Common name: Maslinic acid
Synonyms: Crategolic acid, Crataegolic acid, Masilinic acid, Maslic acid, 2a-Hydroxyoleanoic Acid
CAS NO.: 4373-41-5
Molecular Formula: C30H48O3
Molecular Weight: 472.7
Structure:

Specification: 7%, 10%, 50%, 60%, 85%, 98%( off white to white Powder)
Test method: HPLC
Product Main Quality Items：

Specification	98%
Appearance	white Powder
Contents(Calculated on dry basis by HPLC)	NLT98%
Water contents	NMT2%

Packing: 1kg/bag, 10kg/bag
Storage: Store in cool and dry place and keep away from strong direct light and heat
Shelf Life: Two years when properly stored
Please see the typical HPLC of 70% Maslinic acid as follow:

Please see the typical HPLC of 98% Maslinic acid as follow:

Applications and Health Benefits:

What is Maslinic acid?

Maslinic acid is a compound derived from olive. It is a member of the group of triterpenes known as oleananes.
Recent several studies have proved that maslinic acid exerts a wide range of biological activities, i.e. antitumor, antidiabetic, antioxidant, cardioprotective, neuroprotective, antiparasitic and growth-stimulating.

Health Benefits of Maslinic acid:

1. Maslinic Acid and Cancer

The antitumor activity of maslinic acid has become remarkable in recent years, as evidenced by the higher number of studies that address this issue, compared to those about other biological effects. The vast majority of published references correspond to in vitro experiments that show the anti-proliferative and/or pro-apoptotic effect of maslinic acid, together with plausible mechanisms of action that involve different signaling pathways. Colon cancer cell lines have been extensively used with this aim, but there is no shortage of studies that prove the above-mentioned effects in a wide range of cell lines from other origins. Moreover, this antitumor effect has also been assessed in several animal models, with positive results that reinforce its potential as anticarcinogenic agent.

2. Maslinic Acid and Diabetes

The role of maslinic acid in glucose metabolism has also been extensively studied. Wen et al. provided the first evidence of the inhibitory effect of the triterpene on glycogen phosphorylases (GP), which catalyze the first step of glycogen breakdown. In a first in vitro assay using GPa (activated form of the enzyme) isolated from rat liver, maslinic acid inhibited the enzyme with an IC50 of 99 μM, being 6-fold more potent than caffeine, an established GP inhibitor. Based on this finding, the hypoglycemic activity of the triterpene was evaluated in vivo, using a mouse model of diabetes induced by adrenalin, which is known to indirectly stimulate glycogenolysis and thus increase glucose blood concentration. After the oral administration of maslinic acid (100 mg/kg) for 7 days, fasted plasma glucose appeared to be up to 46% lower, compared to animals that had received only the vehicle. Further work of the same authors went into detail about the mechanism of inhibition of maslinic acid on GP. The crystal structure of the complex GPb (inactivated form of the enzyme)-maslinic acid was determined, which revealed that the triterpene binds at the allosteric activator site, where the physiological activator AMP binds.

3. Maslinic Acid as Antioxidant and Anti-Inflammatory

The antioxidant effect of maslinic acid was first evaluated by Montilla et al. in a model of oxidative status induced by CCl4, which induces lipid peroxidation. Pre-treatment of the rats once daily for 3 days with the triterpene at doses of 50 and 100 mg/kg reduced by approximately 18% plasma levels of endogenous lipid peroxides, at both doses, and by 6.5% and 19%, respectively, the susceptibility of plasma to lipid peroxidation. Similarly, the triterpene isolated from the flowers of Punica granatum prevented the CuSO4-induced oxidation of rabbit plasma LDL, monitored by the formation of dienes, by 33.8%. More recently, Allouche et al. conducted an exhaustive study about the antioxidant properties of several pentacyclic triterpenic diols and acids on LDL particles isolated from human plasma. Maslinic acid not only retarded the initiation and decreased the rate of CuSO4-induced LDL oxidation, but also showed peroxyl radical scavenging activity and a slight metal (copper) chelating effect.
Further research has been done in macrophages, which play a role in the defensive system of the organism in response to activation by a pathogen. Cells were isolated from murine peritoneum and activated with lipopolysaccharide (LPS), a compound that gives rise to a potent inflammatory response mediated by the production of cytokines, such as TNF-α, and also by reactive nitrogen and oxygen species, among others. In this study, the effect of the triterpene was tested on the synthesis of NO, superoxide and hydrogen peroxide. Although maslinic acid did not exert any direct inhibitory effects on the formation of the first two species, the compound did reduce the generation of hydrogen peroxide (IC50 of 46.3 μM), in a way that was similar to that of catalase. In addition, the release of the pro-inflammatory cytokines IL-6 and TNF-α was significantly reduced after treatment with maslinic acid at concentrations of 50 and 100 μM.

4. Maslinic Acid and Cardioprotection

The protective effect of maslinic acid against cardiovascular diseases has been studied using different approaches, which include the assessment of the triterpene in controlling risk factors such as hypertension or hyperlipidemia.
On one hand, experiments with aortic rings isolated from spontaneously hypertensive rats showed that maslinic acid exerted a concentration-dependent relaxation (IC50 of 14.1 μM), after precontraction with phenylephrine [69]. The effect was endothelium-dependent, since the removal of the endothelium attenuated the relaxation. In order to elucidate the underlying mechanism, intact (with endothelium) aortic rings were pre-incubated with NG-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor. This resulted in a diminished relaxation in intact aortic rings, indicating that NO was involved in maslinic acid-induced vasodilation.
On the other hand, in rats fed a high-cholesterol diet for 30 days, the oral administration of maslinic acid (100 mg/kg) for the last two weeks resulted in a hypolipidemic effect, as evidenced by a reduction of more than 70% in serum triglycerides, total cholesterol and LDL-cholesterol. The triterpene also restored the levels of the hepatic marker enzymes lactate dehydrogenase (LDH), alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Similarly, both the glycogen content and the morphological alterations observed in hepatocytes were reversed in maslinic acid-treated animals, compared to controls.
The cardioprotective effect of maslinic acid has also been tested in isoproterenol-induced myocardial infarction in Wistar rats. Animals that had been pre-treated with maslinic acid (15 mg/kg) for 7 days showed an improved serum lipid profile with significantly decreased levels of total cholesterol, triglycerides, LDL-cholesterol, VLDL-cholesterol and increased HDL-cholesterol. The activity of the cardiac marker enzymes creatine kinase (CK), ALT, AST and γ-glutamyl transferase (GGT) significantly decreased. Furthermore, the oxidative status of the animals was evaluated by measuring malondialdehyde (MDA), an indicator of lipid peroxidation, and paraoxonase (PON), an atheroprotective enzyme found in HDL particles. MDA levels were significantly reduced, while the activity of PON increased remarkably in rats that had received maslinic acid, compared to non-treated animals.

5. Maslinic Acid and Neuroprotection

A series of exhaustive studies have demonstrated that maslinic acid may confer neuroprotection in some pathological situations. In a first experiment with primary cultures of rat cortical neurons, cells were incubated with different concentrations of the triterpene (0.1, 1, 10 μM) and subjected to 1 h of oxygen-glucose deprivation followed by reoxygenation (24 h). Maslinic acid dose-dependently attenuated neuronal damage, which was evaluated through observation of morphological changes, release of lactate dehydrogenase (LDH) and neuronal viability [74], and this effect resulted from reduced activity of both caspase-9 and caspase-3. Upstream of caspases, high levels of NO might trigger apoptotic cell death. This gaseous molecule is synthetized in great amounts by the inducible nitric oxide synthase (iNOS) in response to hypoxia, thus inhibition of this enzyme could be the mechanism underlying the protective effect of maslinic acid in oxygen-deprived cortical neurons. Qian et al. observed that when challenged neurons were exposed to the triterpene (10 μM), the amount of NO in the culture medium was rescued to levels close to those found in normoxic conditions, which was correlated with reduced iNOS protein and mRNA levels.