The Integrin Binding Peptide, ATN-161, as a Novel Therapy for SARS-CoV-2 Infection.
The Integrin Binding Peptide, ATN-161, as a Novel Therapy for SARS-CoV-2 Infection.
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整合素结合肽 ATN-161,作为 SARS-CoV-2 感染的新疗法。
DOI:
10.1016/j.jacbts.2020.10.003
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发表时间:
2021-01
期刊:
影响因子:
--
通讯作者:
Bix GJ
中科院分区:
文献类型:
--
作者:
Beddingfield BJ;Iwanaga N;Chapagain PP;Zheng W;Roy CJ;Hu TY;Kolls JK;Bix GJ
SARS-CoV-2 spike protein binds to α5β1 integrin protein and human ACE2/α5β1, facilitating entry into host cells. ATN-161, an integrin binding peptide, inhibits the interaction between the SARS-CoV-2 spike protein and its host binding partners, with 3 sites of binding identified via molecular modeling. ATN-161 inhibits infection in vitro and demonstrates increases in cell viability when administered prophylactically. ATN-161 is well-studied, with the potential for more rapid introduction into clinical trials than many other compounds currently undergoing preclinical evaluation. Many efforts to design and screen therapeutics for the current severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) pandemic have focused on inhibiting viral host cell entry by disrupting angiotensin-converting enzyme-2 (ACE2) binding with the SARS-CoV-2 spike protein. This work focuses on the potential to inhibit SARS-CoV-2 entry through a hypothesized α5β1 integrin−based mechanism and indicates that inhibiting the spike protein interaction with α5β1 integrin (+/− ACE2) and the interaction between α5β1 integrin and ACE2 using a novel molecule (ATN-161) represents a promising approach to treat coronavirus disease-19.
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DOI:
10.29271/jcpsp.2020.supp2.s19
发表时间:
2020-06-01
影响因子:
1
作者:
Asgharpour, Masoumeh;Zare, Elham;Alirezaei, Amirhesam
通讯作者:
Alirezaei, Amirhesam
影响因子:
82.9
作者:
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通讯作者:
Baric RS
DOI:
10.1016/j.bbadis.2004.05.005
发表时间:
2004-08-04
影响因子:
6.2
作者:
Lin, QS;Keller, RS;Zisman, LS
通讯作者:
Zisman, LS
影响因子:
3.7
作者:
Clarke NE;Fisher MJ;Porter KE;Lambert DW;Turner AJ
通讯作者:
Turner AJ
影响因子:
6.3
作者:
Edwards, Danielle N.;Salmeron, Kathleen;Bix, Gregory J.
通讯作者:
Bix, Gregory J.