IngredientsCorosolic acid (CA) is a naturally occurring ursane-type pentacyclic triterpenoid with the molecular formula C30H48O4 and a molecular weight of 472.70 g/mol; its systematic name is 2α,3β-dihydroxy-urs-12-en-28-oic acid. It is also commonly designated by the synonym 2α-hydroxyursolic acid, and carries the CAS registry number 52213-27-1. Like its structural analogs, corosolic acid is a pentacyclic triterpene extracted from plants and has low solubility in water due to its rigid scaffold and hydrophobic properties. The compound belongs to the ursane skeleton class, and its structural analogs include ursolic acid (UA), oleanolic acid (OA), maslinic acid (MA), asiatic acid (AA), and betulinic acid (BA), all of which are natural pentacyclic triterpenes.
Corosolic acid is a pentacyclic triterpenoid predominantly found in medicinal plants such as Lagerstroemia speciosa (Banaba), Eriobotrya japonica, and Orthosiphon stamineus. Lagerstroemia speciosa L. is commonly known as Crepe Myrtle and belongs to the botanical family Lythraceae. This review identified Lagerstroemia speciosa as exhibiting the highest reported concentration of corosolic acid, at 0.89%. Analytical quantification confirms this: remarkable quantities of corosolic acid were found in dried extracts from aerial parts of Lagerstroemia speciosa and Orthosiphon stamineus (14,233 and 1,132 mg/kg, respectively).
Corosolic acid is found in numerous plant species, including Lagerstroemia speciosa L., Tiarella polyphylla D. Don, Datisca cannabina L., Eriobotrya japonica (Thunb.) Lindl., and Perilla frutescens (L.) Britton. Components such as corosolic acid, asiatic acid, arjunolic acid, betulinic acid, and oleanolic acid, known for their hypoglycemic activity in L. speciosa, were also identified in other Lagerstroemia species, including L. indica, L. calyculata, L. crispa, L. floribunda, L. limii, and L. ovalifolia. Corosolic acid has also been isolated from European and South American plants.
Common applications of L. speciosa products include tea bags, dried herbs, ready-to-drink preparations, juice, beverages, as well as capsules and tablets for dietary supplements. As a purified ingredient, corosolic acid is standardized to varying concentrations in commercial extracts—notably, products standardized to 1% and 18% corosolic acid have been used in documented clinical studies. The branded extract Glucosol™ is a well-known standardized product used in multiple research settings.
Banaba (Lagerstroemia speciosa L.) leaf extracts have anti-diabetic properties and have been used as medicine in Southeast Asia, especially in the Philippines. Leaves of the species have been traditionally used over thousands of years as folkloric treatment by native Indians and Japanese for illness and ailments, particularly for lowering blood sugar levels and weight loss. Tea preparations from the leaves of Lagerstroemia speciosa L. have traditionally been used for weight-loss and by diabetics to balance blood sugar levels (Murakami et al., 1993).
Lagerstroemia speciosa, more commonly known as "Banaba" in the Philippines or "Pride of India," has long been used in various forms to treat diabetes and kidney-related ailments. Leaves have been used to treat diabetes mellitus and serve as diuretic and decongestant. Fresh leaves have also been used as an emergency tincture for wounds and sanitizing the surface of the skin, roots are used for treating mouth ulcers, and bark is used as a stimulant, for relief of abdominal pains, and as a febrifuge.
Banaba is also recommended for kidney, bladder problems, and hypertension in traditional practice. The earliest formal scientific documentation of Banaba's blood-glucose–lowering activity came from Garcia in 1940, who published work in the Journal of the Philippine Medical Association describing the hypoglycemic effect of decoctions of L. speciosa leaves administered orally.
Systematic Japanese scientific investigation into Banaba leaf and corosolic acid began in the 1990s, with Murakami and colleagues in 1993 identifying corosolic acid as the active hypoglycemic triterpenoid principle of the leaf extract. Both in-vitro and in-vivo studies on the glucose transporter stimulatory effects of extracts from Lagerstroemia speciosa L. had been described, including the identification of corosolic acid as the active principle of this extract and its hypoglycemic effect.
Chemical analysis revealed that L. speciosa is a storehouse of various phytochemicals, including triterpenoids, acetal, ellagic acid, tannins, alkaloids, sterol, tannic acid, lagerstroemin, flosin B, and reginin A. Six pentacyclic triterpenes—oleonic acid, arjunolic acid, asiatic acid, maslinic acid, corosolic acid, and 2,3-hydroxyursolic acid—with α-glucosidase and α-amylase inhibitory activities were also isolated from L. speciosa.
Although standardized products contain a high level of corosolic acid, it is not entirely clear if observed effects are due to corosolic acid alone or a combination of corosolic acid with tannin components. Ellagitannins such as lagerstroemin are considered co-active constituents that may contribute to the overall antidiabetic profile of Banaba leaf extracts.
At the molecular level, corosolic acid enhances insulin receptor (IR) signaling in skeletal muscle. Studies using L6 myotubes and other insulin-responsive cells demonstrate that corosolic acid increases IR phosphorylation and downstream Protein kinase B (Akt) activation, consequently promoting glucose transporter type 4 (GLUT4) translocation to the cell membrane. These insulin-mimetic effects are potent enough to be blocked by the PI3K inhibitor wortmannin, confirming the involvement of the canonical insulin signaling pathway.
Corosolic acid inhibits the enzymatic activities of several diabetes-related non-receptor protein tyrosine phosphatases (PTPs) in vitro, such as PTP1B, T-cell-PTP, src homology phosphatase-1, and src homology phosphatase-2. One proposed mechanism is corosolic acid's inhibition of PTP1B, which normally attenuates insulin signaling; by inhibiting PTP1B, corosolic acid sustains IR phosphorylation, thereby potentiating insulin action.
Another study reported that corosolic acid inhibited gluconeogenesis by increasing the production of the gluconeogenic intermediate fructose-2,6-bisphosphate in isolated hepatocytes. Cheng reported that corosolic acid represents a new class of allosteric site inhibitors of glycogen phosphorylase (GP), and its glucose-lowering activity could, at least in part, be due to modulation of glycogen metabolism. In addition, Yamada found that corosolic acid increased glucokinase activity without affecting glucose-6-phosphatase activity, suggesting an increase in glycolysis.
Muscle GLUT4 translocation from the low-density microsomal membrane to the plasma membrane was significantly increased in orally corosolic acid–treated mice compared with controls (P < 0.05).
Despite numerous in vitro and animal studies elucidating potential mechanisms involving pathways like AMPK, NF-κB, YAP, and various kinases, a critical gap exists between promising preclinical data and robust clinical validation. Activation of AMPK (AMP-activated protein kinase) by corosolic acid has been documented preclinically, which promotes glucose transport independently of insulin and may also reduce lipogenesis and promote fatty acid oxidation.
Corosolic acid inhibits protein tyrosine phosphatase 1B in vitro, where inhibition of this phosphatase is proposed as a therapy for obesity. Corosolic acid is also a pancreatic lipase inhibitor, the main enzyme for lipid absorption. In a mouse study, corosolic acid acted as a peroxisome proliferator-activated receptor alpha (PPARα) agonist, regulating lipid metabolism and increasing fatty acid beta-oxidation in the liver.
Corosolic acid has the ability to modulate multiple cancer-related signaling pathways and processes, such as the NF-κB, PI3K/Akt, and Wnt/β-catenin pathways, apoptosis, Nrf2, and several other components associated with cellular proliferation or mortality. Studies show that corosolic acid can modulate a diverse range of cancer signaling pathways including NF-κB, PI3K/Akt, and Wnt/β-catenin, and apoptosis.
Accumulating evidence suggests that corosolic acid has anticancer effects through interfering with several processes such as cell proliferation, angiogenesis, invasion, metastasis, and apoptosis. Corosolic acid induces apoptosis in gastric cancer by inhibiting the NF-κB pathway, and in colorectal cancer by activating mitochondria-mediated and caspase-dependent pathways with decreased expression levels of p65, Fas, caspase-8, -9, and -3, and Bcl-2, and increased expression of Bax. In addition, corosolic acid triggers apoptosis by elevating reactive oxygen species (ROS) levels and lowering Bcl-2 levels in lung cancer, and by activating caspase-3/7, -8, and -9 in osteosarcoma.
Preclinical evidence demonstrates that corosolic acid exerts broad-spectrum anticancer activity by inducing apoptosis, autophagy, ferroptosis, and cytotoxicity, while inhibiting tumor cell proliferation, metastasis, and survival signaling pathways, including PI3K/Akt/mTOR, NF-κB, STAT3, and YAP/TAZ. Emerging data also highlight its immunomodulatory role, particularly through suppression of Th17-mediated inflammatory responses, which may further contribute to its antitumor effects.
The cardioprotective benefits of corosolic acid include the restoration of cardiovascular function, preservation of endogenous antioxidants, histological rescue of myofibrils, and reduction of lipid peroxidation in cardiac tissue. The expression of PPAR-γ was enhanced by corosolic acid, and concomitant therapy with the PPAR-γ antagonist GW9662 significantly attenuated this cardiovascular protection, demonstrating that activation of the PPAR-γ pathway is associated with the cardioprotective effect of corosolic acid.
The most extensively investigated clinical application of corosolic acid is glycemic control. The beneficial effects of Banaba and corosolic acid with respect to various aspects of glucose and lipid metabolism appear to involve multiple mechanisms, including enhanced cellular uptake of glucose, impaired hydrolysis of sucrose and starches, decreased gluconeogenesis, and the regulation of related pathways.
Glucosol at daily dosages of 32 mg and 48 mg for 2 weeks showed a significant reduction in blood glucose levels. These findings indicate a moderate glucose-lowering effect—a reduction on the order of 10–15% in postprandial levels—aligned with an α-glucosidase inhibitory effect in vivo. Notably, the effective dose in humans (10 mg) is relatively low, suggesting corosolic acid or Banaba extract has efficacy at nutraceutical dosing levels.
Despite extensive preclinical data demonstrating the multi-target potential of corosolic acid in regulating glucose metabolism, high-quality human evidence supporting its clinical translation is extremely scarce, constituting the most significant "translational gap" in current research. A 2011 systematic review concluded that standardized Banaba leaf extract containing corosolic acid could induce a dose-dependent decrease in blood glucose in patients with type 2 diabetes and was generally "well-tolerated"; however, the original studies on which this conclusion relies were insufficient in terms of design details, sample size, and reporting of specific safety data. Key human evidence is isolated and outdated: the only rigorously designed human trial was published nearly two decades ago. Evidence is therefore assessed as preliminary and limited: positive signals exist in small, short-duration trials, but large, high-quality, placebo-controlled studies are lacking.
Accumulating evidence has indicated that corosolic acid exerts anti-diabetic, anti-obesity, anti-inflammatory, anti-hyperlipidemic, and anti-viral effects. The weight-related evidence is largely indirect and derives from the same small clinical studies as the glycemic data. A 12% decrease in fasting and 60-minute postprandial blood glucose levels was observed after 2 weeks of administration, and the authors also reported an average three-pound weight loss after the 2 weeks. Preclinical evidence in animal models points to mechanisms including pancreatic lipase inhibition and PPARα agonism, but dedicated human weight-loss trials are absent. Evidence is preliminary, predominantly preclinical.
Corosolic acid also exhibits antihyperlipidemic and antioxidant activities. In preclinical models, corosolic acid attenuates hepatic lipid accumulation and inflammatory response via AMPK/SREBPs and NF-κB/MAPK signaling pathways. Corosolic acid is the main active component of Lagerstroemia speciosa and has been known to serve several pharmacological effects, such as antidiabetic, anti-oxidant, and anticancer effects. Evidence for hepatoprotective and hypolipidemic activity in humans remains absent; all relevant data are in vitro or animal-based.
Experimental studies have indicated that corosolic acid plays a pivotal anticancer role in several tumorigenic processes in vitro and in vivo, including cellular proliferation, apoptosis, angiogenesis, lymphangiogenesis, metastasis, and tumor immunity, and it exerts a synergistic effect when administered with other anticancer agents.
Preclinical cytotoxicity data have been reported against a range of cancer cell lines:
More research is required to determine corosolic acid's potential in human clinical trials. All current anticancer evidence is preclinical (in vitro or animal). No human clinical cancer trials have been completed.
The current evidence reports that corosolic acid has been proven a potential sPLA2IIa inhibitor that neutralized sPLA2IIa-induced indirect haemolytic activity and mouse paw edema in a concentration-dependent manner, establishing its anti-inflammatory properties in preclinical models. Human evidence is entirely lacking; evidence is limited to in vitro and animal studies.
Research in diabetic rat models proves that corosolic acid can ameliorate isoproterenol-induced acute myocardial injury, suggesting it may be a viable target for the treatment of cardiovascular diseases. No human cardiovascular trials have been conducted. Evidence is preclinical only.
Accumulating evidence has indicated that corosolic acid exerts anti-viral effects, though published data are primarily in vitro. No controlled human antiviral trials have been reported for corosolic acid. Evidence is preliminary and preclinical.
The following dosages are reported verbatim from cited studies and patent literature; they should not be interpreted as recommended or therapeutic doses.
Glucosol in a soft gel capsule formulation showed a 30% decrease in blood glucose levels compared to a 20% drop seen with a dry-powder filled hard gelatin capsule formulation (P < 0.001), suggesting that the soft gel formulation has better bioavailability than a dry-powder formulation.
A decrease in blood glucose levels has been observed within 2 hours of dosing, and the decrease is typically in the range of 10–15%, although a decrease of 30% has been reported.
Corosolic acid and its structural analogs have low solubilities in water due to their rigid scaffold and hydrophobic properties. Corosolic acid has notable in vitro toxicity, low water solubility, and poor pharmacokinetic properties. These limitations have driven pharmaceutical research into improved delivery systems. Various approaches have been explored, including the synthesis of water-soluble glycoside derivatives, encapsulation in liposomes, complexation with cyclodextrins, development of self-assembling systems, formulation into lipid nanoparticles, and creation of self-microemulsifying drug delivery systems (SMEDDS).
Thorough absorption, distribution, metabolism, and excretion (ADME) studies in multiple species to determine bioavailability (especially comparing different formulations), tissue distribution, clearance mechanisms, and relationships between dose, exposure, and pharmacodynamic markers have been called for but are not yet comprehensively established.
No adverse effects have been observed or reported in any studies involving human subjects receiving Banaba, including one study involving 15 subjects who were given Banaba extract daily for up to 1 year. Acute and chronic clinical studies of corosolic acid (Glucosol™) formulations in normal subjects at a daily dose of 48 mg indicate that their blood sugar levels remain in the normal range (75 to 110 mg/dL) before, during, and after intake, and blood chemistry and hematology profiles did not suggest any significant changes, supporting the safety profile.
According to the research to date, no side effects have been reported in animals, nor have adverse events been viewed or reported in controlled human clinical studies. However, toxicological information from larger studies remains limited.
A clinically significant adverse event has been documented in the peer-reviewed literature. Corosolic acid from Banaba leaves has been used as a traditional herbal medicine for diabetes and kidney disorders; however, a reported case involved the first known instance of a diabetic patient who developed severe lactic acidosis after taking corosolic acid.
A 55-year-old man presented with anorexia, severe abdominal pain, and decreased urine output. He had type 2 diabetes mellitus, stage 3a chronic kidney disease, and gouty arthritis. Before admission he had been taking corosolic acid daily for 1 month and diclofenac daily for joint pains for 1 week.
The authors suggest that the patient had acute kidney injury due to NSAID-induced hypoperfusion, with consequent accumulation of corosolic acid. He may also have had a combination of corosolic acid–related type B lactic acidosis and mild hypoxemia-related type A lactic acidosis. The proposed mechanism: corosolic acid increases fructose 2,6-bisphosphate production, which enhances phosphofructokinase 1 activity and inhibits fructose-1,6-bisphosphatase, resulting in enhanced glycolysis and inhibition of gluconeogenesis, thereby favoring lactic acid production. In the presence of lactic acid, corosolic acid markedly enhances fructose 2,6-bisphosphate production and further favors glycolysis.
Caution is warranted in patients with renal impairment; acute lactic acidosis has been reported.
A case of severe acute lactic acidosis was attributed to the likely accumulation of corosolic acid in a patient with type 2 diabetes mellitus, gouty arthritis, and stage 3a chronic kidney disease with NSAID-induced acute renal impairment. The patient had been taking corosolic acid daily for 1 month. One week prior to admission, NSAID-induced renal hypoperfusion (from self-medication with diclofenac) was thought to have led to subsequent accumulation of corosolic acid.
Given its blood glucose–lowering mechanism, additive hypoglycemic effects are theoretically possible when corosolic acid is used concurrently with antidiabetic pharmaceutical drugs (insulin secretagogues, insulin, or other oral hypoglycemics), though no formal pharmacokinetic drug interaction studies in humans have been published.
A single oral dose toxicity study in rats administered Glucosol at 5 g/kg showed no marked pathological findings (Hamamoto 1999).
Toxicological evaluations indicate that corosolic acid possesses a favorable safety profile at therapeutic doses; however, its clinical translation is hindered by poor aqueous solubility and limited oral bioavailability.
Information regarding safety and efficacy in pregnancy and lactation is lacking. Formal pediatric safety or efficacy data have not been published.
There is potential for skin rashes because the product may be derived from several plant species.
The overall body of evidence for corosolic acid is characterized by a substantial volume of preclinical (in vitro and animal) data but a very limited number of small, often inadequately controlled human trials. Despite numerous in vitro and animal studies elucidating potential mechanisms involving pathways like AMPK, NF-κB, YAP, and various kinases, a critical gap exists between this promising preclinical data and robust clinical validation.
High-quality human evidence supporting its clinical translation is extremely scarce. The existing directly relevant evidence primarily comprises three key studies, which exhibit substantial differences in type, depth, and clinical relevance.
Researchers have called for comprehensive ADME studies, longer-duration trials with larger samples, standardized extraction and quantification protocols, and exploration of improved delivery systems to overcome corosolic acid's inherent bioavailability limitations. Emerging data also highlight an immunomodulatory role through suppression of Th17-mediated inflammatory responses. Toxicological evaluations indicate a favorable safety profile at therapeutic doses.
Health conditions that Corosolic acid may help support.
Corosolic acid is the primary bioactive triterpenoid of banaba leaf (Lagerstroemia speciosa) and has demonstrated blood glucose-lowering effects in human subjects. A clinical trial found that corosolic acid reduced blood glucose levels within 60 minutes. Multiple human studies confirm a 12–30% reduction in fasting blood glucose.
Corosolic acid is the primary bioactive triterpenoid in banaba leaf that acts as an insulin mimetic, promoting GLUT4-mediated glucose uptake and inhibiting alpha-glucosidase, reducing postprandial hyperglycemia and supporting weight management by limiting glucose available for adipogenic conversion.
Corosolic acid is the primary bioactive triterpenoid in banaba leaf, shown to decrease blood glucose within 60 minutes in human subjects in a randomized crossover study. It activates GLUT-4 translocation and inhibits alpha-glucosidase, supporting blood glucose stabilization. A 2-week clinical study in 10 type 2 diabetic subjects using banaba extract showed 30% blood glucose reduction.
Corosolic acid, the primary bioactive of banaba (Lagerstroemia speciosa) leaf, improves insulin sensitivity through AMPK activation and PPAR-γ/PPAR-α upregulation. A 12-week RCT in prediabetics (n=45) with 300 mg/day banaba extract containing 0.3% corosolic acid significantly reduced HbA1c, fasting plasma glucose, and HOMA-IR compared to placebo.
Body systems that Corosolic acid may help support.
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