153386-08-4

Upstream product

• 88-67-5 2-Iodobenzoic acid 
• 371-40-4 4-fluoroaniline 
• 609-67-6 2-Iodobenzoyl chloride 

Downstream Products

• 4322-70-7 2-(4-fluorophenyl)benzo[d]isothiazol-3(2H)-one 
• 1452790-26-9 4-[(Z)-3-phenyl-1-(p-tolylimino)-1H-isochromen-4-yl]butan-2-one 
• 1253388-48-5 2-(4-fluorophenyl)-3,4-diphenylisoquinolin-1(2H)-one 
• 153386-11-9 1-(4-fluorophenyl)-5-(2-iodophenyl)tetrazole 
• 81743-89-7 2-(4-fluorophenyl)benzo[d][1,2] selenazol-3(2H)-one 

Relevant academic research and scientific papers

The Mpro structure-based modifications of ebselen derivatives for improved antiviral activity against SARS-CoV-2 virus

The main protease (Mpro or 3CLpro) of SARS-CoV-2 virus is a cysteine enzyme critical for viral replication and transcription, thus indicating a potential target for antiviral therapy. A recent repurposing effort has identified ebselen, a multifunctional drug candidate as an inhibitor of Mpro. Our docking of ebselen to the binding pocket of Mpro crystal structure suggests a noncovalent interaction for improvement of potency, antiviral activity and selectivity. To test this hypothesis, we designed and synthesized ebselen derivatives aimed at enhancing their non-covalent bonds within Mpro. The inhibition of Mpro by ebselen derivatives (0.3 μM) was screened in both HPLC and FRET assays. Nine ebselen derivatives (EBs) exhibited stronger inhibitory effect on Mpro with IC50 of 0.07–0.38 μM. Further evaluation of three derivatives showed that EB2-7 exhibited the most potent inhibition of SARS-CoV-2 viral replication with an IC50 value of 4.08 μM in HPAepiC cells, as compared to the prototype ebselen at 24.61 μM. Mechanistically, EB2-7 functions as a noncovalent Mpro inhibitor in LC-MS/MS assay. Taken together, our identification of ebselen derivatives with improved antiviral activity may lead to developmental potential for treatment of COVID-19 and SARS-CoV-2 infection.

Discovery and Mechanism of SARS-CoV-2 Main Protease Inhibitors

The emergence of a new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), presents an urgent public health crisis. Without available targeted therapies, treatment options remain limited for COVID-19 patients. Using medicinal chemistry and rational drug design strategies, we identify a 2-phenyl-1,2-benzoselenazol-3-one class of compounds targeting the SARS-CoV-2 main protease (Mpro). FRET-based screening against recombinant SARS-CoV-2 Mpro identified six compounds that inhibit proteolysis with nanomolar IC50 values. Preincubation dilution experiments and molecular docking determined that the inhibition of SARS-CoV-2 Mpro can occur by either covalent or noncovalent mechanisms, and lead E04 was determined to inhibit Mpro competitively. Lead E24 inhibited viral replication with a nanomolar EC50 value (844 nM) in SARS-CoV-2-infected Vero E6 cells and was further confirmed to impair SARS-CoV-2 replication in human lung epithelial cells and human-induced pluripotent stem cell-derived 3D lung organoids. Altogether, these studies provide a structural framework and mechanism of Mpro inhibition that should facilitate the design of future COVID-19 treatments.

Benzisoselenazolone derivative, preparation method and application in anti-coronavirus drugs

The invention belongs to the technical field of anti-coronavirus drug discovery, discloses a benzisoselenazolone derivative, a preparation method and application of the benzisoselenazolone derivativein coronavirus resistance, and relates to synthesis of a

Role of Hetero-halogen (F · · · X, X = Cl, Br, and I) or homo-halogen (X · · · X, X = F, Cl, Br, and I) interactions in substituted benzanilides

A series of halogen-substituted benzanilides have been synthesized and characterized, and crystallization studies directed toward generation of polymorphs have been performed to delineate the importance of interactions involving halogens. The effect of ha

Cyclizations. Part 1. Electrochemical and Photochemical Reactions of 1-(4-Fluorophenyl)-5-(2-halogenophenyl)tetrazoles

Electrochemical reduction of the title compounds, where the halogen substituent is Cl, Br or I, leads to cleavage of the carbon-halogen bond to leave a phenyl radical.Competition then follows between intramolecular radical substitution giving 7-fluorotetrazolophenanthridine and further reduction of the radical, then protonation, giving 1-(4-fluorophenyl)-5-phenyltetrazole.Substitution predominates but reduction and protonation becomes a more competing reaction when the halogen is Br or I.Photochemical reaction of the title compounds shows competition between carbon-halogen bond cleavage to give 7-fluorotetrazolophenanthridine and loss of nitrogen followed by cyclization to give 2-halogenophenyl-5-fluorobenzimidazole.Carbon-halogen bond cleavage predominates and becomes the only reaction when the halogen is I.The fluorine substituent allows the determination of product yields by 19F NMR spectroscopy.