Background: High morbidity and mortality of influenza virus infection have made it become one of the most lethal diseases threatening public health; the lack of drugs with strong antiviral activity against virus strains exacerbates the problem.Methods: Two independent researchers searched relevant studies using Embase, PubMed, Web of Science, Google Scholar, and MEDLINE databases from its inception to December 2022.Results: Based on the different antiviral mechanisms, current antiviral strategies can be mainly classified into virus‐targeting approaches such as neuraminidase inhibitors, matrix protein 2 ion channel inhibitors, polymerase acidic protein inhibitors and other host‐targeting antivirals. However, highly viral gene mutation has underscored the necessity of novel antiviral drug development. Arbidol (ARB) is a Russian‐made indole‐derivative small molecule licensed in Russia and China for the prevention and treatment of influenza and other respiratory viral infections. ARB also has inhibitory effects on many other viruses such as severe acute respiratory syndrome coronavirus 2, Coxsackie virus, respiratory syncytial virus, Hantaan virus, herpes simplex virus, and hepatitis B and C viruses. ARB is a promising drug which can not only exert activity against virus at different steps of virus replication cycle, but also directly target on hosts before infection to prevent virus invasion.Conclusion: ARB is a broad‐spectrum antiviral drug that inhibits several viruses in vivo and in vitro, with high safety profile and low resistance; the antiviral mechanisms of ARB deserve to be further explored and more high‐quality clinical studies are required to establish the efficacy and safety of ARB.

Background: In addition to the COVID-19 waves, the globe is recently facing global monkeypox (MPX) outbreak. As the daily confirmed cases of MPX infection across epidemic and nonepidemic countries are increasing, taking measures to control global pandemic remains crucial. Therefore, this review aimed to provide fundamental knowledge for the prevention and control of future outbreaks of this emerging epidemic. Methods: The review was conducted using PubMed and Google Scholar databases; the search terms used were “monkeypox,” “MPX tropism,” “replication signaling of MPX,” “biology and pathogenicity of MPX,” “diagnosis of MPX,” “treatment of MPX,” “prevention of MPX,” etc. The update epidemic data were collected from the websites of the World Health Organization (WHO), United States Centers for Disease Control and Prevention (CDC), and Africa Center for Disease Control and Prevention (ADCC). High-quality research results published in authoritative journals were summarized and preferred cited. Excluding all duplicates, non-English published references, and irrelevant literature, totally 1,436 articles were assessed for eligibility. Results: It is still difficult to diagnose the patient as MPX simply based on clinical manifestations; therefore, under this situation, employing polymerase chain reaction (PCR) technology to provide confirmed evidence for the diagnosis of MPX seems to be the preferred and indispensable strategy. The treatment approach for MPX infection is mainly symptomatic and supportive; anti-smallpox virus drugs including tecovirimat, cidofovir, and brincidofovir can be employed in severe cases. Timely identification and isolation of confirmed cases, cutting off dissemination routes, and vaccination of close contacts are effective measures to control MPX. Also, smallpox vaccines (JYNNEOS, LC16m8, and ACAM2000) can be under consideration due to their immunological cross-protection among Orthopoxvirus. Nevertheless, given the low quality and scarcity of relevant evidence of current antiviral drugs and vaccines, deeply seeking for the MAPK/ERK, PAK-1, PI3K/Akt signaling, and other pathways involved in MPX invasion may provide potential targets for the treatment, prevention, and control of the epidemic. Conclusions: In response to the current MPX epidemic, the development of vaccines and antiviral drugs against MPX, as well as the rapid and precise diagnostic methods are still urgently needed. Sound monitoring and detection systems should be established to limit the rapid spread of MPX worldwide.

Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder characterized by abnormal protein deposition. With an alarming 30 million people affected worldwide, AD poses a significant public health concern. While inhibiting key enzymes such as β-site amyloid precursor protein-cleaving enzyme 1 and γ-secretase or enhancing amyloid-β clearance, has been considered the reasonable strategy for AD treatment, their efficacy has been compromised by ineffectiveness. Furthermore, our understanding of AD pathogenesis remains incomplete. Normal aging is associated with a decline in glucose uptake in the brain, a process exacerbated in patients with AD, leading to significant impairment of a critical post-translational modification: glycosylation. Glycosylation, a finely regulated mechanism of intracellular secondary protein processing, plays a pivotal role in regulating essential functions such as synaptogenesis, neurogenesis, axon guidance, as well as learning and memory within the central nervous system. Advanced glycomic analysis has unveiled that abnormal glycosylation of key AD-related proteins closely correlates with the onset and progression of the disease. In this context, we aimed to delve into the intricate role and underlying mechanisms of glycosylation in the etiopathology and pathogenesis of AD. By highlighting the potential of targeting glycosylation as a promising and alternative therapeutic avenue for managing AD, we strive to contribute to the advancement of treatment strategies for this debilitating condition.

Purpose. Catechol‐O‐methyltransferase (COMT) participates in the regulation of dopaminergic and adrenergic neurotransmission. COMT Val158Met polymorphism influences the efficacy and safety of opioids, but its association with oxycodone treatment in patients with cancer pain is yet to be elucidated. Hence, this study aimed to investigate the influence of COMT Val158Met polymorphism on oxycodone requirements, drug adverse effects, and pain sensitivity in patients with cancer. Methods. Patients with moderate to severe cancer pain treated with oxycodone were enrolled, of which 101 patients completed the study. All patients were genotyped for COMT Val158Met polymorphism using DNA from blood samples and were categorized into the wild‐type group (n = 50) comprising individuals with the Val/Val genotype and the mutant group (n = 51) encompassing those with the Val/Met or Met/Met genotype. Numerical rating scale (NRS) scores, oxycodone requirements, and the incidence of oxycodone‐related adverse drug reactions were compared between the two groups. Results. Patients in the mutant group exhibited higher NRS scores (6.18 ± 1.40) before the oxycodone treatment than those in the wild‐type (5.48 ± 1.54) group (P = 0.017). Patients in the wild‐type group required more oxycodone (96.00 ± 146.19 mg/24 h) than those in the mutant (77.25 ± 83.91 mg/24 h) group (P = 0.0365). The incidence rates of dysuria (2.0% vs. 16.0%, P = 0.016) and fatigue (0.0% vs. 12.0%, P = 0.013) were significantly lower in the mutant group than those in the wild‐type group. Moreover, patients with at least one Met allele showed a lower risk of suffering from oxycodone‐related side effects than those with the wild homozygote (41.2% vs. 68.0%, P = 0.007). Conclusion. Genetic variations in the COMT Val158Met gene may contribute to variability in the efficacy and safety of oxycodone in cancer pain treatment. The findings from this study emphasize the potential of pharmacogenetics in personalizing pain management. Furthermore, oxycodone therapeutic strategies can be designed based on genetic polymorphisms.

This study assessed the cost-effectiveness of three domestic bevacizumab biosimilars (IBI305, LY01008, and QL1101) and an originator (Avastin) as first-line treatments for nonsquamous NSCLC in China. A network meta-analysis (NMA) using the fractional polynomial (FP) method was used to determine hazard ratios (HRs) for overall survival (OS) and progression-free survival (PFS) without relying on the proportional hazards (PH) assumption. Adjusted OS and PFS curves were used to compare effects. A partitioned survival model was used to evaluate the cost-effectiveness of the biosimilars plus chemotherapy versus the originator plus chemotherapy. The model included cost, utility parameters, scale, and shape determined from previous studies. Probabilistic sensitivity analysis (PSA) and one-way deterministic sensitivity analysis (DSA) were used to assess uncertainty. In a baseline study, LY01008 + chemotherapy, QL1101 + chemotherapy, and bevacizumab + chemotherapy were less effective than IBI305 + chemotherapy. Treatment with LY01008 achieved an additional 0.23 quality-adjusted life-years (QALYs), with a higher cost of $817, leading to an incremental cost-effectiveness ratio (ICER) of $3,552/QALY when compared with that of QL1101. All three biosimilars showed better cost-effectiveness than the originator. The DSA results revealed that the HR-related parameters from the NMA and drug price were the primary sources of uncertainty surrounding incremental net monetary benefits (INMBs). PSA showed that the IBI305 was most likely to be cost-effective when the WTP was 1–3 times the per capita GDP of China in 2022. Sensitivity and scenario analysis confirmed the reliability of the fundamental analysis results. Domestic bevacizumab biosimilars are cost-effective alternatives to first-line treatment for nonsquamous NSCLC in China. IBI305 exhibited the most significant cost-effective advantage among the domestic biosimilars.