Syn-peptides are synthetically manufactured peptides that are similar in structure to a naturally occurring peptide. They are designed to mimic the action of the naturally occurring form. Peptides are essentially short proteins and are used in skincare formulations as they are often small enough to penetrate through the skin. Syn-peptides have been created to combat the appearance of wrinkles, pigmentation and increase the natural protective abilities of the skin. Is Syn-ake Actually Safe? Another study published in the journal Phytotherapy Research demonstrated the anti-snake venom properties of Tamarindus indica seed extract. As a skincare ingredient, Syn-ake can be added to most formulation types, such as serums, moisturizers, or most water-based products. It is generally used as the main anti-aging ingredients but also can be formulated alongside other key ingredients to create a more diverse anti-aging product. Another study published in the Journal of Ethnopharmacology has demonstrated the neutralising properties of Musa paradisiaca juice on phospholipase A2, myotoxic, hemorrhagic and lethal activities of crotalidae venoms.

The venom of the Temple Viper which Syn-ake is designed to mimic, paralyzes the muscles to weaken their prey. Syn-ake was created to mimic this action by creating a synthetic peptide with the same amino acid sequence as the Waglerin-1 peptide. The Waglerin-1 peptide was identified as the cause of the paralysis in the snake’s venom. By creating a chemically similar structure, the synthetic peptide is able to produce a similar effect. It is thought that the molecule is small enough to penetrate the skin and work on the facial muscles, however, due to how deep these muscles are under the skin, only small amounts of the molecule will get through. This means that Syn-ake’s effects are generally temporary, lasting for about a month and reducing the likelihood of off-target effects. Inhibition of protease, hyalunoridase, fibrinogenolytic, procoagulant, anti-edematogenic, anti-ATPase, and alkaline phosphatase The application of -Omics technologies has had a high impact in the study of snake venoms, providing novel and relevant clues for understanding their evolution and composition in their ecological and medical contexts ( 85). In particular, the field of proteomics as applied to venoms, i.e. ‘venomics’ ( 86), has shed light on the complexity of these toxic secretions ( 87, 88). An application of the study of venom proteomes to the field of antivenoms is ‘antivenomics’, a translational venomics applied to the fine characterization of the ability of antivenoms to recognize different components in venoms. In a statement, ENTOD Beauty London noted that the serum is based on a patented anti-aging synthetic tripeptide snake venom neurotoxin developed by Swedish company Pentapharm Ltd.The efficacy of Anacardium occidentale extract against pharmacological actions induced by Vipera russelli venom was observed from the neutralization of phospholipases, proteases, and hyaluronidases, as well as edema, hemorrhage, lethality, and myonecrosis effects

PLA 2 inhibitor and prevention of myofiber breakdown caused by myotoxins I (Asp49) and II (Lys49) of B. asper venom Anti-defibrinogenatic, anti-edematogenic, anti-PLA 2 activity, anti-necrotic, anti-hemorrhagic, anti-coagulant, lipid peroxidase inhibition, superoxide dismutase activity, antiserum action potentiation, anti-lethality, anti-cardiotoxic, and anti-neurotoxic A recent study has scientifically validated the folklore use of Annona senegalensis in the treatment of snakebite by farmers and herdsmen in Northern Nigeria. Inquiries on the sources of information used in this review can be directed to the corresponding author. Author Contributions Recent studies have found that Mucuna pruriens leaves are more effective than the standard drug, anti-venin, for curing snakebite.

Acknowledgments

Syn-ake hasn’t been independently evaluated by the Cosmetic Ingredient Review Expert Panel but the company that produced it has not reported any toxicity or sensitization issues in its research. However, Syn-ake has anecdotally been known to cause adverse reactions in some users, you should start out by adding the smallest possible concentration of Syn-ake to your skincare regime until you know how it will affect your skin. Neuromuscular paralysis leading to respiratory arrest is one of the predominant effects of snakebite envenomings, particularly those caused by species of the family Elapidae, but also by some species of the family Viperidae ( 1, 53). It results from the action of a variety of neurotoxins at the neuromuscular junctions. Post-synaptically acting polypeptides of the three finger toxins (3FTx) family (α-neurotoxins) act by binding with high affinity to the cholinergic nicotinic receptor (AChR) at the motor end-plate of muscle fibers ( 64). Neurotoxicity is also due to the action of PLA 2s at the nerve terminal (β-neurotoxins), by hydrolyzing phospholipids of the plasma membrane, inducing a calcium influx and the consequent alteration of the neurotransmitter exocytotic machinery ( 65). Other types of neurotoxins include the dendrotoxins, present in mamba ( Dendroaspis sp) venom, which are inhibitors of the voltage-dependent potassium channels ( 66). Neurotoxins play a key role in the lethality of snake venoms. Until now, snakebite poisoning remains a public health hazard in tropical countries. Viper snakes are among the most common types of venomous snakes, which are responsible for many envenoming and deaths in most tropical areas. The centerpiece in the therapy of snakebite envenomings is the timely administration of safe and effective antivenoms, which are preparations of IgGs or IgG fragments prepared from the plasma of horses or other animals immunized with venoms of one snake species (monospecific antivenoms) or several species (polyspecific antivenoms) ( 5). Upon parenteral administration in envenomed patients, antivenom antibodies bind to venom components in the circulation or in tissue compartments and contribute to their elimination. Generally, antivenom therapy is complemented by ancillary treatments which vary depending on the pathophysiology of envenomings ( 1). Antivenom efficacy is evaluated at the preclinical level by assessing its capacity to neutralize the lethal action of venoms in animal models, usually mice ( 5, 6). This is the gold standard of antivenom efficacy which is required before antivenoms are introduced into clinical use and as part of the routine quality control of antivenoms by manufacturers and regulatory agencies. The basic protocol for these neutralization assays involves the incubation of venom and antivenom prior to administration in animals. Another experimental option, which is not routinely used in quality control laboratories but which better mimics the actual circumstances of a snake bite, is the rescue-type assay, in which venom is injected first and antivenom is administered afterwards. In addition to lethality, depending on the toxicity profile of venoms, the assessment of neutralization of other toxic activities is also recommended, such as hemorrhagic, myotoxic, dermonecrotic, defibrinogenating, and in vitro coagulant activities, depending on the venom ( 5, 6). Except for the in vitro coagulant activity, the rest of these assays involve the use of high numbers of mice, with the consequent suffering and distress inflicted in these animals because of the toxic action of venoms. Extracts and fractions from Dipteryx alata (Fabaceae) partially neutralized Bothrops jararacussu and Crotalus durissus terrificus venom activities. Hydroalcoholic bark extract from D. alata is active against B. jararacussu venom.