20-Hydroxyecdysone - CAS 5289-74-7
Not Intended for Therapeutic Use. For research use only.
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20-Hydroxyecdysone (Ecdysterone, 20E) is a naturally occurring ecdysteroid hormone which controls the ecdysis (moulting) and metamorphosis of arthropods.
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CAS 5289-74-7 20-Hydroxyecdysone

Reference Reading

1. Antioxidant Properties of Conjugates of 20-Hydroxyecdysone Derivatives with a Polysubstituted Chromanylaldehyde
V. R. Khairullina, A. Ya. Gerchikov, Ya. R. Urazaeva, R. G. Savchenko, and V. N. Odinokov. Kinetics and Catalysis, 2010, Vol. 51, No. 4, pp. 502–506
20-Hydroxyecdysone and its derivatives possess obvious antiradical and antioxidant properties. Their antioxidant effect on blood serum lipid oxidation is comparable with the effects of hydroquinone and butylhydroxytoluene. However, the data characterizing the antioxidant activity (AOA) of 20-hydroxyecdysone and its structural analogues are semiquantitative, so it is impossible to predict the effectiveness of these antioxidants under variable conditions. The parameters used to characterize the AOA of ecdysteroids include the yield of propanedial (final oxidation product), the amount of diene conjugates, the concentration that reduces the rate of oxidation of the model substrate by 50%, and the 2,2-diphenyl-1-picrylhydrazyl radical (DPPH•) accepting efficiency. However, the most objective measure of AOA is the inhibition rate constant determined by kinetic methods.
2. Effect of a novel compound as dietary supplement on growth of decapod crustaceans
Sajal Shrivastava and S. Adline Princy*. RSC Adv.,2015, 5, 65546–65553
Among such economically important marine species, decapod crustaceans specifically play a vital role in the aquaculture and fisheries sector. Hence, understating their physiology can provide significant insights for the development of novel growth enhancers. In decapod crustaceans, the regulation of growth is governed by molt inhibiting hormone, a neurohormone from the crustacean hyperglycemic hormone (CHH) family, synthesized and secreted from the x-organ/sinus gland complex in the eyestalk. CHH family neurohormones formextremely interactive systems to accomplish the integrated function of various physiological processes for decapod crustaceans. A critical role in the ecdysteroid production is played by a key neuropeptide, known asmolt inhibiting hormone.Molt inhibiting hormone is a single-chain 113 amino acid proteohormone composed of a 35 residue signal peptide and a 78 residue mature MIH which play a key role in the regulation of growth and reproduction. Its amino acid sequence exhibits homologies to other neurohormones including crustacean hyperglycemic hormone and vitellogenin inhibiting hormone and hence is designated as belonging to the CHH family neuropeptides. MIH is produced and secreted by the x-organ/sinus gland complex, which acts on the endocrine system, in particular the y-organs, suppressing the production of 20-hydroxyecdysone. Therefore, eyestalk ablation leads to an upsurge in the hemolymph ecdysteroid titer and shortening of the intermolt period, whereas eye-stalk ablated animals injected with crude eyestalk extract show significantly lower ecdysteroid level and delayed molting. Additionally, in vitro studies have also revealed that recombinant MIH and crude eyestalk extracts inhibit 20-hydroxyecdysone production by y-organs. MIH has dual regulation in crustacean physiology. Functional studies have shown that this peptide exerts a stimulatory effect on reproduction by stimulating vitellogenesis in the hepatopancreas. Ecdysteroid hormones profoundly affect growth, differentiation, and metabolism. Regulation of ecdysteroid synthesis, principally achieved by molt inhibiting hormone, is a predominant factor of a complex network that governs the normal growth and proper function of decapod crustaceans. The three residues asparagine (13), serine (71) and isoleucine (72) of MIH interact with the receptor in the y-organs and activate the signaling cascade leading to a significant increase cGMP activity and inhibition of the phantom gene expression. From these observations it is hypothesized that a growth enhancer derived from the residues of MIH responsible for binding to the receptor can lead to a precocious molting and thus stimulates molting.