Correction: Synergistic drug combinations designed to fully suppress SARS-CoV-2 in the lung of COVID-19 patients.

[This corrects the article DOI: 10.1371/journal.pone.

Myrtleciclib, a CDK4/6/9 Inhibitor for the Treatment of Aggressive Cancers.

Background: Selective Cyclin-Dependent Kinase 4/6 inhibitors (CDK4/6i) have revolutionized the treatment of breast cancer and have potential in other cancers, being manageable drugs yet with some bone marrow toxicity. Selective CDK9 inhibitors (CDK9i) never advanced into clinical use, partly due to side effects, including gastrointestinal toxicity, and a small window between activity and cytotoxicity, which results in a narrow therapeutic index (TI).

Method: To overcome the drawbacks of CDK4/6 and CDK9 inhibitors, we have developed myrtleciclib, a selective CDK4/6/9 inhibitor with few non-critical molecular off-targets.

Synergistic drug combinations designed to fully suppress SARS-CoV-2 in the lung of COVID-19 patients.

Despite new antivirals are being approved against SARS-CoV-2 they suffer from significant constraints and are not indicated for hospitalized patients, who are left with few antiviral options. Repurposed drugs have previously shown controversial clinical results and it remains difficult to understand why certain trials delivered positive results and other trials failed. Our manuscript contributes to explaining the puzzle: this might have been caused by a suboptimal drug exposure and, consequently, an incomplete virus suppression, also because the drugs have mostly been used as add-on monotherapies.

Evaluation of the expression and intracellular localization of a 44-kDa calmodulin binding protein during exponential growth and quiescence (G0).

We have previously demonstrated that changes in calmodulin (CaM) levels are associated with G1/S transition of the cell cycle and entry into and release from quiescence (G0). CaM mediates its regulation through the specific interaction with different intracellular proteins called calmodulin binding proteins (CaMBPs). This study was designed to evaluate the expression of the CaMBPs during the cell cycle.

A potent peptidomimetic inhibitor of HSV ribonucleotide reductase with antiviral activity in vivo.

Herpes simplex viruses (HSV) types 1 and 2 encode their own ribonucleotide reductases (RNRs) (EC 1.17.4.