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Policosanol is a valuable compound with potential applications across multiple sectors. Within the pharmaceutical field, policosanol and its main components—triacontanol, octacosanol, and hexacosanol—have shown biological activity, particularly in conditions associated with inflammation and hypercholesterolaemia. Triacontanol, specifically, serves as a plant growth promoter and is widely applied in numerous economically significant crops and microalgae, either as a pure compound or as part of policosanol extracts. This review compiles key studies addressing the bioactivity of policosanol in both plant and animal cells, enabling comparison of the different mechanisms of action. A detailed evaluation of this information opens avenues for further research. Articles were sourced from PubMed and Redalyc using specific key terms: policosanol, inflammatory mechanisms, triacontanol, cellular absorption, photosynthesis, and photoinhibition. Policosanol has been found to interfere with inflammation-related pathways, notably the NF-κB and MAPK signaling cascades. Its cholesterol-lowering capacity results from the suppression of hepatic cholesterol synthesis through the indirect inhibition of HMG-CoA reductase. Triacontanol enhances plant growth and influences biochemical and physiological traits, especially under stress, mainly by improving photosynthetic efficiency. Notably, octacosanol can suppress the activity of triacontanol in plants—a phenomenon not observed in human cells—highlighting key distinctions in how these compounds function in plant versus animal systems, which warrants further investigation.

Gout disease is recognized as one of the most prevalent forms of arthritis worldwide, with an estimated prevalence of around 2.5%. Its pathophysiology is primarily linked to elevated levels of uric acid in the bloodstream, which may result from either increased production or reduced renal excretion. Clinically, it often presents as a swollen, erythematous, and painful joint. The definitive method for diagnosis remains synovial aspiration from the affected joint. While acute attacks typically require management in the emergency department, long-term care is generally provided in primary care settings.This literature review aims to explore gout disease in terms of its clinical features, diagnostic approaches, and treatment strategies, particularly focusing on the role of primary care. A comprehensive search was conducted on the PubMed database using the MeSH term “gout disease” to identify pertinent studies. Gout disease continues to be among the most widespread rheumatologic conditions globally, and unhealthy lifestyle choices, including alcohol intake and high consumption of red and white meats, may exacerbate its incidence. Diagnosis may involve blood tests, radiographic imaging, and joint aspiration. Maintenance therapy, often administered in primary care, includes the use of Allopurinol or other urate-lowering agents.

Digoxin, a cardiac glycoside, is commonly prescribed for the management of congestive heart failure, atrial fibrillation or flutter, and certain cardiac arrhythmias. However, its clinical use is limited by its narrow therapeutic index, which predisposes patients to toxicity. At elevated concentrations, digoxin toxicity can present with gastrointestinal disturbances, visual changes, and cardiac arrhythmias. This systematic review aims to summarize reported cases of digoxin toxicity, focusing on associated risk factors, drug-drug interactions, and clinical manifestations. A comprehensive literature search was conducted using PubMed and Ovid MEDLINE with the keywords “digoxin” and “toxicity.” Clinical and laboratory features of toxicity were extracted and analyzed. Of the 2,399 articles identified, only 10 met the inclusion criteria for final review. In 4 of the 10 cases, diuretics were implicated as interacting medications. Commonly reported symptoms included nausea, vomiting, visual disturbances, bradycardia, and elevated serum digoxin levels. Identified risk factors for toxicity included female sex, advanced age (60–91 years), renal impairment, and concomitant drug use. Notably, toxicity was observed even at therapeutic or low serum digoxin concentrations in the presence of these risk factors. The most frequent clinical manifestations were gastrointestinal symptoms, vision changes, and bradycardia.

Nerve agents are among the most potent and widely recognized chemical weapons. Recently, a new class of nerve agents, known as Novichok, has emerged as both a hazardous and frequently utilized tool in terrorist attacks. Medical professionals must gain a comprehensive understanding of the fundamental chemical and pharmacological properties of Novichok agents. This article provides a detailed review of the history, development, chemical structure, mechanism of action, toxicokinetics, and toxicology of these agents. Additionally, it discusses the latest diagnostic and treatment approaches for poisoning caused by Novichok agents. Contrary to earlier beliefs, Novichok poisoning shares similarities with other organophosphate toxins and can be effectively managed with timely and appropriate treatment. Given the global threat posed by terrorist incidents involving these agents, medical teams need to be well-versed in their characteristics to ensure optimal diagnosis and care for affected individuals.

This study assesses the risk of severe hyperlactatemia (defined as lactate levels > 4 mmol/L) in patients undergoing chronic low-dose aspirin (ASP) therapy and estimates the strength of this association. A case-crossover design was employed, in which individuals who experienced the outcome also served as their own controls, with exposure evaluated during a pre-event period. Additionally, a person-day–based analytical approach was used to compare exposure between case and control periods. Among the case group (ASP exposed/unexposed), the distribution was 127/578, while in the control group it was 547/3,968, yielding an odds ratio (OR) of 1.6 (95% CI: 1.29–1.97; z = 4.31; P < 0.0001). The findings suggest a modest association between low-dose aspirin use (100 mg/day) and elevated lactate levels, particularly in its primary indication for secondary prevention of vascular ischemic events. Although the observed risk is relatively low (OR = 1.6), clinical monitoring is advisable, especially when aspirin is co-administered with agents sharing similar toxicological profiles. Incorporating lactate level assessment into therapeutic management plans may enhance patient safety and therapeutic outcomes.

Producing enantiomerically pure drugs from racemic mixtures has become a critical objective in modern pharmaceutical science. Racemic compounds typically consist of two or more enantiomers, of which only one may be therapeutically active, while the others may be biologically inactive or even toxic, including teratogenic effects. Hence, the ability to effectively isolate the desired enantiomer is essential for ensuring both the safety and effectiveness of pharmaceutical treatments. This mini-review provides an overview of recent innovations in chiral stationary phases (CSPs) employed for the resolution of racemic drugs and mixtures. It covers various classes of CSPs, including those based on Pirkle-type selectors, polysaccharides, polypeptides, inclusion complexes, ligand-exchange mechanisms, macrocyclic antibiotics, and other novel materials. The performance of these phases in a range of separation techniques—such as high-performance liquid chromatography (HPLC), gas chromatography (GC), capillary electrophoresis (CE), supercritical fluid chromatography (SFC), and simulated moving bed (SMB) chromatography—is examined. Emphasis is also placed on the types of molecular interactions between CSPs and target analytes that drive effective enantioseparation.

Azithromycin (AZM), primarily recognized for its antibiotic properties, has gained attention for its ability to modulate the immune system and reduce inflammation. This review explores the impact of AZM on various immune cell types, including T cells, B cells, and natural killer (NK) cells, and its potential in treating chronic inflammatory and autoimmune conditions. AZM inhibits the mTOR signaling pathway in T cells, thereby limiting both T cell proliferation and cytokine production. It also affects B-cell function by modulating pathways such as NF-κB and CD27, thereby influencing antibody synthesis. In NK cells, AZM reduces cytotoxicity and cytokine release while preserving cell viability. The drug’s effects on immune responses, particularly on vaccination responses and reduced antibody levels, have important clinical implications. While AZM shows potential for managing conditions such as graft-versus-host disease and asthma, its varied effects highlight the need for further investigation. Further understanding of these mechanisms is crucial for optimizing AZM’s therapeutic use and minimizing unwanted immune suppression.

This review aims to explore and consolidate the therapeutic potential of colchicine, one of the oldest yet still widely used treatments. Colchicine is an alkaloid compound known for its anti-inflammatory and analgesic effects. It has been effectively used to treat conditions such as gout, familial Mediterranean fever (FMF), and Behcet’s disease. The drug’s mechanism of action involves its interaction with tubulin, a structural component of the cytoskeleton, which disrupts neutrophil functions, including adhesion, migration, and chemotaxis. Colchicine specifically inhibits tyrosine phosphorylation, a key process for neutrophil activation, and affects neutrophil deformability, preventing their extravasation. Additionally, it suppresses the production of superoxide and pro-inflammatory cytokines, such as interleukin 1β and IL-6. The drug also inhibits inflammasome activity, hindering caspase-1 activation and interleukin release. Colchicine has attracted attention during the COVID-19 pandemic due to its potential to treat severe cases and reduce mortality. It is a cost-effective and widely accessible drug with a relatively safe profile. However, its metabolism can be influenced by CYP3A4 and P-glycoprotein inhibitors, as well as by renal and hepatic impairments. Common side effects include gastrointestinal disturbances such as diarrhea, nausea, and vomiting.

Snakebite envenoming remains a significant global health challenge, with high mortality and morbidity rates persisting despite decades of medical attention. Each year, millions are affected by venomous snakebites, often resulting in death or severe disability. Snake venoms exhibit diverse bioactivities, including hemorrhagic, inflammatory, cytotoxic, cardiotoxic, and neurotoxic effects, mainly due to complex mixtures of toxin-rich proteins. Although considerable research has been undertaken, the majority of venom components remain uncharacterized. Recent advancements in proteomics and bioinformatics have enabled more detailed exploration of venom profiles, facilitating the identification and functional prediction of novel toxins. Computational approaches now enable modeling of toxin-target interactions, aiding understanding of venom mechanisms. This review also explores the emerging role of medicinal plants in snakebite treatment, alongside conventional antivenoms. Emphasis is placed on the urgent need to improve access to safe, affordable, and effective antivenoms in low-income tropical regions and to promote their appropriate clinical use.

Over time, the field of psychology has made significant strides in the treatment of psychiatric conditions, including major depressive disorder (MDD), schizophrenia, and Alzheimer’s disease (AD). Depression, also known as clinical depression, is a prevalent mental health condition defined by persistent feelings of sadness, hopelessness, and emptiness, all of which significantly impact the quality of life. According to the World Health Organization (WHO), approximately 3.8% of the global population experiences depression, with 15% of those affected dying by suicide. This review focuses on the emerging role of psychobiotics in treating clinical depression. Recent studies indicate that psychobiotics, which combine probiotics and prebiotics, offer potential therapeutic benefits. These compounds not only introduce beneficial bacteria to the gut but also support the growth of existing gut microbiota. Research on the gut-brain axis has revealed its key role in the effectiveness of psychobiotics, offering promising results for improving mental health. Beyond treating psychological disorders, psychobiotics also contribute to overall health by enhancing gut function.

The growing use of muscle-enhancing steroids, particularly anabolic-androgenic steroids (AAS), has raised significant concerns about their potential adverse effects on cardiovascular health, with heart attacks being a key risk. This study offers an in-depth exploration of the relationship between muscle-enhancing drugs and heart attacks. It examines the physiological processes by which steroids may lead to cardiovascular complications, such as hypertension, dyslipidemia, atherosclerosis, and thrombosis. The research also evaluates the epidemiological data that links steroid use to a higher likelihood of heart attacks and other cardiovascular incidents. In addition, the study addresses the ethical issues surrounding steroid use in sports and fitness, as well as the regulatory measures in place to combat abuse. The importance of interdisciplinary collaboration and evidence-driven strategies to tackle this public health challenge is emphasized. Ultimately, the study advocates increased awareness, more extensive research, and stronger preventive efforts to reduce the cardiovascular risks associated with muscle-enhancing steroids, while encouraging safer alternatives for fitness enhancement.

Creatine is a naturally occurring compound found in muscle tissue that plays a vital role in cellular energy metabolism. While traditionally recognized for its benefits in enhancing skeletal muscle function and exercise performance, recent research has highlighted its potential therapeutic applications in various medical fields. This study reviews the available literature to assess the current state of knowledge regarding creatine’s medical uses and outlines directions for future research. Evidence has demonstrated a correlation between low creatine levels and reduced mental well-being, suggesting a role in the central nervous system. Notably, creatine has been explored as a potential antidepressant—both as a standalone treatment and as an adjunct to selective serotonin reuptake inhibitors (SSRIs)—owing to its newly discovered function as a neurotransmitter. Additionally, long-term investigations into creatine’s molecular mechanisms in the brain have prompted its study in stroke management, where it may support both prevention in high-risk populations and post-stroke rehabilitation. In the context of chronic heart failure, creatine has been linked to cardiomyocyte metabolic dysfunction, particularly regarding disruption of the creatine/phosphocreatine/ATP shuttle. Although studies examining creatine supplementation in cardiovascular disease have produced mixed results, the compound shows promise as a supportive therapy. However, further research is necessary to confirm its efficacy and safety across these medical applications.

Parkinson’s disease (PD) is a chronic and progressive neurodegenerative condition characterized by motor impairments such as tremors and stiffness, along with non-motor symptoms including cognitive decline and depression. While current dopaminergic therapies help manage symptoms, they do not halt the progression of the disease, underscoring the urgent need for treatments that can modify its course. This review explores the potential of repurposing drugs from diverse therapeutic categories—such as immunomodulators, cardiometabolic agents, and anti-infectives—to treat PD. Immunomodulatory compounds such as c-Abl inhibitors (e.g., imatinib and nilotinib) and sargramostim have shown potential to reduce α-synuclein buildup and brain inflammation, though clinical outcomes have been inconsistent. Among cardiometabolic drugs, glucagon-like peptide-1 (GLP-1) receptor agonists, such as exenatide, have shown promising results in improving motor and cognitive function, with phase III trials currently investigating their ability to slow disease progression. Some anti-infective agents, including doxycycline and rifampicin, offer neuroprotective benefits through anti-inflammatory and anti-aggregation mechanisms. Despite ongoing concerns regarding their effectiveness and potential side effects, these repurposed drugs represent promising avenues for PD treatment. Moreover, emerging strategies such as gene therapy, enzyme replacement therapy, and advanced drug-delivery technologies aim to target the underlying disease mechanisms directly. Although no definitive disease-modifying treatment exists yet, the investigation of repurposed and novel therapies provides optimism for future advancements. Further large-scale clinical studies are essential to confirm their safety and therapeutic value.

Herbal substances have long been used as drugs of abuse, with traditional addictive substances like opium and cannabis often being derived from natural, crude plant materials. Cannabinoids and cathinones, for example, are natural derivatives. However, the safety and efficacy of these substances remain significant concerns that require attention and increased awareness. This review highlights various plants, including khat, kratom, salvia, and mandrake, to inform both experts and the general public about the potential risks associated with regular use and synthetic derivatives. Some of these “herbal plants” should be recognized as harmful substances, as prolonged use has been linked to addiction and cognitive impairments. Despite ongoing research, there is still a lack of comprehensive studies addressing these issues. This paper explores the toxicological concerns and key safety risks associated with plant-based products. Ensuring the safety and reliability of herbal remedies is of paramount importance, given ongoing concerns about their use.

Microorganisms are the primary triggers of various inflammatory diseases in the human body. Diseases such as bronchitis, otitis media, pneumonia, conjunctivitis, cystitis, endometritis, and infections of the fallopian tubes and ovaries are routinely treated with antimicrobial agents in global medical protocols. Bacterial infections like chlamydia, streptodermia, scarlet fever, meningitis, and tuberculosis cannot be treated without the application of antimicrobial therapies. Likewise, viral conditions such as herpes, chickenpox, hepatitis C and B, and HIV are now addressed using antiviral treatments. Antibiotics are used to treat fungal infections of the skin, mucous membranes, and nails, as well as systemic mycoses. For protozoal diseases such as giardiasis, amoebic dysentery, trichomoniasis, malaria, and toxoplasmosis, antiprotozoal drugs are prescribed. These therapeutic agents target a wide range of pathogens, including bacteria, viruses, fungi, and protozoa. This article offers a succinct review of various antimicrobial drugs and provides an in-depth analysis of the Russian antimicrobial drug market. 

Artificial intelligence is increasingly being positioned as a transformative tool in pharmaceutical formulation and process development because it can model complex relationships among molecular properties, excipient behaviour, formulation variables, processing conditions, and product performance. Machine learning, deep learning, hybrid modelling, and optimisation algorithms are now used to support decisions that were previously dominated by empirical screening and expert judgement. Despite this promise, the practical translation of artificial intelligence into pharmaceutical development remains uneven. Many models demonstrate high retrospective accuracy but provide limited mechanistic insight, weak interpretability, and uncertain relevance when moved beyond the specific datasets, formulations, equipment, or scales on which they were trained. This critical review examines artificial intelligence in pharmaceutical formulation and process development through three linked lenses: explainability, transferability, and regulatory trust. It argues that these issues are not secondary implementation details but core determinants of whether artificial intelligence can become credible within quality-driven pharmaceutical development. The analysis shows that artificial intelligence can support formulation and process understanding only when predictive performance is accompanied by transparent reasoning, domain-aware validation, lifecycle governance, and evidence of transferability across development contexts. A coordinated pathway involving explainable-by-design models, standardised transferability testing, and regulatory learning environments is required to move pharmaceutical artificial intelligence from technical promise toward justified regulatory trust.

Pharmaceutical development is increasingly moving beyond the traditional emphasis on drug substance performance to include the full experience of medicine use. This shift reflects the recognition that therapeutic value is shaped not only by pharmacology, but also by whether patients can understand, accept, handle, administer, and continue using a product in everyday life. Despite major advances in dosage form engineering, digital health tools, adherence monitoring, and personalised pharmaceutical manufacturing, many innovations remain disconnected from the practical contexts in which medicines are used. A dosage form may be technically sophisticated but still fail if it is difficult to swallow, unattractive to children, burdensome for older adults, incompatible with daily routines, or unsupported by feedback systems that encourage continued use. This narrative review integrates three domains that are often discussed separately: dosage design, adherence logic, and real-world use systems. It argues that patient-centric pharmaceutical technologies should be understood as integrated use systems rather than isolated product features. The central question is how pharmaceutical technologies can be designed to support not only drug delivery, but also patient acceptance, behavioural continuity, and implementation in real healthcare settings. The review concludes that patient-centricity should be treated as a foundational development logic rather than a late-stage product attribute. Future pharmaceutical technologies will require early patient involvement, scalable manufacturing pathways, human factors validation, digital support systems, and regulatory strategies that define success according to real-world usability and patient-defined outcomes.

Smart pharmaceutical systems are emerging as integrated therapeutic platforms that combine physiological sensing, algorithmic interpretation, and automated drug release. They mark a shift from passive delivery technologies toward systems that can respond to changing biological states in near real time. Their promise lies in reducing therapeutic delay, personalising dose adjustment, and extending pharmacotherapy beyond fixed schedules and clinician-mediated titration. The central challenge is that therapeutic intelligence changes the risk profile of pharmaceutical products. A delivery system that senses inaccurately, computes incorrectly, or actuates unpredictably can convert a pharmacological benefit into an autonomous harm pathway. This makes safety assurance inseparable from system architecture, rather than a downstream verification step. The review identifies a recurring sense–control–deliver architecture, but argues that this architecture remains unevenly mature. Glucose-responsive and automated insulin systems provide the strongest clinical evidence, whereas multi-analyte drug monitoring, implantable autonomous platforms, and reinforcement-learning controllers remain closer to proof-of-concept or early translational validation. Four tables organise the system logic, sensor landscape, feedback-control approaches, and safety oversight framework. The review concludes that smart pharmaceutical systems should not be judged solely by pharmacokinetic precision or device performance. Their clinical legitimacy will depend on robust control under uncertainty, interpretable autonomy, resilient human oversight, and regulatory pathways that can evaluate integrated drug–device–software behaviour. Safe therapeutic autonomy will require co-development of engineering validation, clinical governance, and patient-centred design.

The clinical success of mRNA–lipid nanoparticle vaccines transformed lipid nanoparticle technology from a specialised drug delivery field into a central modality for modern biopharmaceutical development. That success demonstrated that nucleic acid therapeutics can be manufactured, distributed, and deployed at unprecedented speed when formulation science, process engineering, and regulatory urgency align. Yet the same success also exposed how dependent LNP products remain on tightly constrained composition, process history, and cold-chain stability. The central problem is that processes optimised rapidly under pandemic conditions do not automatically constitute robust manufacturing platforms. Many LNP processes remain product-specific, empirically tuned, and sensitive to changes in lipid composition, aqueous phase conditions, mixing geometry, and downstream handling. The language of “platform” is therefore often stronger than the underlying evidence for generalisable process robustness. The review maps the structural and functional logic of LNP platforms, evaluates how mRNA delivery requirements shaped formulation choices, and assesses preclinical and manufacturing evidence across laboratory, preclinical, and scalable production contexts. It identifies recurrent fragility points including mixing sensitivity, particle heterogeneity, aggregation, mRNA degradation, storage instability, and incomplete comparability evidence after process change. Five tables summarise platform design, mRNA delivery requirements, manufacturing evidence, fragility points, and a system design strategy for robust LNP production. The post-mRNA era requires a shift from emergency product development to platform-centred system design. LNP manufacturing must become modular, measurable, scalable, and quality-resilient rather than merely reproducible under narrowly defined conditions. Achieving this transition is essential if LNP technologies are to move beyond COVID-19 vaccines into broader therapeutic applications and more equitable global health deployment.

Advanced pharmaceutical technologies are reshaping the meaning of a dosage form. Products such as personalised 3D-printed tablets, long-acting injectable depots, implantable systems, nanoparticulate carriers, and digitally enabled drug-device combinations no longer fit neatly within the traditional categories of tablet, capsule, or simple injection. Their performance depends not only on chemical composition, but also on architecture, spatial distribution, release programming, device function, and sometimes digital feedback. The regulatory challenge is that evidence standards for pharmaceutical products were largely built around assumptions of batch uniformity, reproducible manufacturing, conventional dissolution, standardised stability testing, and population-level bioequivalence. These assumptions remain essential for many products, but they may be insufficient when the dosage form is personalised, structurally heterogeneous, programmable, implantable, or integrated with sensors. This creates uncertainty for both regulators and developers because the critical evidence needed to demonstrate quality, safety, and performance is not always clearly defined. This review critically examines how current regulatory expectations apply to non-traditional dosage systems and where they fail to capture technology-specific risks. It focuses on evidence standards across chemistry, manufacturing, and controls; non-clinical performance testing; clinical evaluation; and post-market evidence generation. The aim is not to propose lower evidentiary thresholds, but to argue for standards that are better aligned with the mechanisms by which advanced dosage systems achieve therapeutic performance. The review concludes that regulatory science must move from a one-size-fits-all model toward a flexible, risk-proportionate system for advanced pharmaceutical technologies. Such a system should preserve high standards for patient protection while allowing evidence requirements to vary according to product complexity, novelty, exposure duration, reversibility, and clinical uncertainty. International coordination, structured regulator-innovator dialogue, and post-market learning will be essential to prevent regulatory evidence standards from lagging behind pharmaceutical innovation.

The pharmaceutical industry is a significant contributor to environmental pollution, yet the sustainability of pharmaceutical technologies themselves has received less sustained attention than clinical efficacy, quality assurance, manufacturability, and cost. Pharmaceutical products are commonly evaluated through therapeutic performance and regulatory compliance, while the material, energy, solvent, water, packaging, and waste implications of their production and disposal remain secondary. This imbalance is no longer defensible as medicines become embedded within wider debates on planetary health, industrial decarbonisation, chemical pollution, and responsible innovation. Current pharmaceutical technology paradigms often depend on linear manufacturing models in which raw materials, solvents, excipients, packaging components, and delivery devices move through production and use before entering waste streams. This model is particularly problematic where complex formulations, multi-material packaging, single-use components, and persistent active substances create environmental burdens that are difficult to recover or neutralise. The problem is not only the presence of pharmaceuticals in the environment, but also the technological logic that normalises excess material throughput as an acceptable cost of product performance. This critical review examines sustainable pharmaceutical technologies through three connected lenses: green manufacturing, excipient burden, and circular design principles. Green manufacturing addresses how pharmaceutical products are synthesised, processed, purified, and scaled. Excipient burden focuses on the hidden environmental and functional load created by supposedly inactive formulation ingredients. Circular design principles extend the discussion beyond production efficiency toward products, packaging, and delivery systems designed for reduction, recovery, reuse, and responsible end-of-life management. The review identifies that continuous manufacturing, flow chemistry, process intensification, biocatalysis, solvent reduction, process mass intensity, and life-cycle assessment provide important but incomplete routes toward greener pharmaceutical production. It also shows that excipients, packaging, and drug delivery systems remain under-theorised in sustainability debates despite their cumulative contribution to material intensity, environmental persistence, and disposal complexity. Five tables present green manufacturing technologies, excipient burden data, circular design principles, environmental risks, and implementation barriers. The central conclusion is that sustainable pharmaceutical technology requires a systems-level transition rather than a collection of isolated green substitutions. Genuine sustainability will depend on integrating green manufacturing with excipient stewardship, circular product design, environmental risk reduction, regulatory adaptation, and cross-sector accountability. The field must therefore move from sustainability as a supplementary efficiency concern toward sustainability as a core design principle of pharmaceutical innovation.

Advanced drug delivery systems have long promised to transform therapy by improving biodistribution, reducing toxicity, enabling intracellular delivery, extending exposure, and opening therapeutic spaces that conventional dosage forms cannot reach. Yet the field remains marked by a persistent translation paradox: thousands of sophisticated carrier systems are reported in the literature, while only a small fraction progress into durable clinical products. This gap is usually explained through biological complexity, manufacturing difficulty, regulatory uncertainty, or inadequate preclinical models. This critical perspective proposes that these explanations, although important, are incomplete. A deeper systemic factor is technological lock-in, defined here as the self-reinforcing dominance of specific drug delivery platforms that shape what researchers, funders, manufacturers, regulators, and companies consider technically feasible and translationally credible. Once a platform accumulates expertise, protocols, supply chains, regulatory familiarity, and publication momentum, alternatives may struggle to compete even when they offer potentially superior solutions. The central argument is that technological lock-in contributes to translational failure by narrowing the drug delivery imagination. Instead of asking which delivery architecture is best suited to a given biological, clinical, manufacturing, and regulatory problem, the field often asks how an incumbent platform can be modified to fit yet another therapeutic challenge. This platform-first logic can lead to repeated optimisation of familiar systems while more disruptive or simpler design spaces remain underexplored. The article critically examines the assumptions that sustain dominant platforms in advanced drug delivery. These assumptions include beliefs that increasing carrier complexity necessarily improves therapeutic performance, that certain materials possess broad translational privilege, that murine and in vitro models can adequately predict human outcomes, and that incremental optimisation is less risky than platform diversification. The perspective argues that these assumptions are not merely technical claims but institutional habits that stabilise lock-in. The proposed conceptual model links critical assumptions, technological lock-in, platform dependency, innovation constraint, and translational failure in a self-reinforcing cycle. In this model, failure does not necessarily disrupt dominant platforms; paradoxically, it may intensify dependence on them because they remain the most familiar, fundable, publishable, manufacturable, and regulatable options. Five tables structure the analysis by summarising translational failure evidence, critical assumptions, failure mechanisms, lock-in case examples, and the proposed model. Breaking technological lock-in requires more than improving individual formulations. It requires deliberate diversification of platform portfolios, stronger interrogation of inherited assumptions, translational assessment that rewards fit-for-purpose simplicity, and innovation policies that lower the cost of exploring alternative delivery architectures. A more resilient advanced drug delivery ecosystem should treat platform diversity not as inefficiency, but as insurance against repeated translational failure.