Maybe Emodin was posted already. Below are old studies. A recent article on COVID-19, talks about using Toremifene plus Emodin and says: "Emodin, an anthraquinone derivative extracted from the roots of rheum tanguticum, has been reported to have various anti-virus effects. Specifically, emdoin inhibited SARS-CoV-associated 3a protein70, and blocked an interaction between the SARS-CoV spike protein and ACE2 (ref. 71). Altogether, network analyses and published experimental data suggested that combining toremifene and emdoin offered a potential therapeutic approach for 2019-nCoV/SARS-CoV-2 (Fig. 6c)."
Antiviral Res. 2007 May;74(2):92-101. Epub 2006 May 15.
Ho TY1, Wu SL, Chen JC, Li CC, Hsiang CY.
Severe acute respiratory syndrome (SARS) is an emerging infectious disease caused by a novel coronavirus (SARS-CoV). SARS-CoV spike (S) protein, a type I membrane-bound protein, is essential for the viral attachment to the host cell receptor angiotensin-converting enzyme 2 (ACE2). By screening 312 controlled Chinese medicinal herbs supervised by Committee on Chinese Medicine and Pharmacy at Taiwan, we identified that three widely used Chinese medicinal herbs of the family Polygonaceae inhibited the interaction of SARS-CoV S protein and ACE2. The IC(50) values for Radix et Rhizoma Rhei (the root tubers of Rheum officinale Baill.), Radix Polygoni multiflori (the root tubers of Polygonum multiflorum Thunb.), and Caulis Polygoni multiflori (the vines of P. multiflorum Thunb.) ranged from 1 to 10 microg/ml. Emodin, an anthraquinone compound derived from genus Rheum and Polygonum, significantly blocked the S protein and ACE2 interaction in a dose-dependent manner. It also inhibited the infectivity of S protein-pseudotyped retrovirus to Vero E6 cells. These findings suggested that emodin may be considered as a potential lead therapeutic agent in the treatment of SARS.
PMID: 16730806
Antiviral Res. 2011 Apr;90(1):64-9.
Schwarz S1, Wang K, Yu W, Sun B, Schwarz W.
The open-reading-frame 3a of SARS coronavirus (SARS-CoV) had been demonstrated previously to form a cation-selective channel that may become expressed in the infected cell and is then involved in virus release. Drugs that inhibit the ion channel formed by the 3a protein can be expected to inhibit virus release, and would be a source for the development of novel therapeutic agents. Here we demonstrate that emodin can inhibit the 3a ion channel of coronavirus SARS-CoV and HCoV-OC43 as well as virus release from HCoV-OC43 with a K1/2 value of about 20 μM. We suggest that viral ion channels, in general, may be a good target for the development of antiviral agents.
PMID: 21356245