Cannabis chemicals block covid virus (in the lab, at least).

Researchers publishing in the Journal of Natural Products have basically opened the door to pot being the next ivermectin with a finding that orally active extracts of Cannabis sativa block the covid virus from reproducing in living cells:

ABSTRACT:
As a complement to vaccines, small-molecule therapeutic agents are needed to treat or prevent infections by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and its variants, which cause COVID-19. Affinity selection–mass spectrometry was used for the discovery of botanical ligands to the SARS-CoV-2 spike protein. Cannabinoid acids from hemp (Cannabis sativa) were found to be allosteric as well as orthosteric ligands with micromolar affinity for the spike protein. In follow-up virus neutralization assays, cannabigerolic acid and cannabidiolic acid prevented infection of human epithelial cells by a pseudovirus expressing the SARS-CoV-2 spike protein and prevented entry of live SARS-CoV-2 into cells. Importantly, cannabigerolic acid and cannabidiolic acid were equally effective against the SARS-CoV-2 alpha variant B.1.1.7 and the beta variant B.1.351. Orally bioavailable and with a long history of safe human use, these cannabinoids, isolated or in hemp extracts, have the potential to prevent as well as treat infection by SARS-CoV-2.

EXCERPT:
To determine if CBDA or CBGA could prevent infection by blocking SARS-CoV-2 cell entry, pseudovirus and live SARS-CoV-2 virus cell infection assays were carried out. We incubated the live SARS-CoV-2 virus with 25 μg/mL of either CBDA, CBGA, or vehicle control (DMSO) and then infected Vero E6 cells. At 24 h postinfection, cells were stained with anti-double-stranded RNA (dsRNA) antibody known to bind specifically to viral RNA. We found an absence of SARS-CoV-2 viral RNA in cells treated with either cannabinoid (Figure 3A). To quantify the level of inhibition, we produced spike protein pseudotyped lentiviral particles with a GFP reporter gene, and HEK 293T cells overexpressing ACE-2 were infected for 48 h with these lentiviral particles following treatment with varying concentrations of CBDA, CBGA, or vehicle control. The number of infected cells was quantified by fluorescence microscopy, and the concentration that reduced pseudovirus infections by half (IC50) was 7.7 μg/mL for CBDA and 8.4 μg/mL for CBGA (Figure 3B,C). The cytotoxicity of these compounds was insignificant at concentrations below 50 μg/mL for Caco2, 293T-ACE2, and Vero cell lines.