Iberdomide (ZENBEXUS™) is a cereblon E3 ligase modulator being developed by Bristol Myers Squibb and its subsidiary Celgene Corporation for the treatment of various haematological malignancies, including multiple myeloma. On 13 August 2026, iberdomide received accelerated approval in the USA for use in combination with daratumumab and hyaluronidase-fihj and dexamethasone for the treatment of adult patients with multiple myeloma who have received at least one prior line of therapy including a proteasome inhibitor and an immunomodulatory agent. On 30 September 2026, iberdomide received conditional approval in China for use in combination with daratumumab and dexamethasone to treat adult patients with multiple myeloma who have received at least one first-line therapy (including a proteasome inhibitor and an immunomodulatory agent). This article summarizes the milestones in the development of iberdomide leading to this first approval for multiple myeloma.
Enlicitide (LIPFENDRA®) is a proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitor being developed by Merck Sharp Dohme for the treatment of dyslipidaemias. On 16 July 2026, enlicitide received its first approval in the USA where it is indicated as an adjunct to diet and exercise to reduce low-density lipoprotein cholesterol (LDL-C) in adults with hypercholesterolaemia, including heterozygous familial hypercholesterolaemia (HeFH). This article summarizes the milestones in the development of enlicitide leading to this first approval for hypercholesterolaemia.
Sodium-glucose cotransporter-2 inhibitors (SGLT-2is) have evolved from glucose-lowering agents to foundational therapies for the management of type 2 diabetes mellitus, heart failure, and chronic kidney disease, with substantial benefits for cardiovascular, kidney, and survival outcomes. As their indications continue to expand, a comprehensive understanding of their safety and tolerability has become increasingly important for optimizing patient care. Building on our recent state-of-the-art review of glucagon-like peptide-1 receptor agonists, this review provides a contemporary synthesis of the evidence on the safety and tolerability of SGLT-2is. We critically appraise data from randomized controlled trials, cardiovascular and kidney outcome trials, pharmacovigilance databases, large observational studies, and systematic reviews and meta-analyses. The available evidence demonstrates that SGLT-2is have a favorable overall safety profile, with genital mycotic infections representing the most consistently observed adverse event. Volume depletion and euglycemic diabetic ketoacidosis remain clinically important but are uncommon and are largely preventable through appropriate patient selection, patient education, and temporary treatment interruption during high-risk clinical situations. Fournier’s gangrene should be regarded as a very rare but serious complication requiring prompt recognition and treatment. In contrast, randomized trials and meta-analyses generally indicate a reduced risk of acute kidney injury, while evidence concerning fracture, lower-limb amputation, hepatotoxicity, pancreatitis, and cancer is less definitive. Although consistent class-wide increases in these latter outcomes have not been established, uncommon or agent-specific risks cannot be excluded, particularly where event numbers are small or follow-up is limited. Overall, treatment discontinuation because of adverse events is low across major cardiovascular, heart failure, and kidney outcome trials, supporting the excellent tolerability of this therapeutic class. Comparative evidence suggests only modest differences among individual SGLT-2is, although definitive conclusions remain limited by the absence of direct, large, randomized head-to-head trials. We also summarize practical strategies for adverse-event mitigation, monitoring, temporary treatment interruption, and individualized patient selection. As the clinical applications of SGLT-2is continue to broaden, ongoing pharmacovigilance, inclusive clinical trials, and comparative safety studies will be essential to further refine their benefit–risk profile and optimize their safe use across diverse patient populations.
Neuropsychiatric involvement in systemic lupus erythematosus remains a significant clinical challenge, encompassing a broad spectrum of manifestations affecting both the central and peripheral nervous systems. Accurate diagnosis and attribution require a structured approach, ideally supported by a multidisciplinary team evaluation and the application of validated attribution models. Recent evidence has reinforced the utility of existing algorithms in improving the attribution of neuropsychiatric events to systemic lupus erythematosus, with advances in laboratory testing and neuroimaging enhancing the ability to establish a causal link between the disease and its clinical manifestations. In parallel, emerging insights into disease pathogenesis are helping to clarify the role of targeted therapeutic strategies, closely tied to attribution processes. High-dose glucocorticoids plus cyclophosphamide remain the cornerstone for severe, inflammatory, neuropsychiatric systemic lupus erythematosus, while rituximab has shown the most consistent signal in refractory disease, albeit mainly in uncontrolled studies. Therapeutic development is progressively expanding along the B-cell lineage, from enhanced CD20 targeting (e.g., obinutuzumab) to profound B-cell depletion via chimeric antigen-T-cell-based strategies, and further toward upstream and parallel pathway modulation, including dual BAFF/APRIL blockade with telitacicept and type I interferon receptor inhibition with anifrolumab, both currently supported by case-based evidence. This narrative review summarizes recent developments in the diagnosis, attribution, pathogenesis, and treatment of neuropsychiatric systemic lupus erythematosus, with the aim of providing clinicians with an updated framework to better recognize and manage this complex and often underappreciated manifestation, ultimately improving patient outcomes.
Prostate cancer remains a leading cause of cancer-related mortality in men worldwide. While hormone therapy is effective in the early stages of advanced disease, multimodal approaches are often required as disease progresses, including radiotherapy, hormonal agents and chemotherapy. In metastatic castration-resistant prostate cancer (mCRPC), tumour cells become resistant to hormone therapy, resulting in poor survival outcomes despite systemic treatments. Among emerging therapies, radioligand therapy targeting prostate-specific membrane antigen (PSMA) has shown promise. PSMA is a transmembrane glycoprotein highly expressed in prostate cancer cells, with minimal expression in normal tissues. This selective distribution enables precision targeting and minimises toxicity. The radiotheranostic agent [177Lu]Lu-PSMA-617 combines PSMA-617, a small molecule ligand, with the beta-emitting radioisotope 177Lutetium. This therapy has demonstrated efficacy in patients with mCRPC who have progressed after androgen receptor pathway inhibitors and taxane-based chemotherapy. Its regulatory approval in the USA, UK and Europe marks a pivotal advancement in prostate cancer management. Clinical trials such as TheraP, VISION and PSMAfore have established the role of [177Lu]Lu-PSMA-617 in mCRPC and its potential additive effects with other anti-tumour therapies are under investigation. Strategies to enhance PSMA expression may further improve therapeutic response. With no relevant drug–drug interaction risk, [177Lu]Lu-PSMA-617 may be safely considered for use in combination with other therapies, a key advantage for frail patients with mCRPC on polypharmacy. Post-treatment management remains a challenge and ongoing research aims to optimise long-term outcomes. This review provides a comprehensive update on [177Lu]Lu-PSMA-617 therapy, from molecular mechanisms to clinical application and outlines future directions in the treatment of advanced prostate cancer.
