Home Cytoskeletal Signaling Integrin antagonist ATN-161

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ATN-161 Integrin antagonist

Cat.No.S8454

ATN-161 is a novel small peptide antagonist of integrin α5β1. It binds to several integrins, including α5β1 and αvβ3, that play a role in angiogenesis and tumor progression.
ATN-161 Integrin antagonist Chemical Structure

Chemical Structure

Molecular Weight: 597.64

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Quality Control

Batch: Purity: 99.82%
99.82

Solubility

In vitro
Batch:

Water : 10 mg/mL (超声加热十分钟，60℃)

DMSO : 3 mg/mL (5.01 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 597.64 Formula

C23H35N9O8S

 Storage (From the date of receipt)
CAS No. 262438-43-7 Download SDF Storage of Stock Solutions

Synonyms Ac-PHSCN-NH2 Smiles CC(=O)N1CCCC1C(=O)NC(CC2=CN=CN2)C(=O)NC(CO)C(=O)NC(CS)C(=O)NC(CC(=O)N)C(=O)N

Mechanism of Action

Targets/IC50/Ki
integrin α5β1
αvβ3
In vitro
ATN-161 interacts with the N-terminus of the β1-domain of integrin α5β1, which may lock this integrin in an inactive conformation. This compound treatment up to 100 μmol/L shows no significant effect on tumor cell proliferation compared with the vehicle-treated control group of cells. However, this chemical significantly inhibits MAPK phosphorylation with maximal effects observed at 20 μmol/L of this compound after 30 minutes of treatment.
In vivo
ATN-161 (Ac-PHSCN-NH2), a 5-mer capped peptide derived from the synergy region of fibronectin that binds to α5β1 and αvβ3 in vitro, blocks breast cancer growth and metastasis. Treatment with this compound causes a significant dose-dependent decrease in tumor volume and either completely blocked or caused a marked decrease in the incidence and number of skeletal as well as soft tissue metastases. Treatment with this peptide results in a significant decrease in the expression of phosphorylated mitogen-activated protein kinase, microvessel density, and cell proliferation in tumors grown in vivo. It is a peptide with a fairly short plasma half-life. compared with the plasma pharmacokinetics of this compound, It is cleared from the tumor with much slower kinetics supporting the hypothesis that this peptide exerts its effects through a durable interaction with its target(s)in the tumor.
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