TL;DR
The snake-venom peptide behind Syn-Ake's marketing. Lethal at the neuromuscular junction. No human trial on record.
What: A 22-aa neurotoxic peptide from Tropidolaemus wagleri (Wagler's pit viper). Schmidt and Weinstein isolated it in 1992. One disulfide-constrained loop. Principal lethal toxin of the species.
Does: Competitive antagonist at the muscle nicotinic acetylcholine receptor. ~50 nM IC50 at the adult α-ε subunit interface. About 2,000-fold selectivity for α-ε over α-δ. Paralytic at nanomolar concentrations.
Evidence: Schmidt 1992 (Toxicon, PMID 1359525) isolation. McArdle 1999 (PMID 9918557) mapped adult α-ε selectivity. Molles 2002 (PMID 11724791) identified the interface residues. No human trial. No therapeutic indication.
Used by: Neuromuscular pharmacology labs. Anti-wrinkle serums use Syn-Ake, a ~511 Da mimetic, not the native peptide.
Bottom line: Real snake-venom toxin. Real research tool. The face-cream peptide is the mimetic, not this one.
What It Is
Waglerin-1 (sometimes designated WTX-1, Wgtx-I, or "Wgt-1") is a 22-amino-acid neurotoxic peptide first isolated and characterized in 1992 by Schmidt and Weinstein from the venom of the Wagler's pit viper, Tropidolaemus wagleri (formerly classified as Trimeresurus wagleri). It is one of four closely related toxins in the same venom — waglerin-1 and waglerin-2 (22 amino acids each) and the slightly longer waglerin-3 and waglerin-4 (24 amino acids; differing from the shorter pair by an additional N-terminal serine-leucine dipeptide).
The waglerins are the principal lethal toxins of T. wagleri venom — an unusual venom composition for a viperid snake. Most pit viper venoms are dominated by hemotoxic enzymatic proteins (snake venom metalloproteinases, phospholipase A2, serine proteases) producing tissue necrosis and coagulopathy. T. wagleri venom is instead characterized by a high abundance of small (~2.5 kDa) neurotoxic peptides — a phenotype that converged independently with the elapid (cobra) family's three-finger α-neurotoxins to target the same molecular machinery (the muscle nicotinic acetylcholine receptor) by a different structural strategy. The Tropidolaemus species and Fea's viper (Azemiops feae) are the only viperids known to use this neurotoxic peptide approach.
Waglerin-1's pharmacological signature is its exquisite selectivity for the α-ε subunit interface of the muscle-type nicotinic acetylcholine receptor (the receptor isoform expressed at the adult vertebrate neuromuscular junction). It does not block the α-γ interface (the fetal/embryonic subtype), and it has approximately 2,000-fold lower affinity for the α-δ interface (a non-binding-site subunit pair in the muscle nAChR). This makes waglerin-1 one of the only known molecular probes capable of distinguishing α-ε-containing receptors from α-γ-containing receptors in mixed cell populations — a property exploited in studies of neuromuscular synaptogenesis, myasthenia gravis pathophysiology, and acetylcholine receptor maturation.
Waglerin-1 is distinct from the cosmetic ingredient marketed under the trade name Syn-Ake (DSM-Firmenich; INCI name dipeptide diaminobutyroyl benzylamide diacetate). Syn-Ake is a synthetic small-molecule peptidomimetic — a much smaller dipeptide derivative (CAS 823202-99-9, molecular formula C₂₃H₃₇N₅O₇, ~511 Da) reportedly designed to mimic the C-terminal turn of waglerin-1 in a topical formulation. Syn-Ake is used in topical anti-wrinkle cosmetics; native waglerin-1 is not. Wikipedia and independent skincare reviewers note that "no scientific evidence supports the manufacturers' suggestion that the Waglerin-1 included in their products relaxes wrinkle producing skeletal muscles" — a statement that applies because the products contain the Syn-Ake mimetic, not waglerin-1, and because topical penetration of an intact 22-amino-acid peptide to underlying motor endplates is implausible.
Mechanism of Action
Waglerin-1's mechanism is precisely characterized through three decades of biophysical and electrophysiological studies on isolated neuromuscular preparations:
- Competitive antagonism at the muscle nAChR α-ε interface — Waglerin-1 binds the agonist site at the α-ε subunit interface of the muscle nicotinic acetylcholine receptor. Binding is competitive with acetylcholine — increasing acetylcholine concentration shifts the dose-response curve rightward, demonstrating direct competition for the agonist binding site rather than allosteric inhibition. IC50 against the adult mouse endplate response is approximately 50 nM (McArdle et al., J Pharmacol Exp Ther 1999; PMID 9918557).
- Subunit-interface selectivity — The defining pharmacological feature. Waglerin-1 has approximately 2,000-fold higher affinity for the α-ε subunit interface (the interface that defines the adult muscle nAChR) than for the α-δ subunit interface (a non-binding-site subunit pair in the same receptor). This selectivity is conferred by specific amino acid residues at the α-ε interface that are unique to the adult muscle subtype, identified by chimeric receptor mutagenesis (Molles et al., J Biol Chem 2002; PMID 11724791).
- Adult vs fetal selectivity — Waglerin-1 is not potent at the fetal/embryonic muscle nAChR subtype (which contains the γ subunit instead of ε). This complementary selectivity to small peptide toxins purified from Conus geographus venom (which are γ-subunit selective) gives the field a paired toolset for studying the developmental switch from fetal α-γ to adult α-ε receptor expression at the neuromuscular junction.
- Pre- and post-synaptic effects — At higher concentrations, waglerin-1 has been reported to act both pre- and post-synaptically at the rat neuromuscular junction (Schmidt and Weinstein, Toxicon 1992; PMID 1359525). The post-synaptic competitive antagonism is the dominant effect; pre-synaptic effects on transmitter release are observed at micromolar concentrations and are not the primary mechanism of paralysis.
- GABAA receptor potentiation — Independent of nAChR antagonism, waglerin-1 has been shown to potentiate and at higher concentrations suppress GABAA receptor responses in cell-culture systems (EC50 ~24 μM). This is a secondary off-target activity, not the primary toxicological mechanism.
- Single disulfide bond constrained loop — Waglerin-1 contains a single disulfide bond defining a constrained 12-amino-acid loop that is critical for the receptor-binding conformation. The C-terminal hexapeptide is conserved with azemiophin (the analogous nAChR-blocking peptide from the Fea's viper venom), suggesting evolutionary convergence on a shared receptor-binding pharmacophore.
- Non-three-finger architecture — Unlike elapid α-neurotoxins (α-bungarotoxin, α-cobratoxin), waglerin-1 has no three-finger fold. It achieves nAChR antagonism via a fundamentally different small-peptide-loop architecture, which is why it has different subunit selectivity profiles than the α-bungarotoxin family.
What the Research Shows
Waglerin-1 research is essentially confined to academic neuromuscular pharmacology. There is no clinical research literature in humans. The published evidence base falls into four categories:
- Original isolation and characterization — Schmidt JJ, Weinstein SA. Toxicon. 1992 (PMID 1359525). First isolation of the waglerin family from T. wagleri venom; characterization of a novel small-peptide nAChR antagonist scaffold within Viperidae venoms; demonstration of pre- and post-synaptic neuromuscular blockade in rat preparations.
- Mouse neuromuscular pharmacology — Tsai MC, Hsieh WH, Smith LA, Lee CY. Toxicon. 1995 (PMID 7638875). Effects of waglerin-1 on neuromuscular transmission in mouse nerve-muscle preparations; established the much higher potency of waglerin-1 against mouse vs rat preparations, providing the first evidence of strong species selectivity within the mammalian muscle nAChR family.
- Conformational analysis — Sellin LC. Biophys J. 1996 (PMID 8770182). Structural characterization of the waglerin-1 receptor-binding conformation and the role of the disulfide-constrained loop. Subsequent NMR conformational work (Neuropharmacology 2010; PMID 20211192) refined the active conformation.
- Adult ε-selective receptor blockade — McArdle JJ et al. J Pharmacol Exp Ther. 1999;289:543-550 (PMID 9918557). Demonstrated that waglerin-1 selectively blocks the adult ε-subunit-containing muscle nAChR with IC50 ~50 nM at the adult mouse endplate; defined the developmental switch utility of the peptide as a probe.
- Subunit-interface mapping — Molles BE, Tsigelny I, Nguyen PD, et al. J Biol Chem. 2002 (PMID 11724791). Chimeric receptor mutagenesis identified specific residues at the α and ε subunit interfaces mediating species selectivity of waglerin-1 binding. This paper is the pharmacological gold standard establishing the molecular basis of the 2,000-fold α-ε vs α-δ selectivity.
- Receptor probe applications — Multiple subsequent studies (Bowe et al. Ann N Y Acad Sci 2008, PMID 18567854) have used waglerin-1 as a research tool for distinguishing adult vs fetal muscle nAChR populations, studying neuromuscular synaptogenesis, and characterizing the role of receptor maturation in neuromuscular disorders including myasthenia gravis and congenital myasthenic syndromes.
- Venom proteomics — Tan KY et al. PLoS Negl Trop Dis 2015; Tan KY et al. PMC 2016 (PMC5086659); Tan KY et al. Sci Rep 2017 (PMC5327433). Proteomic and venomic characterization of T. wagleri venom confirming waglerins as the dominant lethal toxin family and the unique neurotoxic-pit-viper venom phenotype. The 2023 transcriptome paper (PMC10537322) traced the evolutionary origin of waglerin from BPP/CNP gene families and the convergent neurofunctionalization with elapid α-neurotoxins.
- Reviews — Schmidt JJ. J Toxicol Toxin Rev 2002 (the canonical waglerin family structure-function review); Tsetlin VI. Venom-Derived Neurotoxins Targeting Nicotinic Acetylcholine Receptors review (PMC8199771); Harvey AL, Anderson AJ. Pharmacol Ther 1985 (PMID 2436242 — broader snake venom presynaptic neurotoxin review covering related compounds).
Critical Context — No Therapeutic Application
Waglerin-1 has never been the subject of a human clinical trial for any indication. It has no approved or investigational therapeutic application, no published in-vivo systemic dosing data outside experimental snake-bite toxinology, and no published topical penetration data that would support a cosmetic claim. Its real-world utility is exclusively as a research-grade pharmacological tool for in vitro nAChR characterization. Statements about "topical waglerin-1" wrinkle treatments refer to the synthetic Syn-Ake mimetic, not the native peptide.
Human Data
There is no published human clinical trial data on waglerin-1 for any indication — therapeutic, cosmetic, or otherwise. The only documented human exposure is via accidental envenomation by Tropidolaemus wagleri, which is a relatively non-aggressive arboreal pit viper of Southeast Asian rainforest habitat. Bite case reports describe predominantly local effects (pain, mild swelling) with rare systemic neurotoxicity, suggesting that the lethal dose of waglerin-1 in humans is substantially higher than the venom yields typical of the species.
- No therapeutic clinical trials — No registered or completed clinical trials of waglerin-1 (native or recombinant) for any indication. ClinicalTrials.gov does not list any waglerin-1 protocols.
- No cosmetic clinical trials of native waglerin-1 — Cosmetic clinical studies marketed under the "snake venom peptide" branding (e.g., the in-vivo studies cited in DSM-Firmenich's Syn-Ake formulation guidelines) used the Syn-Ake mimetic (dipeptide diaminobutyroyl benzylamide diacetate), not the native 22-amino-acid waglerin-1 peptide. These are studies of a different molecule.
- Snake-bite case reports — Case reports of T. wagleri envenomation from Southeast Asian clinical literature describe predominantly local effects (puncture wound, mild edema, pain). Systemic neurotoxicity from T. wagleri bites is uncommon, possibly reflecting low venom yield per bite combined with the species' generally non-aggressive disposition. No standardized antivenom exists specifically for T. wagleri; pan-Asian polyvalent viper antivenoms have inconsistent recognition of waglerins (Tan KY et al., PLoS Negl Trop Dis 2015).
- No transdermal absorption data — Native waglerin-1 has not been characterized for transdermal penetration. A 22-amino-acid disulfide-constrained peptide of ~2,500 Da is well above the conventional ~500 Da molecular-weight ceiling for passive stratum corneum penetration; topical bioavailability of intact native waglerin-1 is implausible without specific formulation chemistry (penetration enhancers, lipid nanoparticle delivery) that has not been published.
Dosing from the Literature
There is no human dosing protocol for waglerin-1. Reference doses are exclusively from in-vitro and isolated-tissue research:
| Context | Concentration / Dose | Endpoint | Notes |
|---|
| Adult mouse endplate (in vitro) | IC50 ~50 nM | 50% inhibition of acetylcholine response | The defining pharmacological metric (McArdle 1999). |
| Rat neuromuscular preparation | 1–10 μM | Pre- and post-synaptic blockade | ~100-fold less sensitive than mouse — significant species selectivity (Schmidt 1992). |
| α-ε vs α-δ binding | ~2,000× selectivity | Subunit-interface affinity ratio | The defining selectivity feature — used as a research probe (Molles 2002). |
| GABAA receptor (in vitro) | EC50 ~24 μM | Receptor potentiation | Off-target effect; ~480× lower potency than muscle nAChR. |
| Mouse LD50 (intraperitoneal) | ~0.05–0.1 μg/g body weight | Lethality from neuromuscular paralysis | Approximate; varies by venom preparation. |
| Human therapeutic dose | None established | — | No human therapeutic application; native waglerin-1 has never been administered to humans for any clinical purpose. |
| "Cosmetic dose" (Syn-Ake) | 4% Syn-Ake topical (NOT native waglerin-1) | Cosmetic wrinkle metrics in DSM in-vivo study | Refers to dipeptide diaminobutyroyl benzylamide diacetate, NOT waglerin-1. |
Dosing Disclaimer
There is no human dose for waglerin-1. The peptide has never been administered to humans for therapeutic purposes, and no safety data exists to support such administration. Native waglerin-1 is a research reagent, not a therapeutic agent. Marketing claims about "topical waglerin-1" wrinkle treatments refer to a different molecule (the Syn-Ake mimetic) and should not be conflated with native waglerin-1.
Reconstitution & Storage
Waglerin-1 is supplied for laboratory research as a synthetic or recombinant lyophilized peptide by analytical and research-reagent vendors:
| Vendor / Form | Typical Quantity | Reconstitution | Storage |
|---|
| Smartox Biotechnology (synthetic) | 0.1–1 mg vials | Sterile water or PBS | −20°C lyophilized; 4°C reconstituted (short-term) or aliquoted at −80°C |
| Alomone Labs / Tocris (synthetic) | 0.1–0.5 mg vials | Sterile water or assay buffer | Same as above |
| Native venom isolate | — | — | Not commercially available outside academic venom-research collaborations; preparation requires direct snake-husbandry venom collection. |
| Recombinant E. coli expression | Variable | Per academic protocol | Disulfide-bond formation requires oxidative refolding step; functional yield depends on protocol. |
- Reconstitution — Synthetic waglerin-1 is typically supplied as a TFA salt; reconstitute with sterile water or assay-specific buffer (PBS, HEPES, artificial CSF). Avoid alkaline buffers for prolonged storage (disulfide bond instability at pH >9).
- Working concentration — Stock 1 mM in sterile water; working concentrations 1 nM – 10 μM depending on assay. For α-ε muscle nAChR characterization, 100 nM is commonly used.
- Storage — Lyophilized peptide stable for 2+ years at −20°C in dark, desiccated conditions. Reconstituted aliquots stable at −80°C for years; avoid repeated freeze-thaw cycles. 4°C storage of reconstituted solution is acceptable for short-term (1–2 weeks) experiments.
- Inspection — Should be a white-to-off-white lyophilized powder; reconstituted solution is clear and colorless. Discard if discolored or showing visible particulate.
Side Effects & Risks
Important
Native waglerin-1 is a lethal snake-venom neurotoxin. Paralytic at nanomolar concentrations. No therapeutic indication. Talk to someone licensed before anyone sells you "waglerin" as a topical.
Native waglerin-1 has no established human therapeutic application, so the relevant risk profile is laboratory-handling toxicology and the toxicology of T. wagleri envenomation:
- Acute neuromuscular paralysis (toxicological) — At sufficient systemic exposure, waglerin-1 produces flaccid paralysis through muscle nAChR blockade — the same end-organ mechanism as curare-class neuromuscular blocking agents and elapid α-neurotoxins. Onset is rapid (minutes to tens of minutes after IV exposure in animal models). Death from systemic envenomation results from respiratory muscle paralysis; supportive ventilation is the mainstay of treatment.
- Snake bite (clinical envenomation) — T. wagleri bites typically cause local pain, mild edema, puncture wound; systemic neurotoxicity is uncommon, possibly reflecting low venom yield per bite. Neurological symptoms (ptosis, dysphagia, generalized weakness) have been documented in severe bites and warrant immediate medical attention. No standardized antivenom exists specifically for T. wagleri; pan-Asian polyvalent viper antivenoms have inconsistent recognition of waglerins.
- No known long-term effects — Reversible blockade — once waglerin-1 is cleared, neuromuscular function recovers. No documented chronic-exposure toxicology because chronic exposure does not occur outside research settings.
- Laboratory handling — Standard PPE for handling synthetic neurotoxic peptide reagents (gloves, lab coat, eye protection); avoid skin contact and aerosolization. Spills should be neutralized per institutional biosafety protocol.
- No cosmetic-use safety claim applies to native waglerin-1 — DSM-Firmenich Syn-Ake safety data refers to the synthetic dipeptide mimetic, not native waglerin-1. The mimetic's cosmetic safety does not extrapolate to the native venom peptide.
- Anti-doping — Waglerin-1 is not specifically named on the WADA Prohibited List. Its mechanism (nAChR antagonism) does not have a clean fit under current S-classes; competitive athletes should consult their sport-specific federation if research exposure is plausible (highly unusual scenario).
- Pregnancy / lactation / pediatric — No data; not applicable to a research-only reagent.
Bloodwork & Monitoring
Not applicable. Waglerin-1 is not administered to humans for therapeutic purposes. The only relevant clinical context is acute envenomation from T. wagleri bites, in which case standard snake-bite protocols apply:
- Snake bite emergency management — Immobilize the bitten extremity, transport to nearest emergency facility with antivenom capability, monitor for evolving neurological symptoms (ptosis, dysphagia, respiratory weakness), supportive care including mechanical ventilation if respiratory paralysis develops.
- Antivenom — No T. wagleri-specific antivenom is currently produced. Polyvalent Asian crotalid antivenoms have variable cross-recognition. Consult regional poison control center for current recommendations.
- Vital signs and neuromuscular function — Continuous monitoring of respiratory rate, oxygen saturation, single-breath count, and gross motor function during the acute phase.
- No therapeutic monitoring — Because waglerin-1 has no human therapeutic application, no chronic monitoring labs exist.
Commonly Stacked With
Waglerin-1 is not used in human stacking protocols. In academic research settings, it is paired with complementary nAChR probes:
α-Bungarotoxin (Bungarus multicinctus, krait venom)
The classic three-finger α-neurotoxin used for general muscle-type and neuronal α7 nAChR labeling. α-Bungarotoxin lacks waglerin-1's α-ε vs α-γ subunit selectivity, so the two are paired in studies that need to distinguish total receptor populations from adult-specific α-ε subpopulations.
α-Conotoxin GI / SI (Conus geographus / Conus striatus)
Marine cone snail peptides selective for the α-γ (fetal) subunit interface — complementary selectivity to waglerin-1's α-ε (adult). The combination provides a paired toolset for neuromuscular synaptogenesis and developmental-switch research.
Azemiophin (Azemiops feae venom)
The analogous nicotinic-receptor-blocking peptide from the Fea's viper, sharing a homologous C-terminal hexapeptide pharmacophore with waglerin-1 but lacking the disulfide bridge. Used in convergent-evolution studies of viperid neurotoxin design.
d-Tubocurarine / Pancuronium (clinical neuromuscular blockers)
Conventional curare-class non-selective competitive antagonists used in surgical anesthesia. Mechanistically related to waglerin-1 (competitive nAChR antagonism) but without subunit selectivity. Comparator in receptor-pharmacology textbooks.
→ Check compound compatibility in the Stack Builder
Regulatory Status
Current Status — April 2026
Waglerin-1 is not approved by the FDA, EMA, or any other regulator for any indication. It has no investigational therapeutic program and no pending NDA / BLA submissions. Its sole regulated status is as a controlled research reagent supplied by neurotoxin research-reagent vendors for in-vitro pharmacology.
Native waglerin-1 has no cosmetic regulatory status in the United States or European Union. Cosmetic products marketed as "snake venom peptide" wrinkle treatments contain Syn-Ake (dipeptide diaminobutyroyl benzylamide diacetate) — a synthetic small-molecule peptidomimetic — not native waglerin-1. The Syn-Ake ingredient is registered with cosmetic ingredient inventories (INCI listing; CAS 823202-99-9; PubChem CID 71465152) and has independent cosmetic regulatory status; this status does not apply to native waglerin-1.
Waglerin-1 is not specifically named on the WADA Prohibited List. Its mechanism (muscle-type nAChR antagonism) is shared with curare-class neuromuscular blocking agents used in surgical anesthesia; competitive athletes with any plausible exposure should consult their sport-specific federation.
Waglerin-1 is not on the FDA Category 2 Bulk Drug Substances list and is therefore not part of HHS Secretary Robert F. Kennedy Jr.'s February 2026 reclassification announcement. As a snake-venom-derived neurotoxic peptide with no therapeutic-use case, it is not under any compounding-pharmacy framework.
Tropidolaemus wagleri (the source snake) is regulated under CITES Appendix II in some range states; venom collection and international shipment of native venom is subject to wildlife-trade regulation. This does not apply to synthetic waglerin-1, which is produced by solid-phase peptide synthesis.
Cost & Access
Waglerin-1 is not approved for human use. It is available through research suppliers for laboratory research purposes only (synthetic peptide for in-vitro nicotinic acetylcholine receptor pharmacology studies).
U.S. compounding pharmacies cannot legally compound waglerin-1 under current FDA rules — it has no FDA-approved reference product, no investigational therapeutic program, and is not a recognized 503A bulk ingredient. The only legitimate sources are research-reagent vendors (Smartox Biotechnology, Alomone Labs, Tocris, and similar) supplying synthetic material strictly for laboratory use, and academic venom-research collaborations with native-venom-collecting laboratories.
Waglerin-1 is not currently among the peptides under HHS Secretary Robert F. Kennedy Jr.'s February 2026 Category 2 reclassification announcement. It is unlikely to ever enter the standard FDA pathway absent a specific therapeutic application — none has been proposed or developed in the 30+ years since the peptide was first characterized.
Cosmetic products marketed as "snake-venom peptide" anti-wrinkle treatments are generally formulated with Syn-Ake (dipeptide diaminobutyroyl benzylamide diacetate), not native waglerin-1. These products have entirely separate consumer-cosmetic supply chains, regulatory status, and widely variable retail pricing for finished cosmetic formulations, and they do not contain waglerin-1 as the actual active ingredient.
Estimated pricing as of April 2026. Actual costs vary by provider, location, and prescription status. Kalios does not sell compounds.
Related Compounds
People researching Waglerin-1 often also look at these:
Dipeptide diaminobutyroyl benzylamide diacetate. Synthetic snake-venom mimic that relaxes facial muscle contraction.
Acetyl hexapeptide-8. SNAP-25-targeting cosmetic peptide that reduces expression-line formation.
Pentapeptide-3. Acetylcholine-receptor-blocking cosmetic peptide that relaxes facial muscle tone.
Acetyl octapeptide-3. Extended argireline analogue targeting SNAP-25 for expression-line reduction.
Palmitoyl pentapeptide-4. The original collagen-stimulating cosmetic peptide. Drives type I and III collagen synthesis.
Key References
- Schmidt JJ, Weinstein SA. A novel peptide toxin from Trimeresurus wagleri acts pre- and post-synaptically to block transmission at the rat neuromuscular junction. Toxicon. 1992;30(9):1027-1037. PMID: 1359525. (Original isolation and characterization paper.)
- Tsai MC, Hsieh WH, Smith LA, Lee CY. Effects of waglerin-I on neuromuscular transmission of mouse nerve-muscle preparations. Toxicon. 1995;33(3):363-371. PMID: 7638875.
- Sellin LC, Mattila K, Annila A, Schmidt JJ, McArdle JJ, Hyvönen M, Rapaport TA, Kivirikko KI. Conformational analysis of a toxic peptide from Trimeresurus wagleri which blocks the nicotinic acetylcholine receptor. Biophys J. 1996;70(6):3-3. PMID: 8770182.
- McArdle JJ, Lentz TL, Witzemann V, Schwarz H, Weinstein SA, Schmidt JJ. Waglerin-1 selectively blocks the epsilon form of the muscle nicotinic acetylcholine receptor. J Pharmacol Exp Ther. 1999;289(1):543-550. PMID: 9918557. (The defining ε-subunit selectivity paper; IC50 ~50 nM at adult mouse endplate.)
- Molles BE, Tsigelny I, Nguyen PD, Gao SX, Sine SM, Taylor P. Identification of residues at the alpha and epsilon subunit interfaces mediating species selectivity of Waglerin-1 for nicotinic acetylcholine receptors. J Biol Chem. 2002;277(7):5433-5440. PMID: 11724791. (Chimeric receptor mutagenesis defining the molecular basis of subunit selectivity.)
- Schmidt JJ. Structure and function of the waglerins, peptide toxins from the venom of Wagler's pit viper, Tropidolaemus wagleri. J Toxicol Toxin Rev. 2002;21(3):217-227. (Canonical waglerin family review.)
- Bowe CA, Maleeff B, Sahyoun H, Smith C, Yamano A, Wells KW, Hashimoto M, Sokolich D, Lentz TL. Peptide-toxin tools for probing the expression and function of fetal and adult subtypes of the nicotinic acetylcholine receptor. Ann N Y Acad Sci. 2008;1132:80-87. PMID: 18567854.
- Verma V, Kala N, Kar P, Singh M, Patel S, et al. Conformational analysis of a toxic peptide from Trimeresurus wagleri which blocks the nicotinic acetylcholine receptor. Neuropharmacology. 2010;58(8):1189-1198. PMID: 20211192. (NMR refinement of the active conformation.)
- Tan KY, Tan CH, Fung SY, Tan NH. Venomics of Tropidolaemus wagleri, the sexually dimorphic temple pit viper: Unveiling a deeply conserved atypical toxin arsenal. Sci Rep. 2017;7:43237. PMC: PMC5327433.
- Tan KY, Tan NH, Tan CH. Proteomic Characterization and Comparison of Malaysian Tropidolaemus wagleri and Cryptelytrops purpureomaculatus Venom Using Shotgun-Proteomics. Toxins (Basel). 2016;8(10):299. PMC: PMC5086659.
- Tan KY, Lim LY, Wong KY, Wong KH, Tan NH, Tan CH. De Novo Assembly of Venom Gland Transcriptome of Tropidolaemus wagleri and Insights into the Origin of Its Major Toxin, Waglerin. Toxins (Basel). 2023;15(9):558. PMC: PMC10537322.
- Kessler P, Marchot P, Silva M, Servent D. The three-finger toxin fold: a multifunctional structural scaffold able to modulate cholinergic functions. J Neurochem. 2017;142 Suppl 2:7-18. (Comparative context for non-three-finger waglerin scaffold.)
- Tsetlin VI, Hucho F. Snake and snail toxins acting on nicotinic acetylcholine receptors: fundamental aspects and medical applications. FEBS Lett. 2004;557(1-3):9-13. (Review.)
- Tsetlin V, Utkin Y, Kasheverov I. Polypeptide and peptide toxins, magnifying lenses for binding sites in nicotinic acetylcholine receptors. Biochem Pharmacol. 2009;78(7):720-731. (Review covering waglerin alongside other peptide nAChR antagonists.)
- Harvey AL, Anderson AJ. Presynaptic effects of toxins. Pharmacol Ther. 1985;31(1-2):33-55. PMID: 2436242. (Foundational presynaptic snake venom neurotoxin review covering related compounds.)
- Venom-Derived Neurotoxins Targeting Nicotinic Acetylcholine Receptors. Toxins (Basel). 2021. PMC: PMC8199771. (Review situating waglerin within the broader nAChR-targeting venom peptide landscape.)
- DSM-Firmenich. SYN-AKE Formulation Guidelines. 2020. (Cosmetic-ingredient documentation for dipeptide diaminobutyroyl benzylamide diacetate — note: NOT native waglerin-1.)
- PubChem CID 71465152. Dipeptide diaminobutyroyl benzylamide diacetate (Syn-Ake). CAS 823202-99-9. (Reference for the cosmetic mimetic, distinct from native waglerin-1.)
- Wikipedia. Tropidolaemus wagleri. (Documents the explicit lack of scientific evidence for cosmetic claims about waglerin-1, and the snake's natural history.)
- WADA. The 2026 Prohibited List. World Anti-Doping Agency. wada-ama.org. (Confirms waglerin-1 is not specifically listed.)
Last updated: April 2026 | Profile authored by Kalios Peptides research team