Steroid and fatty acid contents from the leaves of Carica papaya.

AIM: To extract and identify the non-polar entities from the leaves of Carica papaya, a plant used for medicinal purpose as folk medicine. MATERIALS AND METHODS: Petroleum ether extract of the Carica papaya leaves was used for this study. Saponification process and methylation process was performed to separate fatty acids and unsaponifiable matters. Phytochemical constituents were separated using chemical process and separated fractions were analyzed by thin layer chromatography (TLC) and gas chromatography coupled with mass spectroscopy (GC-MS). RESULTS: The chemical composition of the steroids, triterpenoids and fatty acid methyl esters (FAMEs) in leaves of Carica papaya, which were analyzed by gas chromatography coupled with mass spectroscopy (GC-MS). A total of 15 fatty acid components were identified in saponifiable matter, from unsaponifiable portion 2 steroids (campesterol, ß- or γ-sitosterol), 1 triterpene (squalene), and 1 diterpene (phytol) were identified. CONCLUSIONS: The results indicate that the extract is rich in non-polar compounds. In this study, GC-MS method is at the central focus for identification of these phytoconstituents. The current method can be used for direct analysis of non-polar entities of plant material.

Design and synthesis of potent antitumor water-soluble phenyl N-mustard-benzenealkylamide conjugates via a bioisostere approach.

A series of new, water-soluble phenyl N-mustard-benzenealkylamide conjugates containing hydrophilic ω-dialkylaminoalkylamide or ω-cyclic aminoalkylamide moieties were synthesized via a bioisostere approach. These compounds have a broad spectrum of antitumor activity against a panel of human tumor cell lines. Of these derivatives, compound 18b effectively suppressed the growth of colon cancer (HCT-116), prostate cancer (PC3), and lung cancer (H460) xenografts. The growth of HCT-116 xenografts was almost completely suppressed when co-treated with compound 18b and 5-fluorouracil. Furthermore, compound 18b can induce DNA cross-linking and cell-cycle arrest at the G2/M phase. Early preclinical studies, including pharmacokinetics in rats, inhibition of the hERG, and 14 days of acute intravenous injection toxicity, suggest that compound 18b is a promising candidate for further preclinical studies.