Tony moly goes sny-AKe, releases intense repair sny-ake wrinkle cream


In 2010 – we saw 3 hit unique cosmetic ingredient which became really popular in Korea : snail mucin, bee venom, and snake venom.


Tony Moly did jump in the hype and released their snail cream, and now they are attacking the SnY-ake hype. Will we have a Tony Moly Bee Venom line later?


Tony Moly intense repair sny-ake wrinkle cream uses the patented Sny-ake ingredient, and mixes it with marine collagen, caviar extracts amongst other anti-wrinkle ingredients to give your skin a rich nutritional sense.


After using the cream for 4 weeks, test subjects saw 10.6% improvement on their wrinkles, and 11.8% improvment after 8 weeks.


SYN®-AKE is a small peptide that mimics the activity of Waglerin 1, a polypeptide that is found in the venom of the Temple Viper, Tropidolaemus wagleri. Clinical trials have shown that SYN®-AKE is capable of reducing mimic wrinkles by inhibiting muscle contractions.


SYN®-AKE is a synthetic tri-peptide derivative that was developed based on the combined expertise of PENTAPHARM in snake venom research and peptide synthesis.


Targeting neuromuscular activity, PENTAPHARM has developed a new snake venomlike active compound which is an antagonist of the muscular nicotinic acetylcholine receptor (nmAChR).

SYN®-AKE has excellent smoothing and fast anti-wrinkle  properties that have been proved in vivo in a short term study (1 month).


Mimic wrinkles are part of the visible face wrinkles. As time passes, these wrinkles persist permanently and get  deeper and deeper: frown lines,  laughter lines and crows feet lines appear more and more due to the repeated movements of facial muscles. SYN®-AKE has been developed as efficient smoothing and anti-wrinkle care particularly effective against expression lines by relaxing facial muscles. This active tri-peptide acts in a manner similar to Waglerin 1, a neuromuscular blocking compound of the venom of the Temple Viper. Acting at  the post-synaptic membrane, SYN®-AKE is a reversible antagonist of the muscular nicotinic acetylcholine receptor (mnAChR). We assume that the tri-peptide is binding to the epsilon subunit of the mnAChR which prevents binding of acetylcholine to the receptor; consequently it remains closed. In the closed state, there is no uptake of sodium ions (Na+) and the muscle stay relaxed.

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