Relevance. Post-infarction chronic heart failure contributes to the development of atrial fibrillation, the most common form of arrhythmia. The search for new drugs with pronounced antiarrhythmic activity is currently relevant.Purpose of the study. To study the sequence of atrial epicardial depolarization in rats with post-infarction chronic heart failure after long-term administration of fabomotizole.Methods. The sequence of atrial epicardial depolarization in rats with post-infarction chronic heart failure caused by anterior transmural myocardial infarction and sham-operated animals was studied using synchronous multichannel cardiac electrochronotopography after a course of fabomotizole administration.Results. Post-infarction chronic heart failure provokes the appearance of an additional excitatory focus in the pulmonary vein lacunae of the left atrium, which is a predictor of atrial arrhythmogenicity. Fabomotizole suppresses an additional arrhythmogenic focus of excitation in the area where the pulmonary veins enter the left atrium, minimizing the risk of developing atrial tachyarrhythmias, including atrial fibrillation.
Introduction. Acute alcohol intoxication (AAI) causes multifactorial damage to organs and tissues. While the clinical manifestations and complications associated with AAI are well known, the underlying mechanisms remain poorly understood.Objective. Studying of the AAI influence on activity of trypsin and indicators of a hemostasis.Materials and methods. AAI was induced by intraperitoneal administration of ethanol (5 g/kg). After 24 hours, trypsin activity was determined in serum, and fibrinogen content and coagulation status were determined in plasma.Results. In rats with AAI, trypsin activity was increased more than doubled in serum. Trpsin, according to current concepts, is a protease-activated receptor (PAR) agonist. The plasma fibrinogen level increased (p < 0.05), indicating activation of the blood coagulation system and a high risk of thrombotic and thromboembolic complications.Conclusion. Data about the sharp increase of the trypsin serum concentrations, an endogenous agonist of PARs receptors, in animals with AAI, raises the question of the contribution of PARs to the development of multiorgan pathology pathognomonic of AAI.
One of the relevant experimental models of autism spectrum disorder (ASD) is the model induced by the administration of propionic acid (PPA), which replicates key behavioral and neurobiological impairments of the disorder, making it promising for the search of new therapeutic agents. The aim of the study was to investigate the effect of fabomotizole on ASD symptoms induced by prenatal administration of propionic acid in Wistar rats during the pubertal period. The ASD model was induced by administering PPA (500 mg/kg subcutaneously) to female rats on days 12–16 of gestation. The resulting offspring (males) received fabomotizole orally at a dose of 10 mg/kg from postnatal day 6 to day 70. Animal behavior was assessed using tests designed to analyze motor and exploratory activity, anxiety, levels of stereotypy, social behavior, and cognitive functions. In male rats with the ASD model induced by prenatal PPA administration, a decrease in exploratory activity, an increase in anxiety, stereotypical manifestations, aggression, reduced social affinity, and impaired cognitive functions were revealed. Fabomotizole at a dose of 10 mg/kg corrected behavioral impairments in male rats with the ASD model, manifested as increased locomotor and exploratory activity, reduced stereotypy, aggressiveness, and anxiety, and improved social and cognitive functions. The obtained data substantiate the promise of developing fabomotizole as a therapeutic agent for ASD.
Relevance. BBP2023 is a new drug candidate of the sydnonimine group, possessing predominantly central vasodilating activity.Objective. To study the pharmacokinetics of the drug candidate BBP2023 in mice after intragastric administration, including an assessment of distribution to organs and tissues.Materials and methods. Experiments were performed on 102 outbred male mice. The animals received a single intragastric dose of BBP2023 at 22.0 mg/kg as an oil emulsion. The total duration of the experiment was 72 hours, during which the animals were euthanized by decapitation at specific time points. Plasma was obtained from blood; homogenates were prepared from internal organs (liver, kidneys, heart, lungs, brain, spleen, muscles, omentum). These were analyzed for the quantitative content of BBP2023 and its metabolites using a previously developed and validated HPLC-MS/MS method. The main pharmacokinetic parameters were calculated using a non-compartmental method.Results. After intragastric administration, BBP2023 was detected in all studied organs and tissues. The time to reach the maximum concentration (0.58 μg/ml) in plasma was 15 minutes, and the elimination half-life was about 7.9 hours. The highest distribution found was to the liver (fr = 2.83), lungs (fr = 1.58), and omentum (fr = 2.62). The minimum value of the elimination rate constant, excluding blood plasma, was observed in brain tissues. The active metabolite BBP2023 A was primarily localized in the kidneys (fr = 16.85) and liver (fr = 4.61). The time to reach the maximum concentration in all organs and tissues ranged from 15 to 45 minutes.Conclusion. The results of the study established that the sydnonimine group drug candidate BBP2023, as well as its active metabolite (BBP2023 A), are detected in mouse brain tissues, which contributes to the realization of cerebral vasodilating activity.
This review presents data on the prevalence and comorbidities of cardiovascular diseases (CVDs), which are risk factors for the development of acute cerebrovascular accident (ACVA) or myocardial infarction (MI) and the risk of adverse outcomes. CVDs have various markers of cerebral damage, it’s manifested by cognitive decline and down to the development of dementia. The primary pathogenetic mechanism for the development of stroke-associated cardiovascular disease is decreasing cerebral blood flow and microcirculatory network density, i.e. the development of cerebrovascular insufficiency. Most patients with cerebral lesions following stroke have concomitant cardiac pathology, which impacts the post-stroke period and patient survival. In turn, stroke causes cardiac complications and/or the development of newly diagnosed cardiovascular diseases due to impaired autonomic regulation of the cardiovascular system and hemodynamic mechanisms.
Relevance. The search for vasodilating agents that predominantly accumulate in brain tissues is an urgent task. One of the drug candidates with cerebral vasodilating activity is BBP2023 a derivative of sydnonymine.Objective. A comparative assessment of the pharmacokinetics of BBP2023 in rabbits after a single administration via different routes.Methods. Experiments were performed using a crossover design on 8 rabbits. The rabbits received a single dose of BBP2023 at 2.0 mg/kg as an oil emulsion intragastrically and rectally, and as an aqueous DMSO solution intravenously and intramuscularly. Blood samples were collected from the marginal ear vein at specific time points. The quantitative determination of BBP2023 and its metabolites in blood plasma was performed using HPLC-MS/MS.Results. It was found that the highest bioavailability values are achieved with intramuscular administration (97.4 %). With intragastric and rectal administration, this indicator averaged 46.1 and 15.3 %, respectively. The maximum concentration of BBP2023 in blood plasma is reached on average 5 minutes after intragastric administration and averages 0.620 μg/ml; the half-life value averages 1 hour. The maximum concentration of the active metabolite BBP2023 A in blood plasma after intragastric administration is detected on average after 25 minutes and is 0.076 μg/ml.Conclusion. The pharmacokinetics of the active pharmaceutical substance of drug candidate BBP2023 was studied in rabbits. The results obtained were used for the subsequent selection of the optimal finished dosage form and route of administration.
Magnesium deficiency is a widespread problem associated with an increased risk of cardiovascular, neurological, and metabolic disorders. The effectiveness of magnesium therapy is largely determined by the bioavailability of the salt used. It is well known that magnesium salts with organic anions are characterized by relatively high bioavailability. This paper presents a detailed analysis of the pharmacological properties of organic magnesium salts: magnesium malate, fumarate, citrate, aspartate, glycinate, threonate, pyroglutamate, orotate, and lactate. The article examines the structural features, elemental magnesium content, anion metabolism, and the effect of anions in the salt on the bioavailability and biodistribution of Mg²+. The feasibility of personalized selection of magnesium salts based on clinical needs is substantiated.
Autism spectrum disorder (ASD) is a neurodevelopmental condition accompanied by alterations in serotonergic, dopaminergic, and noradrenergic systems, as well as delays in early psychomotor and sensorimotor development. One possible approach to correcting these disturbances is the use of BDNF mimetics that regulate synaptic plasticity and neurogenesis. The aim of this study was to investigate the effect of the low-molecular-weight dipeptide BDNF mimetic hexamethylenediamide bis(N-monosuccinyl-L-seryl-L-lysine) (GSB-106) on reflex development and monoamine content in the brain structures of Wistar rats with experimental ASD. The ASD model was induced by administration of sodium valproate (600 mg/kg) on gestation day 12.5. Offspring received GSB-106 orally at a dose of 0.1 mg/kg from postnatal day 7 to 21. The rate of sensorimotor reflex development was evaluated using the “Surface righting” and “Negative geotaxis” tests. Monoamines and their metabolites were quantified by high-performance liquid chromatography with electrochemical detection. GSB-106 improved negative geotaxis performance in both male and female rats with ASD (by 1.8–2.3 times), normalized NA and DOPAC levels in the frontal cortex of females, and reduced DA and 5-HT levels in male brain structures. Thus, GSB-106 exerts a normalizing effect on impaired early behavioral development and monoaminergic systems in rats with an ASD model, suggesting its potential as a promising compound for further investigation.
Reliable primary screening studies using biomodels, which enable rapid and cost-effective identification of the effects of potential medicinal substances, are a crucial step in preclinical research. Therefore, the development of new alternative biological models, taking into account bioethical requirements, is a pressing issue in modern pharmacology. This article presents data on the creation of an alternative zebrafish model for identifying the adaptogenic effects of biologically active substances. Pharmacological validation of the resulting model is conducted. The feasibility of using the resulting model for primary screening of compounds with potential adaptogenic activity is demonstrated.
Relevance. Epilepsy is one of the most common neurological diseases, which is based on a disregulation of the balance between excitatory and inhibitory neurotransmission in the central nervous system. In this regard, the optimization of conditions for the currently used seizure models that reflect the pathophysiology of epilepsy, for the evaluation of the efficacy of potential drugs, remains a relevant task in experimental pharmacology.Objective. Optimization of the conditions of three experimental seizure models induced by intravenous administration of convulsants with different mechanisms of action for subsequent pharmacological evaluation of anticonvulsant and pro-convulsive activities.Materials and methods. Epilepsy was induced in ICR mice by intravenous administration of pentylenetetrazol, bicuculline, or picrotoxin into the lateral tail vein at a constant rate. The seizure threshold was determined as the minimum dose of convulsants. Clonic seizures, generalized clonic seizures, and generalized tonic seizures were recorded using a video camera with subsequent evaluation.Results. Based on the experimental results, optimal administration parameters were established for models of pentylenetetrazole, bicuculline, and picrotoxin-induced seizures, ensuring reproducibility and sensitivity to anticonvulsants. The optimality of the convulsant administration conditions for the models is confirmed by the demonstration of a dose-dependent anticonvulsant effect of diazepam, which statistically significantly increases the seizure threshold and slows the development of a seizure in all models.Conclusion. As a result of this study, the optimal conditions for the administration of convulsants with different mechanisms of action were determined for three experimental seizure models. The obtained results can be used for subsequent preclinical studies of potential compounds possessing anticonvulsant activity.
Given the increasing prevalence of the neurodegenerative diseases worldwide, the development of new methods for correction of neuroinflammation contributing to neurodegenerative diseases is a highly relevant and important issue in the field of biomedical research. Neuroinflammation experimental models are essential tools for developing novel therapies for neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis sclerosis (ALS), epilepsy, and depression. Currently used models can generally be divided into in vitro and in vivo models or according to the method of action on the body – on chemical (exposure to neurotoxins and endogenous substances), genetic (transgenic and knockout animals), physical (injury, stress). Each of these experimental paradigms reproduce neuroinflammation in one aspect and not able to provide a complete picture of this complex process. Another problem is a lack of congruity between experimental model and clinical trials due to an unsuitable choice of the model, its unreliability or experiment conditions. This prevents the search of effective solutions for neurodegenerative disease treatment. Therefore, the current review aims to summarize the different experimental paradigms used to reproduce neuroinflammation and its main strengths and weaknesses, helping to choose the model that better suits each specific research aim.
Parkinson's disease is the second most common neurodegenerative disease, associated with the progressive loss of dopaminergic neurons in the substantia nigra. By the time the first symptoms of the disease appear and, accordingly, the possibility of its diagnosis arises, 50–60 % of dopaminergic neurons in the substantia nigra are lost, and the dopamine level in the striatum decreases by 70–80 %. Modern pharmacotherapy for Parkinson's disease is still predominantly symptomatic and aimed at compensating for the dopamine deficiency in the CNS. In this regard, the development of new antiparkinsonian drugs capable of both slowing down neurodegeneration and stimulating neurogenesis is relevant. Proteins of the neurotrophin family are endogenous neuroprotectors and also activate reparative processes in damaged nervous tissue. This review consolidates current literature on the role of neurotrophins in the pathogenesis of Parkinson's disease and evaluates their potential as a therapeutic strategy.
Aim. To evaluate the comparative pharmacokinetics, bioequivalence, and safety of the test product Ranquilon® 2 mg tablets and the reference drug Ranquilon®1 mg tablets in healthy volunteers under fed conditions.Material and methods. A randomized, open-label, comparative, two-period crossover study was conducted to evaluate the pharmacokinetic parameters, bioequivalence, and safety of two dosage strengths of the drug Ranquilon® — 1 mg tablets and 2 mg tablets. Thirty-six healthy volunteers were randomized into two sequence groups (n =18 per group). Participants in group 1 (sequence RT) received two 1 mg tablets of Ranquilon® in period 1 and one 2 mg tablet of Ranquilon® in period 2. Participants in group 2 (sequence TR) received the study drugs in the reverse order. The washout period between dosing was 7 days. The plasma concentration of the active substance of Ranquilon® (amide N-(6-phenylhexanoyl)glycyl-L-tryptophan) was determined using a validated method of high-performance liquid chromatography–tandem mass spectrometry (HPLC-MS/MS). Vital sings, clinical laboratory parameters (complete blood count and biochemical blood analysis, urinalysis), and 12-lead electrocardiogram (ECG) data were monitored and evaluated during the study. All subjectreported complaints, as well as any deviations from reference ranges in volunteers’ clinical condition, laboratory tests results, and ECG parameters, were considered by the investigators as adverse events (AEs).Results. The mean maximum plasma concentration (Cmax) was 8.00±3.67 ng/ml for the test product and 8.29±3.75 ng/ml for the reference drug. The mean area under the concentration-time curve (AUC0-t) was 18.91±7.49 ng × hr/ml for the test product, and 21.05±8.33 for the reference drug. The calculated 90 % confidence intervals (CI) for the mean ratios (test/reference) of Cmax and AUC0-t were 83.36–107.74 % and 83.06–98.61 %, respectively. Both intervals fall within the predefined bioequivalence range of 80.00–125.00 %. A total of 22 adverse events (AEs) were reported in 13 volunteers. Eight AEs occurred in 5 volunteers (27.8 %) in group 1, and fourteen AEs in 8 volunteers (44.4 %) in group 2. All AEs were mild in severity, resolved spontaneously without sequelae, and required no therapeutic intervention or study-drug discontinuation.Conclusion. Bioequivalence between the test product Ranquilon® 2 mg tablets and the reference drug Ranquilon® 1 mg tablets was conclusively demonstrated at an equivalent dose of 2 mg of the active substance. Both products exhibited favorable and comparable safety profiles.
This article presents literature and our own data on animal models of ischemic and hemorrhagic stroke, using in vivo and in vitro methods. Stroke models are reviewed, including focal ischemia, global complete or transient cerebral ischemia, and combined vascular pathologies. The advantages and disadvantages of experimental models and the mechanisms underlying the consequences of ischemic and hemorrhagic brain injury are discussed.
Relevance. The role of the Sigma1R chaperone in modulating the effects of allosteric modulators of GABAA receptors has been previously demonstrated.However, its influence on processes associated with the orthosteric GABA-binding site and the chloride channel of the receptor remains poorly understood. Despite the established Sigma1R-dependent effect of fabomotizole in the pentylenetetrazole-induced seizure model, the involvement of Sigma1R in its anticonvulsant mechanism under conditions of orthosteric GABA-binding site or chloride channel inhibition remains unclear.Objective. To evaluate the influence of Sigma1R ligands PRE-084, BD-1047, and fabomotizole on seizure thresholds in mouse models of seizures induced by intravenous administration of bicuculline and picrotoxin.Materials and Methods. The study was conducted on male ICR mice. Seizures were induced by intravenous infusion of bicuculline or picrotoxin. Fabomotizole (20 mg/kg), PRE-084 (10 and 20 mg/kg), and BD-1047 (10 and 20 mg/kg) were administered intraperitoneally 90 minutes prior to the convulsant. Threshold doses for the onset of clonic jerks, generalized clonic, and tonic seizures were recorded.Results. An anticonvulsant effect of fabomotizole at a dose of 20 mg/kg was demonstrated, which was attenuated by the Sigma1R chaperone antagonist BD-1047. No intrinsic effects were observed for either the selective Sigma1R agonist PRE-084 or the antagonist BD-1047.Conclusion. The present study demonstrated that the anticonvulsant action of fabomotizole in bicuculline- and picrotoxin-induced seizure models is mediated by Sigma1R activation. The difference between the pharmacological action of fabomotizole and that of the classical agonist PRE-084 suggests the existence of additional, as yet unstudied, mechanisms of Sigma1R interaction with the GABAA receptor, which opens new avenues for further research.
Objective. To study the potential use of Epac regulatory protein inhibitors to prevent alcohol-induced myocardial fibrosis.Materials and Methods. To simulate holiday heart syndrome (HHS), rats were given a 10 % aqueous ethanol solution as the sole fluid source for 10 days, followed by drinking water for 10 days, and then a 10 % aqueous ethanol solution for the following 10 days. Connective tissue and adipose tissue density were assessed in histological preparations obtained from atrial, interatrial septal, and ventricular tissues stained with gallocyanin-eosin and picrofuchsin according to Van Gieson. A scoring system was used to quantify the intensity of the identified pathological changes.Results. Following experimental therapy with ZMEI-3, the degree of connective tissue proliferation in the right atrium and interatrial septum in these animals was significantly lower than that observed in the control group (p = 0.0079 and p = 0.0013, respectively). The intensity of fatty deposits was significantly lower in the right and left atria (p = 0.035 and p = 0.0034, respectively).Conclusion. Experimental therapy with ZMEI-3 in animals with HHS syndrome significantly reduced both the intensity of connective tissue and adipocyte deposits in atrial myocardium and interatrial septum, which may underlie the antiarrhythmic effect of the compound.
Background. Magnesium is one of the body's major cations. The exact number of proteins in the proteome whose activity is associated with magnesium is unknown.Objective. To establish functional categories of magnesium-dependent proteins.Materials and methods. A systems biology analysis was performed using original algorithms for recognizing and classifying magnesium-dependent proteins and a functional linkage method, taking into account protein annotations and Gene Ontology categories. Parametric and nonparametric tests, correlation analysis, and variance analysis were used to test statistical hypotheses.Results. Analysis of protein functional categories revealed that 1,503 GO categories were associated with the biological functions of magnesium. A total of 172 magnesium-dependent proteins in the human proteome are involved in functional responses of the nervous system. These proteins are involved in neurotransmitter homeostasis, neuroplasticity, and neuronal survival.Conclusion. The widespread presence of magnesium in the human proteome confirms its ubiquitous role in supporting physiological function under conditions of adequate supply of this essential element.
Background. Inflammation intensifies lipid peroxidation and damages cell membranes. Therefore, the use of antioxidant and membrane-protective agents in combination with widely prescribed nonsteroidal anti-inflammatory drugs (NSAIDs) can enhance the effect of the therapy. Ethylmethylhydroxypyridine succinate (EMHPS), which has antioxidant and membrane-stabilizing properties, enhances the antiexudative effect of diclofenac sodium and etoricoxib after a single oral administration in rats and mice.Objective. Evaluation of the effect of EMGPS, diclofenac sodium, etoricoxib and combinations of these NSAIDs with EMGPS with a course of oral administration in a collagen-induced arthritis model (CIA) in BALB/c mice.Methods. CIA was modeled by double injection of bovine collagen type II (BC) emulsified with complete Freund's adjuvant into the base of the tail of BALB/c mice, 21 days apart. Arthritis severity, paw edema, hyperalgesia, and motor deficits were recorded. On day 21 after the 2nd BC injection, serum was obtained for evaluation of the concentration of the collagen degradation marker oxyproline and the activity of the antioxidant enzymes catalase and glutathione peroxidase. NSAIDs at a dose of 1 mg/kg, EMHPS at a dose of 25 mg/kg, and combinations of EMHPS with NSAIDs were administered orally daily, starting on day of the 2nd BC injection for 21 days.Results. Mice with CIA developed swelling of the paws, the maximum of an exudative inflammation was observed on days 4–17 after the 2nd injection of BC, then joint deformation was more pronounced, and the concentration of oxyproline in the serum increased. Diclofenac sodium had an antiexudative effect on the 7th day of its administration. Etoricoxib delayed the manifestation of symptoms of arthritis in animals, had an antiexudative effect on the 7th day of its administration, but increased the concentration of oxyproline in serum. EMHPS delayed the manifestation of symptoms of arthritis and reduced the concentration of oxyproline in serum. EMHPS when administered together with diclofenac sodium or etoricoxib had a corrective effect on the severity of symptoms of arthritis and reduced swelling on the 7th day of its administration. EMHPS when administered together with diclofenac sodium or etoricoxib but not NSAIDs and EMHPS per se reduced hyperalgesia on the 7th day of its administration. EMHPS when administered together with diclofenac sodium reduced the level of oxyproline, and when administered with etoricoxib, it prevented the increase in oxyproline level in the serum caused by etoricoxib.Conclusion. The combined use of EMHPS with diclofenac sodium and etoricoxib increases the effect of these NSAIDs in the collagen-induced arthritis model in BALB/c mice.
Relevance. BCRP (Human Breast Cancer Resistance Protein) (ABCG2, MXR; ABCP) is an efflux ATP-dependent transporter protein that plays a crucial role in the pharmacokinetics of a wide range of drugs. To enhance therapeutic safety and predict potential pharmacokinetic drug-drug interactions, international regulatory bodies recommend testing medicinal substances for their affiliation with substrates and inhibitors of BCRP. Preclinical studies are primarily conducted using cell lines that overexpress BCRP in vitro.Objective. The aim was to develop and experimentally validate a methodology for assessing medicinal substances as substrates or modulators of BCRP activity in vivo.Materials and methods. Six sexually mature male rabbits of the Soviet Chinchilla breed, weighing between 3000 g and 4000 g, were used in this study. Sulphasalazine was chosen as the classical substrate for BCRP and was administered intragastrically at a dose of 125 mg/kg. Pharmacokinetic evaluation involved blood sampling from ear veins at time points 0.25 h; 0.5 h; 1 h; 1.5 h; 2 h; 3 h; 5 h; 8 h; 12 h; and 24 h post-administration. Quercetin, known as a potent inhibitor of the transporter, was also administered either as a single dose (100 mg/kg) or chronically (25 mg/kg daily for seven days). After both acute and chronic quercetin administration, sulphasalazine was reintroduced, and its pharmacokinetics were assessed again. Plasma concentrations of sulphasalazine were analyzed by HPLC-MS/MS. Model-independent methods were employed to calculate pharmacokinetic parameters. Differences among groups were evaluated via analysis of variance, assuming a log-normal distribution of data.Results. With a single administration of the BCRP inhibitor quercetin to rabbits, of all the tested pharmacokinetic parameters of sulfasalazine, only Cmax significantly increased, while the remaining parameters (AUC0-t; AUC0-∞ and T1/2) did not significantly change (p > 0.05). With the course administration of the BCRP inhibitor, a significant increase in Cmax values was observed by 3.1 times, AUC0-t and AUC0-∞ by 2.81 times (p = 0.0048**) and 2.49 times (p = 0.0192*), respectively, of the sulfasalazine transporter substrate, indicating a decrease in BCRP activity. In this case, inhibition depends on the duration of quercetin administration, which is confirmed by a significant difference in pharmacokinetic parameters between a series of single and course injections of the substance (p < 0.05).Conclusion. An original method has been developed and experimentally validated for testing medicinal compounds as substrates or modulators of BCRP activity in vivo using male Soviet Chinchilla rabbits as test subjects, with sulphasalazine (125 mg/kg) serving as the transporter substrate and quercetin (administered either as a single dose of 100 mg/kg or as a course of 25 mg/kg/day for seven days) as the inhibitor.
Introduction. The journal "Pharmacokinetics and Pharmacodynamics", published since 2004, has evolved from a narrowly focused periodical on clinical pharmacokinetics to a reputable peer-reviewed journal included in the Supreme Attestation Commission list (K1), in the Unified State List of Scientific Publications — "White List" (level 2) and the DOAJ database. The challenges in the area of modern medicines development require a revision of editorial policy and an expansion of thematic boundaries.Objective. To present a strategic vision for the journal's development, aimed at transforming the publication into an interdisciplinary platform covering the entire lifecycle of a medicinal product — from molecular design to clinical application.Key points. The strategy is based on three key vectors: 1) institutional — renewal of the editorial board, change of the editor-in-chief, and formation of an international editorial council; 2) thematic — integration of related specialties (1.4.16. Medicinal Chemistry, 3.3.6. Pharmacology, Clinical Pharmacology, 3.4.1. Industrial Pharmacy and Medicines Manufacturing Technology, 3.4.2. Pharmaceutical Chemistry, Pharmacognosy) to create a unified publication logistics chain; 3) international — rebranding with a possible name change to position the journal as a global player in the field of translational pharmacology and pharmaceutical sciences, including submission to Scopus and PubMed Central.Conclusion. The implementation of this concept will dramatically expand the pool of authors, increase citation rates, and secure a leading position among national and international pharmaceutical journals, becoming the main integrator of scientific knowledge in the field of innovative drug development.
