Viterilon's first new drug, SIR1-365 tablets, was approved for clinical use in China

Text|Pharmaceutical Mission Hills

The latest announcement by the Center for Drug Evaluation (CDE) of the China National Medical Products Administration, Viterilon (Beijing) Biotechnology Co.
, Ltd.
(Sironax, hereinafter referred to as Viterilon) declared a new class 1 drug SIR1-365 tablets, which has been implied by clinical trials Approved, intended to be developed for the treatment of infectious diseases related to systemic inflammatory response syndrome (SIRS)
.

Viterilon is a global biomedical company focusing on the research and development of "first-in-class" new drugs, co-founded by Dr.
Xiaodong Wang and Dr.
Zhiyuan Zhang
.

Check the CDE official website.

Screenshot source: CDE official website

Public information shows that SIR1-365 is a receptor-interacting protein 1 (RIP1) inhibitor
.

RIP1 is a serine/threonine protein kinase that can regulate a variety of biological signal transduction pathways, such as TNFα-mediated NFκB signal transduction, apoptosis, programmed cell necrosis, and inflammation

According to Viterilon’s official website, in animal experiments, inhibiting RIP1 kinase through small molecule drugs or gene editing can effectively prevent or reduce the development of a series of diseases, including multiple sclerosis (EAE model), Alzheimer’s disease, amyotrophic lateral sclerosis, systemic inflammatory response syndrome
.

In addition, the use of small molecules to inhibit RIP1 kinase can significantly delay the aging process of the male reproductive organs of mice by preventing the programmed necrosis of spermatogonial stem cells and supporting cells in the testis

Previously, Viterilon has registered in the United States to carry out a phase 1 clinical trial, which aims to study the safety and effectiveness of SIR1-365 in patients with severe COVID-19
.

Viterilon was established in 2018 to develop inhibitors for major discoveries in a variety of cell death fields, including apoptosis and necrosis
.

Public information shows that the company’s research and development projects are derived from the breakthrough scientific discoveries of apoptosis, necroptosis and other cell death mechanisms in Dr.

▲The product pipeline of Viterilon (picture source: Viterilon's official website)

For the past many years, Dr.
Xiaodong Wang’s laboratory has been studying the molecular mechanisms of programmed cell apoptosis and programmed cell necrosis, and discovered the important regulatory proteins RIP3 and MLKL (mixed lineage kinase domain-like protein) in cell necrosis
.

They used RIP3 and MLKL gene knockout mice to study the physiological significance of cell necrosis in the body, and found that the cell necrosis signaling pathway regulates the aging of the male mouse reproductive system

The laboratory of Dr.
Zhiyuan Zhang, co-founder of Viterilon, designed a RIP1 inhibitor
.

In mouse experiments, the compound can significantly inhibit the proliferation of seminal vesicle glands and delay the aging of reproductive functions, while the level of male hormones is still maintained at a young level

According to the official website of Viterilon, the current RIP1 inhibitor project (SIR1) has become the fastest-growing product in the research pipeline of Viterilon
.

The clinical approval of SIR1-365 in China means that this RIP1 inhibitor is about to enter clinical studies in China
.

It is hoped that Viterilon SIR1-365 will progress smoothly in clinical research and make more breakthroughs as soon as possible

Reference materials:

[1] Center for Drug Evaluation of China National Medical Products Administration.

[3] Qiu Zhendong, Wang Weixing.

[4]He, S.
, Wang, L.
, Miao, L.
, Wang, T.
, Du, F.
, Zhao, L.
, and Wang, X.
(2009).
Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha.
Cell 137, 1100-1111.

[5]Sun, L.
, Wang, H.
, Wang, Z.
, He, S.
, Chen, S.
, Liao, D.
, Wang, L.
, Yan, J.
, Liu, W.
, Lei, X.
, et al.
(2012).
Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase.
Cell 148, 213-227.

[6]Li, D.
, Meng, L.
, Xu, T.
, Su, Y.
, Liu, X.
, Zhang, Z.
, and Wang, X.
(2017).
RIPK1-RIPK3-MLKL-dependent necrosis promotes the aging of mouse male reproductive system.
Elife 6.