Cordycepin, a nucleoside from Cordyceps mushrooms, has many beneficial properties for health, including anticancer activities. In cancer cells, cordycepin targets various signaling molecules. Here, we review the possible anticancer mechanisms of cordycepin involving the targeting of kinases. Abnormal kinase expression is involved in cancer development and progression through different molecular mechanisms, including phosphorylation, amplification, genetic mutations, and epigenetic regulation. Research suggests that kinases, such as the c-Jun N-terminal kinase (JNK), mitogen-activated protein kinase (MAPK), AMP kinase (AMPK), phosphoinositide 3-kinase (PI3K)/Akt, extracellular signal-regulated kinase (ERK), mammalian target of rapamycin (mTOR), glycogen synthase kinase (GSK)-3β, and focal adhesion kinase (FAK) pathways, can be targeted by cordycepin and disrupting their activity. Given that kinase inhibitors can have crucial roles in cancer treatment, targeting kinases might be one of the molecular mechanisms involved in the anticancer potential of cordycepin.

Osteoarthritis (OA) is characterized by progressive cartilage degeneration. Pharmaceutical intervention remains a main treatment approach. However, drug delivery via intra-articular administration (IA) can be restricted by rapid clearance, the dense and highly negatively charged extracellular matrix (ECM) of cartilage, and uneven distribution of diseased chondrocytes. Nanodrug delivery systems, such as liposomes, micelles, and nanoparticles (NPs), have shown great potential to prolong intra-articular residence, penetrate the ECM, and achieve diseased chondrocyte-specific delivery. In this review, we discuss the challenges associated with intra-articular drug delivery in OA and the nanodrug delivery strategies developed to overcome these challenges. It is anticipated that these nanodrug delivery strategies will advance IA of drugs into broader applications in OA treatment.

While there have been trends in drug discovery from small molecules to new chemical modalities since the large mergers and acquisitions (M&A) of pharmaceutical companies in the late 2000s, trends in interorganizational deal networks have not been well addressed. We investigated the changing trends in interorganizational deals in the pharmaceutical and biotechnology industries. The results demonstrated that there have been changing trends, including a growing number of spinouts from academia and M&A in the United States and Europe. These findings indicates that the traditional network in which large pharmaceutical companies drove drug discovery output has changed, and interorganizational deals among diverse players have become more active.

Familial hypercholesterolemia (FH) is a common autosomal codominant hereditary illness marked by the heightened risk of early atherosclerotic cardiovascular disease and high blood levels of low-density lipoprotein cholesterol (LDL-C). FH patients can have homozygous or heterozygous variants. This condition has been linked to variations in the genes for the LDL receptor (LDLR), apolipoprotein B, proprotein convertase subtilisin/Kexin 9 (PCSK9), and LDLR adaptor protein 1. Drugs such as statins, ezetimibe, and PCSK9 inhibitors are currently widely available, allowing for the theoretical normalization of plasma LDL-C levels mostly in patients with heterozygous FH. However, homozygous FH patients usually have a poor response to traditional lipid-lowering therapy and may have a poor prognosis at a young age. LDL apheresis and novel pharmacological therapies such as microsomal transfer protein inhibitors or anti-angiopoietin-like protein 3 monoclonal antibodies are extremely expensive and unavailable in most regions of the world. Therefore, the unmet need persists for these patients. In this review, we discuss the numerous gene delivery, gene editing, and stem cell manipulation techniques used in this study to correct FH-causing LDLR gene variations in vitro, ex vivo, and in vivo. Finally, we looked at a variety of studies that corrected genetic defects that caused FH using the ground-breaking clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) gene editing technology.

Mitochondria are the powerhouses of cells and modulate the essential metabolic functions required for cellular survival. Various mitochondrial pathways, such as oxidative phosphorylation or production of reactive oxygen species (ROS) are dysregulated during cancer growth and development, rendering them attractive targets against cancer. Thus, the delivery of antitumor agents to mitochondria has emerged as a potential approach for treating cancer. Recent advances in nanotechnology have provided innovative solutions for overcoming the physical barriers posed by the structure of mitochondrial organelles, and have enabled the development of efficient mitochondrial nanoplatforms. In this review, we examine the importance of mitochondria during neoplastic development, explore the most recent smart designs of nano-based systems aimed at targeting mitochondria, and highlight key mitochondrial pathways in cancer cells.

The (re)emergence of multidrug-resistant viruses and the emergence of new viruses highlight the urgent and ongoing need for new antiviral agents. The use of peptidomimetics as therapeutic drugs has often been associated with advantages, such as enhanced binding affinity, improved metabolic stability, and good bioavailability profiles. The development of novel antivirals is currently driven by strategies of converting peptides into peptidomimetic derivatives. In this review, we outline different structural modification design strategies for developing novel peptidomimetics as antivirals, involving N- or C-cap terminal structure modifications, pseudopeptides, amino acid modifications, inverse-peptides, cyclization, and molecular hybridization. We also present successful recent examples of peptidomimetic designs.

Monoclonal antibodies (mAbs) have revolutionized the selective targeting of disease, as well as changing the character of the pharmaceutical industry. Although most attention has focused on conventional antibodies, immunoconjugates and bispecific antibodies (bsAbs) are beginning to show greater potential. Herein, we identify trends in the development and approval of antibody derivatives, as well as the organizations developing these products. Whereas industry development of immunoconjugates has grown steadily over four decades, momentum behind bispecific agents has seemingly expanded only recently. Together, our findings suggest that antibody derivatives provide interesting, albeit still speculative, opportunities for targeted interventions.