ISSUE 01

Abstract:
This review examines the repurposing of established pharmacotherapies for the treatment of ischemic stroke, specifically ticagrelor and abemaciclib. Ticagrelor, reacts to platelet responsibility and increases cerebral blood flow, 1.000 dependent ligand is confirmed, ABEMACICLIB-Dick Strong bondage-attraction shows, indicating its ability to modulate Galactosidase Alpha activity, suitable for conditions that can complicate stroke outcomes Analysis also reveals promising strategies, including cangrelor and tedizolid, suggesting a diverse range of therapies to improve stroke management Structural analysis of protein-ligand interactions Provide insights into manufacturing optimization about and highlights the effectiveness of existing drugs in new clinical settings Findings advocate further experimental verification of the efficacy and safety of these recycled drugs in clinical practice, and ultimately aimed at improving patient outcomes in dementia care. 

Keywords: 

Stroke, Ticagrelor, Abemaciclib, Drug Reuse, P2Y12 Receptor Antagonist, Galactosidase Alpha, Molecular Docking, Virtual Screening, Treatment Seekers 

Introduction:

A stroke is a serious medical condition defined as a sudden interruption of blood flow to the brain, resulting in immediate neurological damage that can affect movement, speech, and cognitive function[1].Types of strokes there are two main types: ischemic and hemorrhagic [2] . Accounts for about 87%, when it occurs when blood vessels supplying blood to the brain is damaged, due to local thrombus in a blood vessel or embolism or embolism , bleeding in body in other parts of the In contrast, blood vessels in the brain rupture, leading to hemorrhage and increased intracranial pressure and ischemia; This condition can also be divided into subarachnoid hemorrhage, where bleeding occurs in the space around the brain, and intracranial hemorrhage, where bleeding occurs within the brain capillaries themselves, major causes of mortality and longevity occurs worldwide[3] .The World Health Organization estimates that measles kills 5 million people each year, permanently 50 others in the form of It disables one million people and affects 15 million people each year as a fifth disease most common in the United States of epilepsy emphasizes the high immediate health costs and the need for effective treatment and prevention strategies[4].

Current treatment options for stroke focus primarily on restoring blood flow and preventing further nerve damage. Major therapies include thrombolytic therapy, such as recombinant tissue plasminogen activator (tPA), which is used to pop clots in acute bleeding episodes but tPA must be administered over a limited period of time—frequently most within 3 to 4.5 hours of symptom onset—to be effective in many patients[5] . Use is limited Mechanical thrombectomy is an alternative that involves physically removing large blood vessels and has proven effective for specific patients with major ischemic stroke[6] . Furthermore, antiplatelet agents such as aspirin and clopidogrel are commonly used for secondary prevention reduce the risk of stroke recurrence[7]. Limitations of there is a need; Many patients do not have access to emergency clinics for timely intervention, in contrast to tPA in hemorrhage. Furthermore, advanced interventional techniques such as thrombectomy are generally limited, especially in rural or underserved areas [8]. These challenges underscore the critical need for alternative therapies that can be delivered safely and effectively regardless of time or patient status[9].

Abemaciclib, a cyclin-based kinase inhibitor, offers a convenient recycling strategy in this regard. Bemaciclib, a specific inhibitor of CDK4 and CDK6, is used to treat hormone receptor positive breast cancer [10]. Abemaciclib disrupts the cell cycle by inhibiting these kinases, leading to cancer cell apoptosis and cell cycle arrest [11]. But emerging research suggests that abemaciclib may have neuroprotective effects due to its ability to modulate cellular processes associated with inflammation and apoptosis, which are important in stroke [12]. Preliminary studies, suggested that inhibitory drugs. The CDK edge will promote neuronal survival and neurodegenerative diseases and reduced inflammatory responses in injury models, suggesting potential applications in trauma therapy [13].

The aim of this study is to evaluate the efficacy of abemaciclib as a neuroprotective therapy in stroke, with a focus on the effects of neurogenesis and functional recovery in preclinical models 9140. We assume that abemaciclib administration would significantly reduce vascular cell death in ischemic stroke models compared to controls. Improvements in neuronal function and behavioral outcomes, and these neuroprotective effects are mediated by modulation of cell cycle regulatory pathways, and this reduction in turn leads to an inflammatory response in the brain. This study may pave the way for new therapeutic strategies in the management of stroke, ultimately improving patient outcomes.

Abstract:
Bacterial infections, clogged pores, and excessive sebum production are the causes of acne. Around 20% of people globally and up to 80–90% of teenagers suffer with acne vulgaris, a prevalent dermatological disorder. It appears when sebaceous glands overproduce sebum, or oil, which clogs pores when combined with dead skin cells. As a result, Cutibacterium acnes (formerly known as Propionibacterium acnes) bacteria can develop in an anaerobic environment. Inflammation brought on by the bacterial activity might result in papules, pustules, nodules, or cysts. Acne can be made worse by hormone imbalance, stress, high-glycemic diets, and bad skincare practices. The two main categories of treatments are herbal (plant-based) and synthetic (chemical-based).

Keywords: 

Clogged pores, inflammation, synthetic & herbal treatments, bacterial infection.

Introduction:

Treatments for acne fall into: 

Synthetic (based on chemicals): These consist of hormonal medicines (oral contraceptives), antibiotics (clindamycin, erythromycin), retinoids (tretinoin, adapalene), and benzoyl peroxide. These substances function by unclogging pores, eliminating germs, and lowering sebum production. Prolonged usage, however, can cause skin irritation, dryness, and antibiotic resistance.

Herbal (Plant-Based): Made from medicinal plants including aloe vera, tea tree oil, neem (Azadirachta indica), turmeric (Curcuma longa), and green tea (Camellia sinensis) that contain antibacterial, anti-inflammatory, and antioxidant chemicals. With few adverse effects, they work by preventing bacterial development, lowering sebum, and encouraging skin repair. Because of their holistic approach and biocompatibility, herbal medicines are becoming more and more popular.

1. Materials and Procedures

1. Design of the Study

This study compares the effectiveness, safety, cost, and consumer preference of herbal and synthetic acne and pore management therapies using a survey and literature review methodology.

To examine the performance metrics of both therapy modalities, the study aggregates information from consumer surveys, published research publications, clinical trials, and pharmaceutical databases.

2. Sources of Data

Data was gathered from the sources listed below:

Scientific databases: ResearchGate, ScienceDirect, PubMed, and Google Scholar.

WHO, AYUSH, and Statista reports are examples of institutional and regulatory sources.

Market and consumer research: assessments of Indian consumers' preferences for herbal and synthetic skincare products conducted between 2021 and 2023.

Clinical studies: Peer-reviewed clinical data contrasting synthetic drugs (benzoyl peroxide, salicylic acid, retinoids, etc.) with herbal extracts (neem, aloe vera, turmeric, tea tree oil, green tea, (antibiotics). (1).

3. Selection Standards

Criteria for inclusion:

research papers released from 2010 to 2025.

research on pore therapy and acne vulgaris.

research that compared herbal and synthetic formulations, either clinical or observational.

articles on cost-effectiveness, safety, efficacy, or customer happiness.

Criteria for exclusion:

studies with ambiguous formulation details or insufficient clinical data.

studies that employ synthetic chemicals or botanicals for purposes other than dermatology.

studies on animals without a human connection.

4. Survey Specifications

Five primary criteria served as the basis for the comparison analysis:

Effectiveness:  Lesion clearance %, recurrence rate, and time required for noticeable acne reduction.

Safety and Tolerability: The frequency of photosensitivity, dryness, redness, or irritation.

Accessibility and Cost: The market pricing (₹/g) and the product's availability in local or online marketplaces.(2).

Consumer Preference: based on survey results from 500 people between the ages of 18 and 35 who suffer from acne.

5. Analysis Method

For each parameter, a comparison grading matrix was created, with 1 denoting poor and 5 denoting good.

Based on reported clinical outcomes (decrease in lesion count, erythema, and dryness %), average efficacy and tolerability were determined.

The frequency (%) of using herbal versus synthetic products was used to examine consumer preference data.

Market retail values gathered from pharmacy and e-commerce databases were used to compare costs.

6. Materials Taken into Account

Review of Herbal Ingredients:

Neem, or Azadirachta indica,

Aloe vera, or Aloe barbadensis

The turmeric plant, Curcuma longa

Tea tree oil, or Melaleuca alternifolia

Green tea, Camellia sinensis

Review of Synthetic Agents:

Peroxide benzoyl

Salicylic acid

Tretinoin and Adapalene (Retinoids)

Erythromycin and Clindamycin are topical antibiotics.

Hormonal therapies based on oral contraceptives(3).

7. Method of Evaluation

To assess the benefits, drawbacks, and results of each category, comparative data were collated into tabular form.

Clinical efficacy percentages were used to validate the findings in the literature, including:

In just one week, benzoyl peroxide reduced germs by 98%.

In six weeks, neem extract can reduce lesions by 40–50%.

Tea tree oil has fewer negative effects and is just as effective as 5% benzoyl peroxide.

Due to a variety of data sources, statistical interpretation concentrated on qualitative tendencies rather than quantitative meta-analysis.(4).

 8. Moral Points to Remember

There was no direct testing on humans or animals because this is a review and survey-based study.

All of the data came from publicly accessible consumer data and previously published, ethically approved research studies.(5).

Abstract:
Dysregulated cytokine signalling via the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway is the main cause of rheumatoid arthritis (RA), a chronic autoimmune disease marked by ongoing synovial inflammation and joint damage. JAK1 is a prospective therapeutic target because it is one of the JAK family members that is essential in mediating pro-inflammatory responses. In order to find new JAK1 inhibitors among FDA-approved medications, the current work used a computational drug repurposing strategy that combined molecular docking and virtual screening based on Morgan fingerprints. Nineteen structurally comparable candidates were obtained from the DrugBank database using tofacitinib as a reference molecule. The anticancer medication Ribociclib had the highest binding affinity (–9.1 kcal/mol) against JAK1, outperforming Tofacitinib (–8.8 kcal/mol), according to docking tests conducted using CB-Dock2. Strong target engagement was confirmed by interaction analysis, which showed robust hydrogen bonding and hydrophobic interactions with important active site residues such as Leu959, Glu966, and Asp1003. The PDB-REDO model refinement enhanced structural precision, boosting the trustworthiness of docking results. Additionally, Ribociclib's pharmacokinetic profile as a systemically active medication is consistent with its strong gastrointestinal absorption and restricted blood–brain barrier permeability, according to the BOILED-Egg model analysis. All of these results point to Ribociclib as a viable repurposing option for JAK1 inhibition in rheumatoid arthritis, deserving of additional in vitro and in vivo validation to investigate its safety and therapeutic efficacy in inflammatory conditions.

Keywords: 

Clogged pores, inflammation, synthetic & herbal treatments, bacterial infection.

Introduction:

The chronic, systemic autoimmune disease known as rheumatoid arthritis (RA) mostly affects synovial joints, causing inflammation, bone erosion, and cartilage degradation1. It is typified by gradual joint deformity, pannus development, and chronic synovitis, which eventually lead to pain, stiffness, and loss of function2. Approximately 1% of people worldwide suffer from RA, which is a leading cause of disability globally and more common in women than in men3. In addition to joint involvement, RA is linked to systemic consequences such anaemia, lung fibrosis, and cardiovascular disease, all of which drastically lower the quality of life and life expectancy of those who are affected4.

Environmental factors, immune dysregulation, and genetic vulnerability interact intricately in the pathogenesis of RA5. Tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) are pro-inflammatory cytokines released by activated T cells, B cells, and macrophages that promote inflammation and tissue destruction6. The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is essential to this inflammatory signalling because it sends cytokine-mediated signals to the nucleus and controls the expression of genes linked to inflammatory responses and immune activation7.

JAK1 is one of the four members of the JAK family (JAK1, JAK2, JAK3, and TYK2) that is especially important for the spread of inflammatory cytokine signalling8. JAK1 inhibition is a desirable target for RA therapy since it has been demonstrated to lower the synthesis of inflammatory mediators and inhibit immune cell activation9. JAK inhibitors that are currently on the market, such as tofacitinib, baricitinib, and upadacitinib, have shown clinical effectiveness in managing the symptoms of RA10. However, side effects, expensive treatment costs, and long-term safety concerns frequently restrict their use, highlighting the need for new and better options.

One effective method for finding novel therapeutic applications for already-approved medications is drug repurposing, sometimes referred to as drug repositioning11. Because the pharmacokinetic and toxicity profiles of these drugs are already well established, this strategy lowers development time, expense, and risk. By forecasting chemical interactions at the target level, computational techniques like molecular fingerprinting, virtual screening, and molecular docking have sped up the process of finding repurposing candidates in recent years. 

Antineoplastic, antiproliferative, and anti-inflammatory qualities are demonstrated by ribociclib, a selective cyclin-dependent kinase (CDK4/6) inhibitor that has been authorised for the treatment of breast cancer12. It was thought that Ribociclib would also inhibit JAK1, providing therapeutic potential in RA, given the structural closeness between kinase domains.

This work identified new JAK1 inhibitors for RA using a computational drug repurposing strategy that combined molecular docking and virtual screening based on Morgan fingerprints. The lead molecule was Tofacitinib, while Ribociclib was the best-scoring contender, outperforming Tofacitinib (–8.8 kcal/mol) with a binding affinity of –9.1 kcal/mol. According to these results, ribociclib may be a viable repurposing option for JAK1 inhibition in RA, which calls for more experimental verification.

Disease Selection: Rheumatoid Arthritis (RA)

The study's target illness is rheumatoid arthritis (RA), a chronic inflammatory disease that causes cartilage degradation, bone erosion, and disability due to persistent inflammation of the synovial joints13. About 1% of people worldwide suffer from RA, which is primarily a female condition. It is linked to extra-articular consequences such pulmonary fibrosis and cardiovascular disease14. Cytokines such as IL-6, TNF-α, and IFN-γ, which mainly signal via the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway, are responsible for the dysregulated immunological activation that underlies the pathophysiology of RA15.

A key player in the pathogenesis of RA, JAK1 is a vital modulator of pro-inflammatory cytokine signalling among the JAK family16. JAK1 inhibition is a useful therapeutic approach since it inhibits several cytokine-driven inflammatory pathways. JAK1 was chosen as the primary target for this structure-and ligand-based therapeutic repurposing study due to its verified molecular target, well-characterized signalling mechanism, and clinical significance17.

Selection of FDA-Approved Lead Compound: Tofacitinib

Because of its proven effectiveness in treating RA, tofacitinib, a small molecule JAK inhibitor that has FDA approval, was chosen as the study's lead medication. By specifically blocking JAK1 and JAK3, it alters the cytokine signalling that triggers immunological and inflammatory reactions. For computational similarity-based drug screening, the compound's established mechanism of action, clinically verified pharmacokinetics, and safety profile serve as a trustworthy benchmark. The receptor model was the crystal structure of JAK1 coupled to a ligand (PDB ID:3EYG). 

The availability of experimental and structural data that support precise ligand-based virtual screening and molecular docking validation further supported the selection of tofacitinib as a reference ligand.

Ligand-Based Drug Repurposing (Morgan Fingerprinting)18

For ligand-based drug repurposing, the DrugBank database was used, with an emphasis on FDA-approved medications. Using Tofacitinib as the reference ligand, a virtual screening method based on Morgan fingerprints was used. Tanimoto similarity coefficients between compounds can be calculated thanks to Morgan fingerprints, which encode the molecular structure by taking into account atom habitats within a specified radius. 

Because of its effectiveness and precision in discovering compounds that share substructural similarities with known inhibitors, this approach was chosen. For additional investigation, compounds with a Tanimoto similarity score of ≥ 0.7 were shortlisted as possible hits. Out of the 19 structurally similar medications found in the database, the FDA-approved anticancer medication Ribociclib has the highest similarity score to Tofacitinib.

Binding Interaction and Validation

Based on interaction profiles and binding affinity (kcal/mol), the docking results were examined. Protein–ligand interactions, such as hydrogen bonding, hydrophobic contacts, and π–π stacking interactions, were visualised using Discovery Studio Visualiser19. 

Ribociclib had the highest binding affinity (–9.1 kcal/mol) among the 19 tested drugs, outperforming Tofacitinib (–8.8 kcal/mol). Ribociclib's significant binding potential within the JAK1 active pocket was confirmed by the interaction study, which showed that it interacted with important active site residues like Leu959, Glu966, and Asp1003.

Molecular Docking Studies20

CB-Dock2, a sophisticated web-based docking platform that uses AutoDock Vina to estimate binding affinities and interaction poses between ligands and target proteins, was used to perform molecular docking simulations. Based on the ideal cavity score and anticipated binding energy, CB-Dock2 automatically selects the top five possible binding cavities and produces docking data. 

The Protein Data Bank (PDB) provided the crystal structure of human Janus Kinase 1 (JAK1) (PDB ID: 3EYG). Water molecules were eliminated, polar hydrogens were added, and the active site surrounding the co-crystallized ligand was defined in order to prepare the structure before docking. In the pathogenesis of rheumatoid arthritis (RA), this location is the ATP-binding pocket that activates the JAK-STAT pathway.

The reference ligand was the lead chemical, Tofacitinib, a JAK inhibitor for RA that has FDA approval. In order to evaluate comparative affinities, a total of 19 structurally comparable FDA-approved medications found using Morgan fingerprint-based virtual screening were also docked with JAK1. The CB-Dock2 platform, which offers an effective interface for ligand-protein interaction analysis, was chosen due to its accuracy in identifying the binding pocket and dependability in determining Vina scores.

Binding affinity (kcal/mol), cavity size, and Vina score were used to assess the docking results; stronger binding interactions were indicated by lower (more negative) energy values. In contrast to Tofacitinib (-8.8 kcal/mol), the anticancer medication Ribociclib showed the highest binding affinity (-9.1 kcal/mol), suggesting a possibly stronger and more stable binding to JAK1. To find important hydrogen bonds, hydrophobic contacts, and electrostatic interactions that contribute to complex stability, docking poses were visualised using Discovery Studio Visualiser.

Data Analysis

The Morgan fingerprint Tanimoto similarity scores and binding energies of the docked compounds were used to rank them. Key amino acid residues involved in ligand stabilisation inside the JAK1 active site were identified by analysing interaction patterns. To determine the stability and dependability of docking, parameters such RMSD, hydrogen bond formation, and contact type were examined. 

Multiple stabilising contacts with important JAK1 residues, such as Lys908, Glu966, and Asp939, were shown by ribociclib, a CDK4/6 inhibitor with well-established anticancer effects. This suggested robust binding and possible inhibitory efficacy. Through pharmacological repurposing, this implies that Ribociclib may alter the JAK-STAT signalling system, providing therapeutic benefits in rheumatoid arthritis.

Statistical and Computational Tools

Descriptive statistical techniques were used to examine the connection between binding energies and molecular similarity scores. Matplotlib and Seaborn were used for data visualisation and correlation charting, while Python (version 3.10) modules like RDKit were used for fingerprint generation and similarity index computation. The combination of structure-based (CB-Dock2 docking) and ligand-based (Morgan fingerprinting) screening methods provide a thorough evaluation for finding new medication repurposing candidates that target JAK1 in rheumatoid arthritis.

Abstract:
Imatinib effectively targets the constitutive activation of the c-KIT receptor tyrosine kinase, which is the primary cause of gastrointestinal stromal tumours (GISTs). However, the development of new inhibitors is required due to developed medication resistance and ongoing, lifelong administration with related side effects. Using a hybrid in silico drug repurposing approach, our study quickly identified possible c-KIT antagonists that could overcome imatinib resistance by utilising the established safety of FDA-approved medications. The methodology combines structure-based blind molecular docking against the human c-KIT kinase domain (PDB ID: 8S16) using AutoDock VINA with ligand-based screening via SwissSimilarity, utilising Imatinib as a reference to locate structurally similar FDA-approved medicines (Tanimoto coefficient ≥0.988). This method investigated possible allosteric sites while screening for both strong binding affinity and great structural similarity. Several of the top 10 compounds with high anticipated binding affinities were identified via molecular docking. Interestingly, the chemical CHEMBL475796 performed better than the reference standard, imatinib (−11.2 kcal/mol), with a Vina score of −12.0 kcal/mol. Because they are currently FDA-approved, the identified lead compounds—in particular, CHEMBL475796—are well-positioned for quick translational development. To verify c-KIT inhibitory effectiveness and efficacy against imatinib-resistant GIST phenotypes, a thorough in vitro and in vivo validation process is the next essential step.

Keywords: 

Gastrointestinal Stromal Tumours (GISTs), c-KIT, Imatinib, Drug Repurposing, In Silico Drug Discovery, Virtual Screening, Molecular Docking, Blind Docking, SwissSimilarity, Tyrosine Kinase Inhibitor, AutoDock VINA, Tanimoto Coefficient, FDA-approved drugs.

Introduction:

Gain-of-function mutations in the gene encoding the receptor tyrosine kinase, c-KIT, which result in its constitutive, ligand-independent activation, are usually the pathogenesis of gastrointestinal stromal tumours (GISTs), the most prevalent mesenchymal malignancy of the gastrointestinal tract [1]. In most cases of GIST, the primary oncogenic mechanism that promotes unchecked cell proliferation and survival is this hyperactivated signalling. By specifically targeting the mutant c-KIT protein, imatinib, a tyrosine kinase inhibitor, revolutionised the treatment of GIST [2–3]. The nearly unavoidable emergence of acquired drug resistance, frequently brought on by secondary c-KIT mutations, severely limits the benefits of imatinib despite its early clinical success and causes disease progression in the majority of treated patients [4]. Furthermore, continuous, life-long administration is required and is frequently associated with dose-limiting side effects, including periorbital edema, fatigue, and gastrointestinal issues.

By utilising the established safety and pharmacokinetic information of currently approved FDA drugs, drug repurposing offers a quicker and more affordable discovery pathway for the search for new therapeutic compounds that can overcome imatinib resistance and provide a safer profile [5–6]. For this, computational techniques—in particular, molecular docking and virtual screening—have been crucial in quickly sorting through enormous chemical libraries to find potential candidate compounds. Potential repurposed medications that show efficacy against GIST cell lines, including imatinib-resistant phenotypes, have been effectively identified by previous in silico research [7-8].

The current study uses a mixed computational approach to more fully investigate the landscape of putative c-KIT inhibitors. [9–10] This work combines structure-guided blind molecular docking to evaluate the pharmaceuticals' binding affinity and interactions with the c-KIT kinase domain with ligand-based screening, which uses the molecular structure of the well-known inhibitor imatinib to find structurally similar FDA-approved medications.[11–13] In order to quickly identify and rank high-potential drug candidates for repurposing in the treatment of GIST, this hybrid approach prioritises approved medications that are both structurally similar to the established first-line agent and anticipated to exhibit favourable receptor binding. It focusses on mechanisms that may circumvent acquired resistance and minimise side effects.[14–15].

Abstract:
The beauty and cosmeceutical industries have been greatly impacted by the quick development of artificial intelligence (AI) and machine learning (ML), which has resulted in the creation of novel, individualised, and scientifically based products. Researchers and formulators may now examine vast databases pertaining to consumer preferences, ingredient performance, and skin physiology thanks to AI and ML technologies, producing more individualised and efficient skincare products. These resources help with formulation optimisation, product stability forecasting, and evaluating any adverse effects likeallergy or irritation. Additionally, by providing real-time, data-based recommendations, AI-powered skin analysis systems and virtual try-on applications have revolutionised the consumer experience. In the cosmetics industry, machine learning algorithms are also essential for digital marketing, regulatory compliance, and quality control. Notwithstanding the many advantages, there are drawbacks to combining AI and ML, such as concerns about data privacy, algorithm transparency, and expensive implementation costs. The purpose of this review is to provide an overview of the present uses, benefits, drawbacks, and potential future developments of AI and ML in cosmetic science, emphasising their expanding contribution to the integration of pharmaceutical research and contemporary cosmetic innovation.

Keywords: 

Artificial Intelligence, Machine Learning, Cosmeceuticals, Personalized Skincare, Formulation Optimization, Skin Analysis, Virtual Try-On, Cosmetic Innovation

Introduction:

The conventional formulation methods used in the cosmetics business have given way to extremely complex, technologically advanced systems. Machine learning (ML) and artificial intelligence (AI) have become potent instruments in recent years that are revolutionising the wayProducts for cosmetics are created, assessed, and customised. These technologies make it possible to make data-driven choices in areas including skin analysis, formulation optimisation, ingredient selection, and consumer recommendation systems. AI describes computer programs that are able to carry out operations like pattern recognition, problem solving, and decision making that normally call for human intellect. Algorithms in machine learning, a branch of artificial intelligence, learn from data and gradually get better at what they do. These methods, when used in beauty science, enable researchers to examine vast datasets of skin types, consumer preferences, and formulation characteristics in order to produce individualised and successful solutions. The use of AI in the cosmetic and cosmetics industries has increased because to the growing need for safe formulas, customised skincare, and effective product creation. Every facet of cosmetic research and marketing is changing due to technology, from virtual try-on systems and AI-powered skin diagnostic tools to predictive modelling of formulation stability. Furthermore, new avenues for intelligent, adaptable cosmetic treatments are being opened by the integration of AI with nanotechnology and biotechnology. With a focus on formulation creation, dermatological analysis, quality control, and customised beauty care, this paper attempts to examine the uses, benefits, difficulties, and possibilities of AI and ML in the cosmetics industry. The study also emphasises how these technologies usher in a new era of intelligent cosmetics by bridging the gap between pharmaceutical research and cosmetic innovation.