Thiazolidin-4-ones is an important heterocyclic ring system of a pharmacophore and a privileged scaffold in medicinal chemistry. This review is focused on the latest scientific reports regarding biological activities of thiazolidin-4-ones published in 2020 and 2021. The review covers recent information about antioxidant, anticancer, anti-inflammatory, analgesic, anticonvulsant, antidiabetic, antiparasitic, antimicrobial, antitubercular and antiviral properties of thiazolidin-4-ones. Additionally, the influence of different substituents in molecules on their biological activity was discussed in this paper. Thus, this study may help to optimize the structure of thiazolidin-4-one derivatives as more efficient drug agents. Presented information may be used as a practical hint for rational design of new small molecules with biological activity, especially among thiazolidin-4-ones.

Spinal cord injury (SCI) is a pathological neurological condition that leads to significant motor dysfunction. It is a condition that occurs as a result of tragic accidents, violent acts, or as a consequence of chronic diseases or degenerative changes. The current treatments for patients with SCI have moderate efficacy. They improve the quality of life of patients, but they are still doomed to long-term disability. In response to the modern directions of research on possible therapeutic methods that allow for the recovery of patients with SCI, a scientific review publication is needed to summarize the recent developments in this topic. The following review is focused on the available pharmacological treatments for SCIs and the problems that patients face depending on the location of the injury. In the following review, the research team describes problems related to spasticity and neuropathic pain; possible therapeutic pathways are also described for neuroprotection and the improvement of neurotransmission within the injured spinal cord, and the review focuses on issues related to oxidative stress.

Preterm labor is a leading cause of neonatal morbidity and mortality, with inflammation playing a central role in its pathogenesis. This structured literature review summarizes the role of the nuclear factor kappa B (NF-κB) signaling pathway in term and preterm labor and critically evaluates current evidence on natural and synthetic NF-κB modulators as potential therapeutic approaches. The narrative overview covers publications through June 2026. Experimental, translational, and review studies were synthesized narratively. NF-κB integrates hormonal, mechanical, infectious, and sterile inflammatory signals in gestational tissues, promoting the expression of pro-inflammatory cytokines, cyclooxygenase-2, prostaglandins, chemokines, and contraction-associated proteins that drive uterine activation. While tightly regulated NF-κB activation is essential for physiological term labor, it’s premature or excessive activation contributes to inflammation-associated preterm labor. Natural compounds and synthetic agents consistently attenuate excessive NF-κB signaling and downstream inflammatory responses in preclinical models, supporting their potential as candidate therapeutic strategies. However, clinical evidence remains limited. Future research should prioritize tissue-specific, context-dependent modulation of NF-κB and establish the safety, optimal therapeutic windows, and clinical efficacy of NF-κB-targeted interventions during pregnancy.

Preterm labor is a leading cause of neonatal morbidity and mortality, with inflammation playing a central role in its pathogenesis. This structured literature review summarizes the role of the nuclear factor kappa B (NF-κB) signaling pathway in term and preterm labor and critically evaluates current evidence on natural and synthetic NF-κB modulators as potential therapeutic approaches. To ensure comprehensive identification of relevant studies, a structured literature search informed by PRISMA 2020 reporting recommendations was performed, including studies published through August 2025. Experimental, translational, and review studies were synthesized narratively. NF-κB integrates hormonal, mechanical, infectious, and sterile inflammatory signals in gestational tissues, promoting the expression of pro-inflammatory cytokines, cyclooxygenase-2, prostaglandins, chemokines, and contraction-associated proteins that drive uterine activation. While tightly regulated NF-κB activation is essential for physiological term labor, its premature or excessive activation contributes to inflammation-associated preterm labor. Natural compounds and synthetic agents consistently attenuate excessive NF-κB signaling and downstream inflammatory responses in preclinical models, supporting their potential as candidate therapeutic strategies. However, clinical evidence remains limited. Future research should prioritize tissue-specific, context-dependent modulation of NF-κB and establish the safety, optimal therapeutic windows, and clinical efficacy of NF-κB-targeted interventions during pregnancy.