15356-74-8Relevant articles and documents
Dihydroactinidiolide, a natural product against Aβ25-35 induced toxicity in Neuro2a cells: Synthesis, in silico and in vitro studies
Das, Mamali,Prakash, Sengodu,Nayak, Chirasmita,Thangavel, Nandhini,Singh, Sanjeev Kumar,Manisankar, Paramasivam,Devi, Kasi Pandima
, p. 340 - 349 (2018)
Synthesis of natural products has speeded up drug discovery process by minimizing the time for their purification from natural source. Several diseases like Alzheimer's disease (AD) demand exploring multi targeted drug candidates, and for the first time we report the multi AD target inhibitory potential of synthesized dihydroactinidiolide (DA). Though the activity of DA in several solvent extracts have been proved to possess free radical scavenging, anti bacterial and anti cancer activities, its neuroprotective efficacy has not been evidenced yet. Hence DA was successfully synthesized from β-ionone using facile two-step oxidation method. It showed potent acetylcholinesterase (AChE) inhibition with half maximal inhibitory concentration (IC50) 34.03 nM, which was further supported by molecular docking results showing strong H bonding with some of the active site residues such as GLY117, GLY119 and SER200 of AChE. Further it displayed DPPH and (.NO) scavenging activity with IC50 value 50 nM and metal chelating activity with IC50 >270 nM. Besides, it significantly prevented amyloid β25-35 self-aggregation and promoted its disaggregation at 270 nM. It did not show cytotoxic effect towards Neuro2a (N2a) cells up to 24 h at 50 and 270 nM while it significantly increased viability of amyloid β25-35 treated N2a cells through ROS generation at both the concentrations. Cytotoxicity profile of DA against human PBMC was quite impressive. Hemolysis studies also revealed very low hemolysis i.e. minimum 2.35 to maximum 5.61%. It also had suitable ADME properties which proved its druglikeness. The current findings demand for further in vitro and in vivo studies to develop DA as a multi target lead against AD.
β-Carotene autoxidation: Oxygen copolymerization, non-vitamin A products, and immunological activity
Burton, Graham W.,Daroszewski, Janusz,Nickerson, James G.,Johnston, James B.,Mogg, Trevor J.,Nikiforov, Grigory B.
supporting information, p. 305 - 316 (2014/05/06)
Carotenoids are reported to have immunological effects independent of vitamin A activity. Although antioxidant activity has been suggested as a basis of action, the ability of carotenoids to autoxidize to numerous non-vitamin A products with immunological activity is an alternative yet to be fully explored. We have undertaken a systematic study of β-carotene autoxidation and tested the product mixture for immunological activity. Autoxidation proceeds predominantly by oxygen copolymerization, leading to a defined, reproducible product corresponding to net uptake of almost 8 molar equivalents of oxygen. The product, termed OxC-beta, empirical formula C40H60O 15 versus C40H56 for β-carotene, contains more than 30% oxygen (w/w) and 85% β-carotene oxygen copolymers (w/w) as well as minor amounts of many C8-C18 norisoprenoid compounds. No vitamin A or higher molecular weight norisoprenoids are present. The predominance of polymeric products has not been reported previously. The polymer appears to be a less polymerized form of sporopollenin, a biopolymer found in exines of spores and pollen. Autoxidations of lycopene and canthaxanthin show a similar predominance of polymeric products. OxC-beta exhibits immunological activity in a PCR gene expression array, indicating that carotenoid oxidation produces non-vitamin A products with immunomodulatory potential.
Total synthesis of (±)-dihydroactinidiolide using selenium-stabilized carbenium ion
Dabdoub, Miguel J.,Silveira, Claudio C.,Lenard?o, Eder J.,Guerrero Jr., Palimécio G.,Viana, Luiz H.,Kawasoko, Cristiane Y.,Baroni, Adriano C.M.
scheme or table, p. 5569 - 5571 (2011/02/24)
A new, short total synthesis of dihydroactinidiolide 1 is described using selenium carbenium ion-promoted carbon-carbon bond formation as the key step. Our synthetic strategy starts with a lactonization reaction between 1,3,3-trimethylcyclohexene 13 and α-chloro-α-phenylseleno ethyl acetate 14, affording the key intermediate, α-phenylseleno-γ-butyro lactone 15, which reacted via a selenoxide elimination to the target compound 1.
