urs-12-ene-3,28-diol/Urs-12-ene-3,28-diol, (3β)-/(3S,4aR,6aR,6bS,8aS,11R,12S,12aS,14aR,14bR)-8a-(Hydroxymethyl)-4,4,6a,6b,11,12,14b-heptamethyl-1,2,3,4,4a,5,6,6a,6b,7,8,8a,9,10,11,12,12a,14,14a,14b-icosahydro-3-picenol/urs-12-ene-3beta,28-diol/12-URSEN-3BETA,28 DIOL/3B,28-DIHYDROXY-URSA-12-EN/(3β)-Urs-12-ene-3,28-diol/12-URSEN-3B,28-DIOL/Uvaol,Urs-12-ene-3,28-diol/(3S,4aR,6aR,6bS,8aS,11R,12S,12aS,14aR,14bR)-8a-(Hydroxymethyl)-4,4,6a,6b,11,12,14b-heptamethyl-1,2,3,4,4a,5,6,6a,6b,7,8,8a,9,10,11,12,12a,14,14a,14b-icosahydro-3-picenol/Urs-12-ene-3β,28-diol/Urs-12-ene-3b,28-diol/Uvaol
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
523.7±50.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:545-46-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
The ethanolic extract of the leaves of Eriobotrya japonica exhibited inhibitory activity against phosphodiesterase-4D (PDE4D), which is a therapeutic target of inflammatory disease. Subsequent bioassay-guided fractionation led to the isolation of a new triterpene (1), together with seven known triterpenoids, methyl corosolate (2), ursolic acid (3), oleanolic acid (4), methyl maslinate (5), α-amyin (6), 3β,19α,23-trihydroxy-urs-12-ene (7) and uvaol (8). The structure of compound 1 was established as 3β-hydroxyl-21β-acetoxyl-urs-12-en-28-carboxylate on the basis of interpretation of its 1D and 2D NMR and HR-ESI-MS spectroscopic data. The bioassay results verified compounds 2, 3 and 8 inhibited PDE4D2 effectively with the IC50 values of 3.06, 2.18 and 5.17 μM, respectively, which may provide a novel mechanism for the anti-inflammatory activity of the leaves of E. japonica.
Eriobotrya japonica; PDE4 inhibitors; triterpenoid
Bioactive triterpenoids from the leaves of Eriobotrya japonica as the natural PDE4 inhibitors.
Tan BX1, Yang L1, Huang YY2, Chen YY2, Peng GT1, Yu S1, Wu YN2, Luo HB2, He XX1.
The limiting factor for the use of Cisplatin in the treatment of different type of cancers is its toxicity and more specifically urogenital toxicity. Oxidative stress is a well-known phenomenon associated with Cisplatin toxicity. However, in Cisplatin treated group, abnormal animal behavior, decreased body weight, cellular and sub-cellular changes in the kidney and sperm abnormality were observed. Our investigation revealed that Cisplatin when administered in combination with a natural product derivative (Urs-12-ene-3α,24β-diol, labeled as IN0523) resulted in significant restoration of body weight and protection against the pathological alteration caused by Cisplatin to kidney and testis. Sperm count and motility were significantly restored near to normal. Cisplatin caused depletion of defense system i.e. glutathione peroxidase, catalase and superoxide dismutase, which were restored close to normal by treatment of IN0523. Reduction in excessive lipid peroxidation induced by Cisplatin was also found by treatment with IN0523. The result suggests that IN0523 is a potential candidate for ameliorating Cisplatin induced toxicity in the kidney and testes at a dose of 100mg/kg p.o. via inhibiting the oxidative stress/redox status imbalance and may be improving the efflux mechanism.
Copyright ? 2017 Elsevier Inc. All rights reserved.
Cisplatin; Histopathology; Oxidative stress; Sperm motility; Urogenital
IN0523 (Urs-12-ene-3α,24β-diol) a plant based derivative of boswellic acid protect Cisplatin induced urogenital toxicity.
Singh A1, Arvinda S2, Singh S3, Suri J2, Koul S4, Mondhe DM5, Singh G6, Vishwakarma R4.
2017 Mar 1
Uvaol, a triterpene present in olives and virgin olive oil, has been shown to possess anti-inflammatory properties and antioxidant effects. However, until now, no studies have demonstrated its potential effects on allergic inflammation. The aim of this study was to evaluate the anti-inflammatory effects of uvaol in a mouse model of allergy characterized by eosinophil-dominant inflammation in actively sensitized mice. The anti-inflammatory effect of uvaol was analyzed in two murine models of allergic inflammation (pleurisy and asthma). In these models, Swiss mice were sensitized and challenged with ovalbumin (OVA). In the pleurisy model, the pleural eosinophilic inflammation and IL-5 concentrations were examined 24h after the OVA challenge, while in the asthma model were examined the airway inflammation via bronchoalveolar lavage (BAL) fluid cytology and lung histopathology analyses. Our results showed that uvaol decreased the accumulation of eosinophils and the concentration of IL-5 in pleural effluent. Uvaol also demonstrated important anti-inflammatory activity by inhibiting production of IL-5 and influx of leukocytes, mainly of eosinophils, in BAL fluid, but without interfering with levels of reactive oxygen species in leukocytes. Moreover, the eosinophil infiltration, mucus production, number of alveoli that collapsed, and IL-5 levels in the lung were clearly decreased by uvaol treatment. These findings indicate that uvaol can be a good candidate for the treatment of allergic inflammation by inhibiting eosinophil influx and IL-5 production in ovalbumin-induced allergy.
Copyright ? 2016 Elsevier B.V. All rights reserved.
Eosinophil; IL-5; Inflammation; Triterpene; Uvaol; Uvaol (PubChem CID: 92802)
Uvaol attenuates pleuritis and eosinophilic inflammation in ovalbumin-induced allergy in mice.
Agra LC1, Lins MP2, da Silva Marques P3, Smaniotto S2, Bandeira de Melo C3, Lagente V4, Barreto E5.
2016 Jun 5