Artificial intelligence (AI) is increasingly shaping the pharmaceutical industry. This ACCP commentary examines the implications of AI for industry-based clinical pharmacists across the pharmaceutical life cycle, including drug development, regulatory affairs, medical affairs, health economics and outcomes research, and pharmacovigilance. Artificial intelligence-enabled tools may support target identification, clinical trial design, regulatory intelligence, evidence synthesis, medical content generation, real-world evidence analysis, economic modeling, adverse event processing, and safety signal detection. As these tools mature, the role of the clinical pharmacist is likely to shift from primarily task execution toward clinical interpretation, quality assurance, strategic decision-making, and governance of AI-supported outputs. However, AI implementation also introduces important risks and practical implementation challenges. These limitations reinforce the need for clinical pharmacists to remain actively engaged as human-in-the-loop experts who can assess whether AI-generated insights are scientifically valid, clinically relevant, ethically sound, and appropriate for decision-making. Ultimately, AI may expand the reach and efficiency of pharmaceutical industry functions, but successful integration will depend on pharmacist leadership in evaluation, oversight, and responsible implementation.

While clinicians commonly prescribe neuromodulators for the treatment of refractory or unexplained chronic cough, no trials have directly compared these treatments. Furthermore, although guidelines recommend non-pharmacological management involving physiotherapy and speech-language therapy, few trials have evaluated its effectiveness.

Parkinson's disease (PD) affects 11.77 million people worldwide, projected to reach 17.27 million by 2035. Current dopamine replacement therapies provide symptomatic relief but lack disease-modifying effects. Drug repurposing offers advantages: reduced development time (3-12 vs 10-17 years) and costs ($40-80 million vs $1-3 billion). To examine the pathophysiological connections between cancer and PD and evaluate the therapeutic potential of repurposing anticancer drugs through shared molecular mechanisms. Analysis of shared pathways, including mitochondrial dysfunction, ubiquitin-proteasome dysregulation, protein aggregation, neurotrophic factors, apoptotic genes, Dual Tyrosine Kinase Inhibition, microRNAs, and inflammation. Examination of repurposed anticancer agents in preclinical and clinical PD studies. Mitochondria-targeted metformin analogues showed 1000-fold increased potency in MitoPark models, although Mito-Q failed in human trials. Ixazomib enhances α-synuclein clearance via autophagy in preclinical models. Nilotinib showed poor CNS penetration (< 0.3% in CSF), resulting in worsening motor outcomes. Relatlimab, trehalose, and lapatinib demonstrated preclinical benefits through inhibition of α-synuclein spread, mTOR-independent autophagy, and multi-pathway neuroprotection, respectively. The AZA-PD Phase 2 trial (azathioprine) demonstrated a favourable safety and tolerability profile and offered valuable insights into peripheral immune modulation in early PD, though it did not meet its primary endpoint of slowing disease progression. Key barriers include poor CNS penetration, narrow therapeutic windows (70% neuronal loss at diagnosis), differential safety requirements, and timing-dependent efficacy necessitating early intervention. Mechanistic convergence provides a rationale for repurposing drugs; however, clinical success requires addressing the unique challenges of neurodegeneration. Future approaches should focus on precision medicine, innovative delivery systems, and multi-target interventions rather than direct therapeutic translation.

Guideline Title: 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Release Date: February 19, 2026. Prior Version(s): None; de novo guideline. Developer: American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines, in collaboration with multiple partner societies including the Society of Hospital Medicine. Target Population: Adults aged 18 years or older with acute pulmonary embolism.

Targeting the intrinsically disordered oncoprotein c-Myc remains challenging due to its lack of druggable pockets, hindering small-molecule inhibitor development for decades. Antibody-based strategies utilizing TRIM21-mediated targeted protein degradation (TPD), such as TRIM-Away, offer a promising alternative for endogenous c-Myc degradation but are limited by ineffective intracellular antibody delivery and uneven endogenous TRIM21 levels in various cancer cells. To overcome these, herein we disclose an acid-responsive nanoplatform using amorphous carbonated calcium phosphate nanoparticles (ACCP NPs) for effective intracellular co-delivery of TRIM21 and antibodies. Under mild biomimetic conditions, TRIM21-antibody complexes were effectively mineralized and encapsulated in the formed nanoparticles. Following endocytic uptake, these acid-sensitive ACCP NPs disassembled in endo/lysosomes, facilitating subsequent endo/lysosomal escape and cytosolic cargo release, leading to eventual intracellular TPD. In vitro, mineralized TRIM21-antibody complexes from ACCP NPs effectively degraded various intracellular targets, particularly c-Myc, across diverse cell types, including those that are TRIM21-deficient. Specifically, m-T21-c-Myc Ab nanoparticle degraded c-Myc via the ubiquitin-proteasome system and concurrently reduced MAX levels, synergistically inhibiting c-Myc transcriptional activity. In vivo, m-T21-c-Myc Ab significantly suppressed tumor growth without major organ toxicity. This work establishes ACCP NP-based TPD as a versatile and efficient platform for TRIM21/antibody-mediated degradation and a promising strategy for targeting other "undruggable" proteins.

Atrial fibrillation (AF) is increasing in incidence, prevalence, and lifetime risk, and contributes to substantially greater health care costs and increased risks of stroke, heart failure, and mortality. Improving adherence to evidence-based recommendations equitably in AF is critical to advancing clinical care, patient outcomes, and public health. The writing committee developed a comprehensive set of 5 performance measures, which are appropriate for public reporting or pay-for-performance programs, and 16 quality measures, which are useful to clinicians and health care organizations for quality improvement. The writing committee selected the measures from the strongest recommendations (Class 1 or 3) in the "2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation." The purpose of the writing committee's performance measures is meant to ensure that patients with newly diagnosed AF receive a basic clinical evaluation, with an emphasis on secondary prevention for patients at all stages of AF, documenting stroke risk, and, if indicated, providing appropriate anticoagulation. AF quality measures cover a variety of topics including measuring and addressing health inequities, optimizing antiarrhythmic or anticoagulant treatment, engaging in shared decision-making for rate- versus rhythm-control strategies, and, in appropriate patients, offering catheter ablation for those with heart failure with reduced ejection fraction. The performance and quality measures are intended to advance the quality and equity of AF care across all patient populations with AF.