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racterizing unidentified mechanisms of gemR and on identifying agents with anti-tumor efficacy in these gemR models.Helminth infections are among the most common infectious diseases in underdeveloped countries. AZ-33 cell line Helminths suppress the host immune responses and consequently mitigate vaccine efficacy and increase severity of other infectious diseases. Helminth co-infections might suppress the efficient immune response against SARS-CoV-2 at the early stage of the infection and may increase morbidity and mortality of COVID-19.At times, combination therapy has proven to be very effective. While no cure is available to date, herein we put forward with rationale and supporting evidence that if administrated simultaneously, a combination of FDA-approved drugs comprising ivermectin, famotidine, and doxycycline may provide robust chemoprophylaxis effective against COVID-19.The COVID-19 pandemic has been humbling for the biomedical community, pointing out as much about what we do not know as what we do. Among these learnings are lessons about immune-based measures to prevent or treat a new biothreat. This article summarizes lessons learned from two experimental approaches for passive immunity, convalescent plasma and monoclonal antibody therapy. Two early reports of outcomes, both of which appeared within hours of one another, reveal the importance of blending past learning with a forward-looking approach. These also present cautionary lessons as the world looks to new vaccines to help eradicate this deadly scourge.Acute respiratory distress syndrome (ARDS) is one of the critical stages of COVID-19, leading to lung injury and hemolysis. Dysfunctional hemoglobin (Hb) suffers low-level oxygenation, overloaded iron, and down-regulation of hemeoxygenase-1 (HO-1), representing potential therapeutic interventions. This Viewpoint outlines the Hb-HO-1 system as a host-cell target, and proposes possible therapies, including iron chelation and CO therapies, against COVID-19 with ARDS.Guided by evolutionarily signaled vulnerabilities in the structure of SARS-CoV-2, we identify epitopes in free monomers of the spike protein that steer the generation of induced or administered antibodies geared at promoting destabilization of the virus quaternary structure, thereby hampering infectivity.The evolutionary change of SARS-CoV-2 is of the outmost concern. With a more stable phenotype, mutation D614G has become dominant. Its structural impact prompts the development of an antibody that destabilizes the virus quaternary structure where it is most vulnerable. Vaccine-related antigenic regions are different from the proposed epitope, hence avoiding therapeutic redundancy.SARS-CoV-2 has developed a substantial number of mutations, especially in the S-protein. With the advancement of the pandemic, accumulations of further mutations at the S-protein receptor-binding domain could enhance the infectivity and pathogenicity of the virus. Prediction and evaluation of such mutations are essential for understanding the potential development of more pathogenic strains and for COVID-19 management.Ivacaftor-tezacaftor and ivacaftor-tezacaftor-elexacaftor are new breakthrough cystic fibrosis (CF) drug combinations that directly modulate the activity and trafficking of the defective CF transmembrane conductance regulator protein (CFTR) underlying the CF disease state. Currently, in the hospital setting, there are no therapeutic drug monitoring assays for these very expensive, albeit, life-saving drugs. A rapid and precise novel method for the quantification of ivacaftor, its metabolites, tezacaftor, and elexacaftor, in human plasma was developed and validated using multiple reaction monitoring mass spectrometry (MRM/MS). The MRM/MS analytical method was validated at a concentration range of 0.0025-1 μg/mL for ivacaftor, ivacaftor-M1, ivacaftor-M6, tezacaftor, and elexacaftor in human plasma. The method displayed good accuracy (90.62-94.51%) and reproducibility (99.91-100%) including at low concentrations 0.01 μg/mL. With a mobile phase consisting of [acetonitrile/water]/0.1% formic acid (7030 v/v) at a flow rate of 0.5 mL/min, a linear correlation was observed over a concentration range of 0.0025-1 μg/mL in human plasma for ivacaftor (R2 = 0.9865105), ivacaftor-M1 (R2 = 0.9852684), ivacaftor-M6 (R2 = 0.9911764), tezacaftor (R2 = 0.98742470), and elexacaftor (R2 = 0.9897608). The reported method can accurately quantify ivacaftor, ivacaftor-M1, ivacaftor-M6, tezacaftor, and elexacaftor at low concentrations in human plasma. We have established a cost-efficient and timely method for measuring ivacaftor, its metabolites, and tezacaftor with or without elexacaftor in human plasma suitable for high-throughput applications in the hospital settings or clinical trials.Fibroblast growth factors 19 and 21 (FGF19 and FGF21) have biological actions that render them promising clinical candidates for treatment of metabolic diseases, particularly dyslipidemia and nonalcoholic steatohepatitis (NASH). These two atypical endocrine FGFs employ an accessory receptor β-klotho (KLB) to signal through classical FGF receptors (FGFRs). FGF19 and FGF21 bind to KLB via their C-terminus, to orient the N-terminus for productive interaction with FGFRs. The C-terminal peptides have been shown to competitively inhibit this biological agonism. We report here an assessment of the structural relationship in the C-terminal sequences of FGF19 and FGF21 that led to the identification of a sustained-acting peptide optimized for pharmacological use. It demonstrates high potency and selectivity to antagonize FGF19 and FGF21 in cells coexpressing FGFRs and KLB. This peptide was also effective in blocking FGF19 and FGF21 mediated downstream gene expression (i.e., Fos and Egr1) in vivo. In DIO mice, this antagonist alters metabolic function as assessed by changes in body weight, food intake, and plasma insulin. Thus, the selective inhibition of KLB could constitute a medicinal approach to treat diseases associated with excess FGF19 or 21 activity and separately serve as an effective tool to promote a deeper assessment of atypical FGF biology.