{"id":2965,"date":"2026-08-26T11:41:13","date_gmt":"2026-08-26T10:41:13","guid":{"rendered":"https:\/\/officialcorepeptides.brandloom.net\/it\/?post_type=product&p=2965"},"modified":"2026-08-26T11:41:14","modified_gmt":"2026-08-26T10:41:14","slug":"buy-syn-ake-in-switzerland","status":"publish","type":"product","link":"https:\/\/officialcorepeptides.ch\/it\/product\/buy-syn-ake-in-switzerland\/","title":{"rendered":"Syn-AKE (200MG)"},"content":{"rendered":"

What Is Syn-AKE?<\/h2>\n

Syn-AKE, also known as Dipeptide Diaminobutyroyl Benzylamide Diacetate, is a synthetic dipeptide with the amino acid sequence \u03b2-Ala-Pro-Dab-NHBzl. It belongs to a class of biomimetic peptides designed to emulate the neuromuscular blocking activity of Waglerin-1, a peptide found in the venom of the Temple Viper (Tropidolaemus wagleri). For those looking to buy Syn-AKE in Switzerland<\/strong>, Core Peptides offers high-quality research-grade material for laboratory applications.<\/p>\n

As a dipeptide a peptide composed of two amino acids with a modified C-terminal benzylamide Syn-AKE features a unique structure that allows it to interact with nicotinic acetylcholine receptors (nAChR) at the neuromuscular junction. The peptide is commonly supplied as the diacetate salt with the molecular formula C23H37N5O7 and a molecular weight of approximately 495.58 g\/mol. Its INCI name is Dipeptide Diaminobutyroyl Benzylamide Diacetate, and it is identified by CAS number 823202-99-9.<\/p>\n

Syn-AKE Research Overview<\/h2>\n

Syn-AKE has attracted research interest as a tool for investigating neuromuscular junction signaling, nicotinic acetylcholine receptor pharmacology, and synaptic transmission. The peptide’s design a synthetic mimic of the active region of Waglerin-1 enables it to reversibly antagonize muscular nicotinic acetylcholine receptors (mnAChR) at the postsynaptic membrane.<\/p>\n

Research interest in Syn-AKE centers on its ability to modulate neuromuscular transmission through competitive inhibition of acetylcholine binding. Specifically, by binding to the nAChR, Syn-AKE prevents acetylcholine from activating the receptor, thereby reducing muscle contraction. Consequently, this mechanism positions Syn-AKE as a valuable compound for studying receptor-ligand interactions, neuromuscular modulation, and synaptic transmission.<\/p>\n

When researchers choose to buy Syn-AKE in Switzerland<\/strong> for laboratory studies, they gain access to a compound that may help elucidate mechanisms of nAChR antagonism, neuromuscular junction physiology, and receptor pharmacology at the molecular level.<\/p>\n

How Does Syn-AKE Work?<\/h2>\n

Syn-AKE exerts its biological effects through reversible antagonism of muscular nicotinic acetylcholine receptors (mnAChR) at the postsynaptic membrane. The peptide’s mechanism involves several well-characterized steps.<\/p>\n

Nicotinic Acetylcholine Receptor Binding<\/h3>\n

Syn-AKE acts as a reversible antagonist at the muscular nicotinic acetylcholine receptor (mnAChR). Research suggests that the peptide binds to the C-loop of the \u03b11 subunit of the nAChR, thereby inhibiting acetylcholine from binding to the receptor. As the muscular nicotinic ACh receptors are reversibly blocked, the ion channel remains closed, preventing the depolarization that would normally trigger muscle contraction.<\/p>\n

In previous studies, acetylcholine has been shown to bind to the C-loop of subunit \u03b11, the allosteric site of the nAChR. Syn-AKE appears to compete for this binding site, thereby attenuating the nicotinic response.<\/p>\n

Neuromuscular Junction Modulation<\/h3>\n

Syn-AKE is a postsynaptic peptide, meaning it acts on the receiving side of the neuromuscular junction. By occupying some of the receptors at the nerve-to-muscle junction, the peptide reduces the micro-movements that drive muscle contraction. In muscle cell contraction assays, Syn-AKE has been shown to reduce contraction frequency by up to 82% at optimal concentrations, demonstrating potent but reversible neuromuscular modulation.<\/p>\n

Reversible Antagonism<\/h3>\n

Unlike botulinum toxin, which enzymatically cleaves SNARE proteins and produces irreversible effects, Syn-AKE acts as a reversible antagonist of the neuromuscular postsynaptic nicotinic acetylcholine receptor. This reversible mechanism allows for the study of receptor dynamics and the recovery of function following peptide administration.<\/p>\n

Researchers who buy Syn-AKE in Switzerland<\/strong> for research purposes can investigate these mechanisms across diverse experimental models of neuromuscular transmission, receptor pharmacology, and synaptic signaling.<\/p>\n

Why Is Syn-AKE Studied?<\/h2>\n

Researchers study Syn-AKE primarily for its potential relevance to nicotinic acetylcholine receptor pharmacology, neuromuscular junction physiology, and synaptic transmission. The peptide’s ability to reversibly antagonize nAChR makes it a valuable tool for understanding the molecular basis of neuromuscular signaling and receptor-ligand interactions.<\/p>\n

Syn-AKE’s connection to the Waglerin-1 venom peptide has made it a focus of neuropharmacology and biomimetic research. For instance, the peptide represents a synthetic approach to studying the neuromuscular blocking activity of natural venom components without the toxicity of the natural compound. This enables researchers to investigate receptor binding kinetics and structure-activity relationships in a controlled laboratory setting.<\/p>\n

Moreover, researchers study Syn-AKE in the context of receptor pharmacology and drug development. Head-to-head comparisons in in vitro assay systems suggest that Syn-AKE may achieve faster onset of neuromuscular modulation compared to other peptides. Therefore, this makes it a useful reference compound for investigating nAChR antagonists and their effects on synaptic transmission.<\/p>\n

Researchers who buy Syn-AKE in Switzerland<\/strong> from Core Peptides can incorporate this peptide into their studies on nAChR pharmacology, neuromuscular junction signaling, and receptor-mediated modulation of muscle contraction.<\/p>\n

Syn-AKE Research Areas<\/h2>\n\n\n\n\n\n\n\n\n\n\n\n\n
Research Area<\/th>\nDescription<\/th>\n<\/tr>\n<\/thead>\n
Nicotinic Acetylcholine Receptor Pharmacology<\/strong><\/td>\nInvestigating Syn-AKE’s binding affinity and antagonism of nAChR<\/td>\n<\/tr>\n
Neuromuscular Junction Signaling<\/strong><\/td>\nStudying Syn-AKE’s effects on neuromuscular transmission and muscle contraction<\/td>\n<\/tr>\n
Synaptic Transmission<\/strong><\/td>\nExamining Syn-AKE’s modulation of neurotransmitter release and receptor activation<\/td>\n<\/tr>\n
Receptor-Ligand Interactions<\/strong><\/td>\nExploring the molecular basis of nAChR binding and antagonism<\/td>\n<\/tr>\n
Reversible Neuromuscular Blockade<\/strong><\/td>\nPreclinical research into reversible nAChR antagonism and receptor dynamics<\/td>\n<\/tr>\n
Biomimetic Peptide Research<\/strong><\/td>\nInvestigating synthetic mimics of natural venom peptides<\/td>\n<\/tr>\n
Muscle Contraction Modulation<\/strong><\/td>\nStudying Syn-AKE’s effects on contraction frequency and amplitude<\/td>\n<\/tr>\n
Receptor Binding Studies<\/strong><\/td>\nInvestigating the molecular interactions between Syn-AKE and nAChR subunits<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Scientific Research on Syn-AKE<\/h2>\n

Researchers have conducted scientific studies on Syn-AKE in both in vitro and preclinical settings, deriving evidence from receptor-binding assays, muscle contraction assays, and molecular docking experiments. The peptide originates from research on the Temple Viper venom peptide Waglerin-1 and represents a synthetic biomimetic approach to studying nAChR antagonism.<\/p>\n

In Vitro Evidence<\/h3>\n

In vitro studies using receptor-binding assays have demonstrated that Syn-AKE acts as a reversible antagonist of muscular nicotinic acetylcholine receptors (mnAChR). The peptide binds to the C-loop of the \u03b11 subunit of the nAChR, inhibiting acetylcholine from binding to the receptor. Researchers have characterized this mechanism through electrophysiological and pharmacological studies.<\/p>\n

Muscle cell contraction assays have shown that Syn-AKE reduces contraction frequency by up to 82% at optimal concentrations, demonstrating potent but reversible neuromuscular modulation. Furthermore, head-to-head comparisons in in vitro assay systems suggest that Syn-AKE may achieve faster onset of neuromuscular modulation compared to other peptides.<\/p>\n

Structural and Synthetic Studies<\/h3>\n

Researchers have developed synthetic routes for Syn-AKE, including an optimized Hofmann-type rearrangement as a final step to build the target skeleton. The synthesis of H-\u03b2-Ala-Pro-DabNHBz diacetate (a muscular nicotinic acetylcholine receptor antagonist) has been delineated through this five-step synthetic pathway.<\/p>\n

The peptide’s structure has been characterized with the sequence \u03b2-Ala-Pro-Dab-NHBzl and molecular formula C23H37N5O7. Research-grade material is typically supplied as a lyophilized powder with verified HPLC purity \u226598%.<\/p>\n

Clinical Studies<\/h3>\n

Syn-AKE has been studied in clinical research for its effects on wrinkle formation and expression lines. For example, a 2021 double-blind, randomized clinical trial examined the effects of a peptide serum containing Syn-AKE on skin appearance. However, researchers should note that the peptide is supplied for laboratory research purposes only. Scientists who buy Syn-AKE in Switzerland<\/strong> should remain aware of these evidence considerations.<\/p>\n

Syn-AKE Compared With Related Peptides<\/h2>\n\n\n\n\n\n\n\n\n\n
Peptide<\/th>\nRelationship to Syn-AKE<\/th>\nKey Differences<\/th>\n<\/tr>\n<\/thead>\n
Waglerin-1<\/strong><\/td>\nNatural venom peptide; Syn-AKE is a synthetic mimic<\/td>\nWaglerin-1 is a 22-amino acid peptide from snake venom; Syn-AKE is a synthetic dipeptide with similar activity<\/td>\n<\/tr>\n
Argireline (Acetyl Hexapeptide-8)<\/strong><\/td>\nBoth studied for neuromuscular modulation<\/td>\nArgireline targets the SNARE complex; Syn-AKE targets nAChR at the postsynaptic membrane (different mechanism)<\/td>\n<\/tr>\n
SNAP-8<\/strong><\/td>\nBoth are synthetic peptides for neuromodulation research<\/td>\nSNAP-8 inhibits SNARE complex assembly; Syn-AKE is an nAChR antagonist<\/td>\n<\/tr>\n
Leuphasyl (Pentapeptide-18)<\/strong><\/td>\nBoth studied for neuromodulation<\/td>\nLeuphasyl is an enkephalin analog targeting opioid receptors; Syn-AKE targets nAChR<\/td>\n<\/tr>\n
Botulinum Toxin<\/strong><\/td>\nBoth modulate neuromuscular transmission<\/td>\nBotulinum toxin enzymatically cleaves SNARE proteins with irreversible effects; Syn-AKE is a reversible nAChR antagonist<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Research Applications<\/h2>\n

Researchers utilize Syn-AKE in a variety of laboratory research applications, primarily in the fields of neuropharmacology, receptor biology, and neuromuscular research. Key research applications include:<\/p>\n