1. Membrane Transporter/Ion Channel
    Neuronal Signaling
  2. nAChR
  3. α-Conotoxin Vc1.1 TFA

α-Conotoxin Vc1.1 TFA 

Cat. No.: HY-125777A
Handling Instructions

α-Conotoxin Vc1.1 TFA is a disulfide-bonded peptide isolated from Conus victoriae and is a selective nAChR antagonist. α-Conotoxin Vc1.1 TFA inhibits α3α5β2, α3β2 and α3β4 with IC50s of 7.2 μM, 7.3 μM and 4.2 μM, respectively, and has less inhibitory effect on other nAChR subtypes. α-Conotoxin Vc1.1 TFA has the potential for neuropathic pain reserach.

For research use only. We do not sell to patients.

Custom Peptide Synthesis

α-Conotoxin Vc1.1 TFA Chemical Structure

α-Conotoxin Vc1.1 TFA Chemical Structure

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Description

α-Conotoxin Vc1.1 TFA is a disulfide-bonded peptide isolated from Conus victoriae and is a selective nAChR antagonist. α-Conotoxin Vc1.1 TFA inhibits α3α5β2, α3β2 and α3β4 with IC50s of 7.2 μM, 7.3 μM and 4.2 μM, respectively, and has less inhibitory effect on other nAChR subtypes. α-Conotoxin Vc1.1 TFA has the potential for neuropathic pain reserach[1][2].

IC50 & Target

IC50: 7.2 μM (α3α5β2), 7.3 μM (α3β2) and 4.2 μM (α3β4)[1]

In Vitro

The α-Conotoxin Vc1.1 is first discovered using a PCR screen of cDNAs from the venom ducts of Conus victoriae. α-Conotoxin Vc1.1 inhibits nicotine-evoked membrane currents in isolated bovine chromaffin cells in a concentration-dependent manner and preferentially targets peripheral nAChR subtypes over central subtypes. The three-dimensional structure of Vc1.1 comprises a small alpha-helix spanning residues Pro6 to Asp11 and is braced by the I-III, II-IV disulfide connectivity seen in other alpha-conotoxins. The cysteine spacing within the sequence of α-Conotoxin Vc1.1 suggests that it is a member of the 4/7 subclass of α-conotoxins, which includes the extensively studied conotoxins MII, EpI and PnIB[1].

In Vivo

α-Conotoxin Vc1.1 (0.18-18 μg/μL; intramuscular injection; daily; for 7 days; male Sprague-Dawley rats) treatment suppresses pain behaviors and also accelerates functional recovery of injured neurons in CCI rats[1].

Animal Model: Outbred male Sprague-Dawley rats (3-4 months old; 250-350 g) bearing with chronic constriction injury (CCI)[1]
Dosage: 0.18 μg/μL, 1.8 μg/μL or 18 μg/μL
Administration: Intramuscular injection; daily; for 7 days
Result: Suppressed pain behaviors and also accelerates functional recovery of injured neurones.
Molecular Weight

1921.00

Formula

C₇₃H₁₀₄F₃N₂₃O₂₇S₄

Sequence

{Gly}{Cys}{Cys}{Ser}{Asp}{Pro}{Arg}{Cys}{Asn}{Tyr}{Asp}{His}{Pro}{Glu}{Ile}{Cys}-NH2 (Disulfide bridge:Cys2-Cys8;Cys3-Cys16)

Sequence Shortening

GCCSDPRCNYDHPEIC-NH2 (Disulfide bridge:Cys2-Cys8;Cys3-Cys16)

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

References
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Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2

Keywords:

α-Conotoxin Vc1.1nAChRNicotinic acetylcholine receptorsAnalgesicdisulfidepeptideneuropathicα3α5β2α3β2α3β4Inhibitorinhibitorinhibit

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α-Conotoxin Vc1.1 TFA
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HY-125777A
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