA 98).
Some studies proposed that anolignan B, termilignan B, and arjunic acid are the main constituents responsible for the antibacterial activity of the root extract, since they were highly active against several bacterial pathogens (Bacillus cereus, Escherichia coli, Klebsiella pneumoniae, and Staphylococcus aureus), with minimum inhibitory concentrations (MICs) in the range of 1.9–31 µg/mL.
A critical distinction applies throughout this section: the direct scientific evidence for isolated arjunic acid specifically is sparse and largely preclinical (in vitro and animal). The much larger body of clinical and preclinical research pertains to whole Terminalia arjuna bark extract or to the closely related compound arjunolic acid. Where evidence relates specifically to arjunic acid, this is noted explicitly.
Preclinical evidence (arjunic acid specific):
Arjunic acid (AA) is described as one of the major active components of Terminalia arjuna known for its health benefits. One study evaluated the cardioprotective potential of Terminalia arjuna extract (TAE) and AA against cobalt chloride (CoCl₂)-induced hypoxia damage and apoptosis in rat cardiomyocytes; TAE (50 μg/ml) and AA (8 μg/ml) significantly (p < 0.001) protected H9c2 cells, as evidenced by cell viability assays, against CoCl₂ (1.2 mM)-induced cytotoxicity. TAE and AA pretreatments protected the cells from oxidative damage by decreasing the generation of free radicals (ROS, hydroperoxide, and nitrite levels) and retained mitochondrial membrane potential by alleviating the rate of lipid peroxidation induced by CoCl₂ treatment.
Preclinical evidence (arjunolic acid and bark extract, shared mechanistic relevance):
Arjunolic acid, a potent principle from the bark of Terminalia arjuna, has been shown to provide significant cardiac protection in isoproterenol-induced myocardial necrosis in rats; to further explore its mechanism, antiplatelet activity, anticoagulant assays, electrocardiographic changes, serum marker enzymes, antioxidant status, lipid peroxide, and myeloperoxidase (MPO) were measured and compared with acetyl salicylic acid (ASA).
In vivo findings indicate that arjunolic acid may be a promising cardioprotective agent against LPS-stimulated cardiotoxicity, at least in part, through upregulation of cardiac antioxidants, reduction of lipid peroxidation, and inhibition of inflammation and cardiac cell death.
Clinical evidence (whole bark extract):
Evidence from various in vitro, in vivo, and clinical trials reveals the pleiotropic effects of Terminalia arjuna such as anti-atherogenic, hypotensive, inotropic, anti-inflammatory, anti-thrombotic, and antioxidant actions for treatment of various cardiovascular disorders. A double-blind, randomized controlled trial on patients with chronic heart failure (Maulik et al., 2016, Phytomedicine) has been identified in the clinical literature. Arjuna has been used in the indigenous system for the treatment of cardiac ailments since 500 BC; however, there is a lack of vigilance studies during long-term therapy, and the present clinical study was planned to examine the long-term safety of Arjuna as an adjunct drug in chronic coronary artery disease (CAD) patients.
During one study period, a total of 35 patients of chronic CAD were enrolled to receive Arjuna bark extract powder (500 mg three times daily) along with conventional drugs, while the control group (35 patients) received conventional drugs alone.
Overall, both clinical and preclinical studies clearly indicate possible therapeutic potential of Terminalia arjuna bark in a wide range of cardiovascular diseases; many of these studies are randomized, double-blind, and placebo-controlled; however, there are some striking shortcomings in most of these studies which need to be addressed in future studies. Though various pharmacological studies and clinical trials support its benefit in CVD as per traditional use, new clinical trials using more rigorous state-of-the-art technology and in a larger population setup are warranted to assess the traditional putative efficacy of Terminalia arjuna.
Terminalia species have been evaluated to a limited extent for potential hepatoprotective, cardiovascular, cholesterol-reducing, dermatologic, antimicrobial, antioxidant, and urate-lowering effects; however, clinical trial data are lacking to recommend use for any indication.
Evidence strength: For isolated arjunic acid in cardiovascular applications — preliminary; restricted to in vitro and one or two animal studies. For the parent plant extract, there is moderate-quality evidence from small randomized controlled trials, but with methodological limitations.
The antioxidant activity of isolated arjunic acid has been directly demonstrated in laboratory models. In a study from the Department of Pharmacology, Tibet Nationalities Institute, arjunic acid was found to be a strong antioxidant and a free radical scavenger, more potent than ascorbic acid, in microsomes lipid peroxidation, DPPH, hydrogen peroxide-induced RBC hemolysis, and DCFHâ‚‚-DA assay (p < 0.05). However, no significant difference was observed in the RBC autoxidative hemolysis assay (p > 0.05).
Evidence strength: In vitro only. No clinical trials have evaluated arjunic acid specifically as an antioxidant supplement in humans.
Arjunolic acid plays an effective role in exerting protection against both type I and type II diabetes and also ameliorates diabetic renal dysfunctions. The FXR agonism findings for arjunic acid noted above suggest a possible mechanism for lipid-modulating effects, though this remains at the in-silico and in-vitro stage. The main mechanism behind the anti-hyperlipidemic activity involves the anion exchange property, where anions of phytochemicals in the plant bind with the bile acid anions in the intestine and convert cholesterol into bile acid, which is then excreted in stool, leading to a decrease in serum LDL cholesterol level.
Evidence strength: Preclinical (in-silico, in vitro, animal models). No human clinical trials specifically assessing arjunic acid for glucose or lipid metabolism have been identified in the peer-reviewed literature.
T. arjuna has been reported to exhibit hepatoprotective activity against paracetamol-induced hepatic injuries. Administration of aqueous extracts of T. arjuna bark before paracetamol/CClâ‚„ administration led to a significant reduction in sGOT, sGPT, sALP, and SB levels, almost comparable to silymarin in CClâ‚„-induced hepatocarcinoma. Another study indicated that methanolic extracts of T. arjuna stems and their phytochemicals also exhibit hepatoprotective activity.
Evidence strength: Preclinical animal studies; no clinical trials specifically on arjunic acid for liver conditions identified.
As described under mechanisms of action, arjunic acid isolated from Terminalia sericea roots showed direct antibacterial activity in vitro. Methanolic and water extracts of T. arjuna bark showed significant inhibition zones against 22 tested bacteria, including eight uropathogens, with MIC values between 0.16 and 2.56 mg/mL. The chloroform extract showed no antibacterial activity. The aqueous extract of T. arjuna bark also demonstrated strong antifungal effects against eight Candida species, with MIC values ranging from 0.16 to 0.64 mg/mL.
Evidence strength: In vitro only. No clinical trials on the antimicrobial effects of arjunic acid or arjuna preparations in infectious disease contexts have been identified.
While direct anticancer work on arjunic acid itself is limited, there is active interest in using arjunolic acid as a scaffold for synthetic derivatives. Diverse research groups have utilized arjunolic acid as a template for synthesizing various semi-synthetic derivatives, which have been evaluated for their anti-cancer, anti-diabetic, and antioxidant properties. Arjunolic acid (AA) is a pentacyclic triterpenoid with promising anticancer properties. A series of novel AA derivatives containing a pentameric A-ring with an enal moiety, combined with additional modifications at C-28, were designed and prepared. For one active derivative, the anticancer molecular mechanism of action in PANC-1 cells showed induction of cell-cycle arrest at G0/G1 phase and significant inhibition of wound closure rate of PANC-1 cancer cells in a concentration-dependent manner; additionally, the compound synergistically increased the cytotoxicity of Gemcitabine, especially at a concentration of 0.24 μM.
Evidence strength: Preclinical derivatives research only. No clinical oncology evidence for arjunic acid or its direct analogues.
Arjunic acid as a purified isolated compound is not used in standardized human dosing protocols. Dosages in the scientific literature refer exclusively to bark extract preparations and to preclinical experimental concentrations:
No established human therapeutic dosage for purified arjunic acid has been defined in any regulatory monograph or clinical pharmacopoeia identified in the available literature.
It is clearly documented that this plant has a good safety profile when used in conjunction with other conventional drugs. Extracts of T. arjuna are well tolerated.
A directly relevant in-vitro pharmacokinetic study specifically examined arjunic acid's potential to inhibit cytochrome P450 enzymes in human liver microsomes. Alcoholic and aqueous bark extracts of T. arjuna, arjunic acid, arjunetin, and arjungenin were evaluated for their potential to inhibit CYP3A4, CYP2D6, and CYP2C9 enzymes in human liver microsomes. While alcoholic and aqueous bark extract of T. arjuna showed potent inhibition of all three enzymes with IC₅₀ values less than 50 μg/mL, arjunic acid, arjunetin, and arjungenin did not show significant inhibition of CYP enzymes in human liver microsomes. Enzyme kinetics studies suggested that the extracts of arjuna showed reversible non-competitive inhibition of all three enzymes in human liver microsomes.
This finding is pharmacologically significant: it suggests that the CYP-inhibitory potential of whole bark extracts observed in vitro may be attributable to complex mixture components rather than to arjunic acid itself.
Caution is warranted for people who are at risk of bleeding or who are taking blood-thinning medications because arjuna may inhibit platelet aggregation. While this caution relates to the plant as a whole, the antiplatelet mechanism is partly attributable to the triterpenoid fraction that includes arjunic acid.
The evidence shows that there is no interaction of T. arjuna with other cardiovascular drugs, and T. arjuna can therefore be used safely along with these drugs. The pharmacovigilance study monitored 35 CAD patients receiving bark extract powder at 500 mg three times daily alongside aspirin, beta-blockers, ACE inhibitors, and statins, with hemogram, liver function tests, and kidney function tests conducted every 6 months.
Arjuna may pose potential risks and should be avoided during pregnancy. Given the lack of sufficient safety data, its use should also be avoided during lactation. Information regarding safety and efficacy in pregnancy and lactation is lacking.
No potential mutagenic effects were observed with arjunic acid in the Salmonella microsome assay (TA 98). This suggests the compound does not exhibit direct mutagenicity under these test conditions, though more comprehensive genotoxicity profiling in human-relevant models remains limited.
There is a paucity of data regarding the exact molecular mechanism of its action, appropriate form of drug administration, whether whole crude drug or aqueous or alcoholic extract should be used, toxicological studies, and its interaction with other drugs. Experimental studies demonstrate the versatile effects of arjunolic acid, but still, further investigations are necessary to identify the functional groups responsible for its multivarious effects and to study the molecular mechanisms as well as the probable side effects/toxicity owing to its long-term use.
Arjunic acid occupies a specific but relatively underexplored niche within the broader pharmacology of Terminalia arjuna. The following summarizes the state of evidence:
Health conditions that Arjunic acid may help support.
Arjunic acid is a principal triterpenoid saponin from Terminalia arjuna bark identified as a primary cardioactive compound. It contributes to arjuna's anti-ischemic, antioxidant, and antiatherogenic properties documented in PubMed-indexed reviews and experimental studies. It boosts endogenous antioxidant defense systems relevant to arterial protection.
Body systems that Arjunic acid may help support.
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