Cardiotoxin Analog (CTX) IV (6-12) (TFA)

Cardiotoxin Analog (CTX) IV (6-12) TFA is a membrane active peptide that specifically targets negatively charged phospholipid membranes (such as phosphatidylserine and phosphatidylinositol) and can be isolated from the venom of the Taiwan cobra. Cardiotoxin Analog (CTX) IV (6-12) TFA is a snake venom cardiotoxin that binds to cell membranes and embeds into lipid bilayers through hydrophobic interactions and electrostatic attraction, thereby destroying the stability of membrane structure. Cardiotoxin Analog (CTX) IV (6-12) TFA can induce membrane lipid disorder and cell lysis, exhibiting hemolysis and cytotoxicity[1][2].

Product Specifications

CAS Number

[2918768-05-3]

UNSPSC

12352209

Target

Apoptosis

Type

Peptides

Related Pathways

Apoptosis

Field of Research

Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/cardiotoxin-analog-ctx-iv-6-12-tfa.html

Purity

99.53

Solubility

H2O : 50 mg/mL (ultrasonic)

Smiles

NCCCC[C@@H](C(N)=O)NC([C@H](CC1=CNC2=CC=CC=C12)NC([C@H](CC3=CC=CC=C3)NC([C@H]4N(C([C@H]5N(C([C@H]([C@@H](C)CC)NC([C@H](CC(C)C)N)=O)=O)CCC5)=O)CCC4)=O)=O)=O.OC(C(F)(F)F)=O

Molecular Formula

C50H71F3N10O9

Molecular Weight

1013.16

References & Citations

[1]Kaneda N, et al. The amino acid sequence of cardiotoxin-analogue IV from the venom of Naja naja atra. FEBS Lett. 1976 Nov;70 (1) :217-22. |[2]Dufourcq J, et al. Structure-function relationships for cardiotoxins interacting with phospholipids. Toxicon. 1982;20 (1) :165-74. |[3]Aoki Y, et al. Highly efficient in vivo delivery of PMO into regenerating myotubes and rescue in laminin-α2 chain-null congenital muscular dystrophy mice. Hum Mol Genet. 2013 Dec 15;22 (24) :4914-28.|[4]Randazzo D, et al. Persistent upregulation of the β-tubulin tubb6, linked to muscle regeneration, is a source of microtubule disorganization in dystrophic muscle. Hum Mol Genet. 2019 Apr 1;28 (7) :1117-1135.|[5]Fan W, et al. Hsp70 Interacts with Mitogen-Activated Protein Kinase (MAPK) -Activated Protein Kinase 2 To Regulate p38MAPK Stability and Myoblast Differentiation during Skeletal Muscle Regeneration. Mol Cell Biol. 2018 Nov 28;38 (24) :e00211-18.|[6]Dalle S, et al. Cardiotoxin-induced skeletal muscle injury elicits profound changes in anabolic and stress signaling, and muscle fiber type composition. J Muscle Res Cell Motil. 2020 Dec;41 (4) :375-387.|[7]Liu Y, et al. MicroRNA-200c-5p Regulates Migration and Differentiation of Myoblasts via Targeting Adamts5 in Skeletal Muscle Regeneration and Myogenesis. Int J Mol Sci. 2023 Mar 5;24 (5) :4995.|[8]Mahdy MA, et al. Comparative study of muscle regeneration following cardiotoxin and glycerol injury. Ann Anat. 2015 Nov;202:18-27.|[9]Wang Y, et al. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models. Int J Mol Sci. 2022 Nov 2;23 (21) :13380.

Shipping Conditions

Blue Ice

Storage Conditions

-80°C, 2 years; -20°C, 1 year (Powder, sealed storage, away from moisture)

Scientific Category

Peptides

Clinical Information

No Development Reported

Citation 01

Antioxidants (Basel) . 2023 Sep 13;12 (9) :1754.|Antioxidants (Basel) . 2024 Sep 1;13 (9) :1069.|Cell Death Dis. 2022 Sep 29;13 (9) :838.|Cell Death Discov. 2022 Apr 30;8 (1) :236.|Commun Biol. 2022 Nov 9;5 (1) :1201.|Adv Sci (Weinh) . 2025 Aug 31:e12354.|Int J Mol Sci. 2023 Mar 5;24 (5) :4995.|Mol Ther. 2025 May 6:S1525-0016 (25) 00360-0.