The Glucagon-Like Peptide-1 Receptor (GLP-1R) and the Hypocretin/Orexin Receptor Type 2 (HCRTR2) are critical G protein-coupled receptors that govern metabolism and neuroendocrine function. Clinical observations suggest a functional overlap, particularly in the regulation of appetite, energy homeostasis, and sleep/wake cycles. Sleep disturbance profoundly disrupts neuroendocrine and metabolic homeostasis, contributing to obesity, impaired glucose regulation, elevated appetite, and altered reward signalling. This study employed an integrated computational approach, combining Network Pharmacology, Molecular Docking, and Molecular Dynamics simulations to elucidate the molecular crosstalk and predict the structural basis for dual-target modulation. Network Pharmacology analysis of target genes revealed a significant overlap of 51 common targets between GLP-1R and HCRTR2. which were enriched in Gene Ontology terms related to cAMP-mediated signalling, circadian regulation, synaptic vesicle organisation, and peptide hormone binding. KEGG pathway enrichment revealed significant clustering in dopaminergic reward pathways, adipocytokine signalling, and lipid-metabolic regulation, indicating shared involvement in neuroendocrine and metabolic homeostasis. To validate this convergence structurally, cross-docking of cognate Ligands was performed using the Schrödinger suite on 7LCJ and 4S0V. The core experiments involved cross-docking the GLP-1R agonist, Danuglipron, with HCRTR2, and the established Orexin antagonist, Suvorexant, with GLP-1R. Both cross-docking pairs showed favourable binding affinities. The stability of both cross-docked complexes was further confirmed via Molecular dynamics simulation, which demonstrated low-deviation dynamics and persistent binding interactions. These results provide strong molecular and structural evidence that the GLP-1R and HCRTR2 signalling axes converge on common molecular hubs, offering an atomic-level mechanism for their functional interdependence and explaining potential polypharmacological effects of existing drugs. This is the first of its kind, comprehensive in silico framework demonstrating molecular convergence between GLP-1R and HCRTR2.

Long-term exposure to fluoride during early development is associated with impairments in neurobehavioral functions, oxidative stress, and molecular alterations in the developing brain. However, the mechanisms by which fluoride disrupts neurodevelopment, as well as the potential of natural flavonoids such as naringin to counteract these effects, are not well characterised. This study aimed to investigate the neurodevelopmental harms of fluoride and evaluate the multi-target neuroprotective efficacy of naringin using behavioural, biochemical, antioxidant, proteomic, and gene expression approaches in rats. Adult male and female Wistar rats and their offspring were exposed to sodium fluoride with or without naringin throughout development. Neurodevelopmental and behavioural assessments were performed along with estimation of serum and urine fluoride levels. Brain oxidative stress markers and biochemical parameters were analysed, followed by proteomic profiling (LC–MS/MS), functional enrichment analysis, and PCR validation of selected molecular markers. Fluoride exposure did not significantly affect most neonatal reflexes but produced selective impairments in specific sensorimotor parameters and pronounced behavioural deficits during post-weaning stages. Rats exposed to fluoride exhibited increased oxidative stress, altered antioxidant enzyme activities, and elevated fluoride levels in both serum and urine, highlighting systemic and neuronal toxicity. Proteomic analysis indicated a dysregulation of pathways linked to mitochondrial function, calcium signalling (including pathways associated with CALM2), synaptic plasticity, and apoptosis. PCR analysis confirmed alterations in key neuronal and stress-related genes. Co-treatment with naringin significantly alleviated behavioural impairments, restored antioxidant balance, reduced fluoride accumulation, mitigated dysregulation across multiple molecular pathways, and lessened changes in both proteomic and transcriptional markers. Fluoride exposure was associated with neurodevelopmental toxicity involving oxidative imbalance, mitochondrial dysfunction, calcium-related signalling disturbances, and alterations in synaptic pathways. Naringin attenuated many behavioural, biochemical, and molecular alterations, indicating a protective effect across multiple targets. These findings support further investigation of naringin as a potential protective compound against fluoride-induced neurodevelopmental alterations.

Antisense oligonucleotides represent a promising class of therapeutic agents due to their high specificity in modulating gene expression. These short, single-stranded synthetic sequences (typically 13-25 nucleotides) function by binding to complementary RNA targets, thereby influencing RNA processing or translation, primarily through RNase H-mediated degradation. Over the past decade, significant advances in chemical modifications and delivery strategies have led to a notable increase in the number of ASO-based therapies that have reached the market. Despite this progress, several challenges persist, including poor stability in biological fluids, limited cellular uptake, and safety concerns related to off-target effects and immunogenicity. This review provides a comprehensive overview of the mechanisms of action of ASOs, their pharmacological applications, current market status, and clinical progress. Special attention is given to evaluating in vitro and in vivo ASO stability using nanotechnology-based delivery approaches to improve pharmacokinetics/ pharmacodynamics and structural modifications to enhance therapeutic potential. Additionally, we discuss the associated adverse effects and propose strategies to mitigate them.

ABSTRACT Chronic wounds pose a major clinical challenge due to a complex pathophysiological condition. It is characterized by persistent inflammation, excessive oxidative stress, and a high risk of bacterial infection, which hinders tissue repair. To address this, a multifunctional hydrogel dressing based on gallic acid conjugated chitosan (G‐CHI) and integrated with simvastatin and heparin‐functionalized Ag/Zn‐doped bioactive glass (HBG). The incorporation of gallic acid improved the structural integrity and viscoelastic behavior of the hydrogel. The release kinetics study demonstrated controlled liberation of Ag + and Zn 2+ ions within biologically safe limits over 24 h, while simvastatin exhibited diffusion‐controlled release behavior. The hydrogel also exhibited desirable adhesive properties, indicating its suitability as a wound dressing material. In vitro biofunctional assays showed enhanced antioxidant activity (~75% free radical scavenging), hemocompatibility (< 5% hemolysis), and effectiveness against both Staphylococcus aureus and Escherichia coli (> 90% efficacy in time kill assay). Further, synergistic release of simvastatin and bioglass showed enhanced proliferation of fibroblast (NIH 3T3), keratinocyte (HaCaT), and endothelial cells (SVEC), accompanied by increased collagen deposition compared to control groups. These findings suggest that the synthesized hydrogel (BSG‐CHI) provides a favorable microenvironment for tissue regeneration and wound management applications.

Accurate prediction of cytochrome P450-mediated victim drug-drug interactions (DDIs) is critical for the safe use of central nervous system (CNS) drugs, particularly in populations at high risk of polypharmacy. This study evaluated the utility and limitations of in vitro human liver microsomal data for predicting victim DDIs of CNS compounds metabolized by CYP1A2, CYP2B6, CYP2D6, and CYP3A4. Reaction phenotyping with isoform-selective inhibitors quantified the fractional metabolic contribution (fm,cyp) of each enzyme, and inhibition parameters for fluvoxamine (CYP1A2), ticlopidine (CYP2B6), cinacalcet/paroxetine (CYP2D6), and ketoconazole (CYP3A4) were incorporated into a mechanistic static model using unbound hepatic inlet concentrations as surrogates for site of inhibition exposure. Predictions for CYP2B6-, CYP2D6-, and CYP3A4-mediated interactions were generally within 3-fold of observed clinical values. In contrast, CYP1A2 substrates showed high sensitivity to fm,cyp values exceeding 0.9, resulting in underprediction (eg, ramelteon-fluvoxamine, 66-fold) or overprediction (eg, tacrine). Contributing factors may include incomplete characterization of minor metabolic pathways, hepatic accumulation of inhibitors, and limitations of static modeling assumptions. Overprediction of select CYP3A4 interactions, such as lurasidone-ketoconazole, likely reflects underestimation of the fraction escaping intestinal metabolism. These findings indicate that human liver microsome-based reaction phenotyping provides valuable guidance for early DDI risk assessment, particularly for CYP2B6, CYP2D6, and CYP3A4 substrates, but small deviations in fm,cyp for CYP1A2 substrates can lead to substantial underestimation of clinical risk. Integration with physiologically based pharmacokinetic modeling and refined fm,cyp estimates may enhance prediction accuracy and better inform safe CNS drug use, especially in populations prone to polypharmacy. SIGNIFICANCE STATEMENT: Accurate prediction of P450-mediated drug-drug interactions is essential for safe central nervous system drug therapy, especially in patients at high risk of polypharmacy. This study shows that human liver microsome-based reaction phenotyping reliably predicts CYP2B6, CYP2D6, and CYP3A4 interactions, whereas small deviations in fm,cyp for CYP1A2 substrates can cause substantial under- or overprediction. Incorporating physiologically based pharmacokinetic modeling and refined fm,cyp estimates can enhance drug-drug interaction risk assessment and guide safer coadministration of central nervous system-active drugs with potent P450 inhibitors.

The emergence of Plasmodium falciparum strains resistant to conventional antimalarial medications such as chloroquine, mefloquine, pyrimethamine, and sulfadoxine underscores the urgent need for novel therapeutic agents. Metallo-aminopeptidase PfA-M1, a zinc-dependent enzyme that catalyzes host hemoglobin degradation into heme, represents a validated target for P. falciparum malaria treatment. In the present study, an in-silico molecular approach was applied to evaluate cinnamoyl sulfonamide hydroxamate derivatives (NMJ 1–8) against PfA-M1 (PDB ID: 4X2U, 1.50 Å resolution, Zn2⁺-dependent). Orally available aminopeptidase inhibitor tosedostat bound to the PfA-M1. Extra-precision docking, MMGBSA binding energy analysis, and induced-fit docking demonstrated favorable ligand–protein interactions with IFD docking scores ranging from − 1984.16 to − 1989.93 kcal/mol. Among these, NMJ-2 and NMJ-3 showed the strongest binding affinities and were subjected to molecular dynamics (MD) simulations. The MD results confirmed the formation of stable complexes, highlighting persistent interactions with crucial residues HIS500, GLU463, GLU519, and HIS496. Bioisosteric replacement further optimized NMJ-2 and NMJ-3 derivatives, all of which satisfied ADME pharmacokinetic parameters. Importantly, the interaction patterns of NMJ-2 and NMJ-3 overlapped with those of the reference inhibitor tosedostat, indicating their potential to inhibit PfA-M1 activity in P. falciparum. These findings suggest that NMJ-2 and NMJ-3 are promising scaffolds for future antimalarial drug development and require further preclinical validation.

Background and Aim: Chronic fluoride exposure causes neurotoxicity, oxidative stress, neuroinflammation, and cognitive impairment, posing a significant public health concern. This study investigated the neuroprotective potential of melatonin against fluoride-induced neurotoxicity and cognitive dysfunction in male and female Wistar rats, with emphasis on oxidative stress, neuroinflammation, apoptosis, and sirtuin 1 (SIRT1) signaling. Materials and Methods: Four-week-old Wistar albino rats (n=8 per group per sex) were exposed to sodium fluoride (NaF, 50 ppm in drinking water) alone or co-treated with melatonin (10 or 20 mg/kg, oral) for 8 weeks. Cognitive function was assessed using the Morris Water Maze (MWM) and Novel Object Recognition Test (NORT). Serum fluoride, brain SIRT1, oxidative stress markers (malondialdehyde [MDA], superoxide dismutase [SOD]), apoptosis markers (caspase-3, B-cell lymphoma 2 [Bcl-2]), inflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6]), acetylcholinesterase (AChE) levels, and hippocampal histopathology were evaluated. Results: NaF exposure significantly elevated serum fluoride, reduced brain SIRT1, increased oxidative stress, apoptosis, neuroinflammation, AChE activity, and caused hippocampal neuronal damage, leading to impaired learning and memory in both sexes (p < 0.05). Melatonin co-treatment (both doses) significantly attenuated these changes by lowering serum fluoride, restoring SIRT1 levels, reducing MDA, caspase-3, TNF-α, IL-6, and AChE, while increasing SOD and Bcl-2. It also improved behavioral performance in the MWM and NORT and preserved hippocampal neuronal morphology. Effects were comparable between sexes and between the two melatonin doses. Conclusion: Melatonin effectively mitigates fluoride-induced neurotoxicity and cognitive dysfunction in Wistar rats by modulating oxidative stress, neuroinflammation, apoptosis, and SIRT1 signaling. These findings highlight melatonin as a promising neuroprotective agent against environmental fluoride toxicity, with potential translational relevance for fluorosis-endemic areas.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder with multifaceted risk factors, including diet and metabolic dysfunction. The rising prevalence of AD and diabetes has drawn attention to their shared pathophysiological mechanisms. The "cafeteria diet," characterized by high-fat, high-sugar, and energy-dense foods, has emerged as a significant contributor to metabolic dysfunctions, including obesity and insulin resistance, which are risk factors for both diabetes and neurodegenerative diseases. This study explores the effects of the cafeteria diet on cognitive impairment, AD pathology, and its potential role in exacerbating diabetes-related neurological complications. Animal models were subjected to cafeteria diets, mimicking human dietary patterns, to investigate changes in brain structure, amyloid-beta accumulation, tau hyperphosphorylation, and cognitive function. Additionally, metabolic profiling demonstrated the development of insulin resistance and other hallmarks of diabetes, which were closely correlated with the severity of cognitive deficits. Neuropathological analyses revealed exacerbated amyloid-beta accumulation and increased neuroinflammation, linking dietary-induced diabetes to AD pathophysiology. These findings underscore the critical role of dietary habits in modulating the risk and progression of AD, highlighting the importance of interventions targeting metabolic health to mitigate cognitive decline. This study emphasizes the need for further research to unravel the molecular mechanisms underlying the diet-diabetes- AD axis and develop targeted therapeutic strategies.

Immunotherapeutics offer promise for colon cancer treatment but are often limited by tumor heterogeneity. This study reports the development of mannose-functionalized (Mannosylated) liposomes co-encapsulating Levamisole (LEV) and Lipopolysaccharide (LPS) that targets M2-Tumor associated macrophages (TAMs) and enhance therapeutic efficacy. Liposomes were prepared by thin-film hydration method and optimized using Box-Behnken design. FT-IR analysis confirmed mannose conjugation at 1644 cm-1, indicating amide bond formation. The optimized formulation exhibited a particle size of 169.5 ± 0.71 nm, encapsulation efficiencies of 50.28 ± 2.64% (LEV) and 95.76 ± 0.10% (LPS) and demonstrated controlled drug release of LEV in vitro at pH 1.2, 6.8, and 7.4 conditions. In vivo evaluation in CT26 orthotopic colon tumor model showed enhanced tumor localization, significant tumor regression and improved survival outcomes in formulation treated group when combined with 5-fluorouracil (5-FU). qRT-PCR analysis revealed downregulation of M2 macrophage markers (CD206, Arg1). Phagocytosis assay demonstrated significantly higher phagocytic clearance (p < 0.05). Although the delayed-type hypersensitivity (DTH) assay showed a decline in % DTH response, histopathology of spleen and thymus implied enhanced lymphocyte cellularity with acute inflammatory infiltrations confirming elevated immune activation. The Mannosylated liposomal system effectively delivers immunomodulators to modulate the tumor microenvironment and enhance 5-FU based therapy in colon cancer.

Around 100 million individuals with diabetes in India are at risk of developing diabetic wounds in their lifetime. These wounds cause severe reductions in the quality of life of patients due to increased economic burden and risk of limb amputations. Indigenous wound dressings offer cost-effective solutions for the management and healing of such wounds. Loading of bioactive formulations in passive dressing material has led to successful intervention in hampered wound healing cascades. The role of traditional wound healing formulations, such as aloe vera, turmeric, and cinnamon oil extracts loaded in hydrogels, hydrocolloids, sponges and other dressing materials, has been reported earlier. Tamra Bhasma and Yasad Bhasma are two types of Ayurvedic formulations (Bhasmas) cited in the Indian traditional medicinal text “Rasa-shastra”. These Bhasmas have been studied in isolation and show beneficial attributes, such as free radical scavenging, hepatoprotective activity and anti-inflammatory effects. The present work is aimed at studying the combinatorial effect of Tamra Bhasma and Yasad Bhasma in conjunction with the potent anti-microbial “cinnamaldehyde nanoemulsion (NE)” loaded in two different forms of a polyvinyl alcohol (PVA) matrix: hydrogel and sponge. In vitro studies on three cell lines, NIH 3T3, HaCaT and HuVECs, showed sustained release of these Bhasmas and NE, leading to enhanced cell proliferation, cell migration, free radical scavenging and collagen formation. Compared with the PVA hydrogel and sponge controls, the developed bioactive wound dressing shows promise for the healing and management of infected diabetic wounds.

SH2 (Src Homology 2) domains play a crucial role in phosphotyrosine-mediated signaling and have emerged as promising drug targets, particularly in cancer therapy. STAT3 (Signal Transducer and Activator of Transcription 3), which contains an SH2 domain, plays a pivotal role in cancer progression and immune evasion because it facilitates the dimerization of STAT3, which is essential for their activation and subsequent nuclear translocation. SH2 domain-mediated STAT3 inhibition disrupts this binding, reduces phosphorylation of STAT3, and impairs dimerization. This study employed an in silico approach to screen potential natural compounds that could target the SH2 domain of STAT3 and inhibit its function. The phytomolecules (182455) were retrieved from the ZINC 15 database and were docked using various modes like HTVS, SP, and XP. The phytomolecules exhibiting higher binding affinity were selected. MM-GBSA was performed to determine binding free energy, and the QikProp tool was utilized to assess the pharmacokinetic properties of potential hit compounds, narrowing down the list of candidates. Molecular dynamics simulations, thermal MM-GBSA, and WaterMap analysis were performed on compounds that exhibited favorable binding affinities and pharmacokinetic characteristics. Based on docking scores and binding interactions, ZINC255200449, ZINC299817570, ZINC31167114, and ZINC67910988 were identified as potential STAT3 inhibitors. ZINC67910988 demonstrated superior stability in molecular dynamics simulation and WaterMap analysis. Furthermore, DFT was performed to determine energetic and electronic properties, and HOMO and LUMO sites were predicted for electronic structure calculation. Additionally, network pharmacology was performed to map the compounds’ interactions within biological networks, highlighting their multitarget potential. Compound-target networks elucidate the relationships between compounds and multiple targets, along with their associated pathways and help to minimize off-target effects. The identified lead compound showed strong potential as a STAT3 inhibitor, warranting further validation through in vitro and in vivo studies.

Drug-induced liver injury is a major clinical and pharmacological challenge, often driven by oxidative stress and inflammation. This study aimed to develop a sesamol derivative with enhanced hepatoprotective efficacy via NRF2/HO-1 pathway activation. A focused virtual library of sesamol derivatives was generated through reaction-based enumeration and evaluated utilizing molecular docking and molecular dynamics simulations. Among 189 designed compounds, compound 133840-3CaBen (SMD) demonstrated superior binding to the KEAP1-NRF2 interface and was selected for synthesis and biological evaluation. In vitro antioxidant assays revealed that SMD exhibited a 4.5-fold lower IC50 compared to sesamol. In HepG2 cells, SMD conferred up to 62.99% protection against paracetamol-induced toxicity. In vivo, SMD (100 & 200 mg per kg b.w. orally) significantly restored liver enzyme profiles, and antioxidant markers (CAT, GSH, GPx, SOD) and reduced MDA levels. ELISA analysis confirmed NRF2, HO-1, and γ-GCS upregulation with a concomitant decrease in TNF-α and IL-6. Histopathological examination of H&E-stained liver sections corroborated these findings, showing preserved hepatic architecture with minimal necrosis, inflammation, and vacuolation, especially in the SMD group, comparable to silymarin. Collectively, our findings suggest that structural modification of sesamol into SMD confers hepatoprotection, likely through upregulation of NRF2/HO-1 pathway proteins. These findings highlight SMD as a promising lead compound for developing NRF2-targeted hepatoprotective agents.

Atherosclerosis is a serious cardiovascular disease because of its asymptomatic behavior at its initial stage. This study investigates the hemodynamics in an idealized stenosed carotid artery using Fluid - Structure Interaction (FSI) approach to enumerate the interaction of arterial wall and blood flow. This study evaluated the hemodynamic parameters such as velocity, wall shear stress (WSS), oscillatory shear index, relative residence time (RRT), endothelial stimulation potential (ESP), vorticity and helicity. A non - Newtonian Carreau - Yasuda model was used to mimic the non - Newtonian behavior and a linear isotropic material was used for arterial wall. An idealized plaque was added in the arterial wall at the sinus region that induced approximately 20 % stenosis. The results reveal signification variations in the hemodynamic patterns near the stenosis, with increased velocity, high OSI, and reduced WSS at critical locations. Elevated OSI at the sinus suggest turbulent flow patterns and disruption of endothelial layers that potentially accelerate atherosclerosis progression. The study also highlights the plaque induced flow disturbances that include recirculation zones and altered helicity contours that impair particle retention and plaque growth. The relative residence time metric (RRT) emphasize prolonged blood residence at the sinus, contributing to accumulation of lipids and progression of plaque. The study underscores the importance of FSI in capturing realistic behavior as compared to rigid wall assumption. The study gives important information about how atherosclerosis develops and how vulnerable plaque is. Future research that incorporates patient-specific geometries and hyperelastic artery properties could improve these findings and increase predictive models for ischemic stroke and related cardiovascular disorders.

Glioblastoma (GBM) is the most prevalent and deadly primary brain tumor. The current treatment for GBM includes adjuvant chemotherapy with temozolomide (TMZ), radiation therapy, and surgical tumor excision. There is still an issue because 50% of patients with GBM who get TMZ have low survival rates due to TMZ resistance. The activation of several DNA repair mechanisms, such as Base Excision Repair (BER), DNA Mismatch Repair (MMR), and O-6- Methylguanine-DNA Methyltransferase (MGMT), is the main mechanism via which TMZ resistance develops. The zinc-finger DNA-binding enzyme poly (ADP-ribose) polymerase-1 (PARP1), which is activated by binding to DNA breaks, affects the activation of the MGMT, BER, and MMR pathway deficiency, which results in TMZ resistance in GBM. PARP inhibitors have been studied recently as sensitizing medications to increase TMZ potency. The first member of the PARP inhibitor family to be identified was Olaparib. It inhibits PARP1 and PARP2, which causes apoptosis in cancer cells and DNA strand break. Olaparib is currently investigated as a radio- and/or chemo-sensitizer in addition to being used as a single agent because it may increase the cytotoxic effects of other treatments. This review addresses Olaparib and its significance in treating TMZ resistance in GBM.

BACKGROUND:This study aims to identify patterns and predictors of medical device-related adverse events (MDAEs) among radiotherapy patients. Understanding MDAEs is crucial for optimizing patient safety during radiotherapy. METHODOLOGY:An observational study conducted from August to December 2023 involved 139 patients undergoing radiotherapy. Demographics, clinical characteristics, and AE reports were collected from patient datasheets and analyzed using SPSS Version 28. RESULTS:Study findings revealed that patients with head and neck cancer were significantly associated with higher rates of skin (OR: 3.56, CI: 1.59-7.96) and mucous membrane reactions. Specific dose ranges, particularly 800-2800 cGy, also predict mucous membrane reactions (OR: 11.12, CI: 3.42-36.1). Furthermore, smokeless habits significantly influenced both skin (OR: 6.04, CI: 1.99-18.3) and mucous membrane reactions (OR: 8.77, CI: 2.57-29.9). In contrast, head and neck cancer patients had reduced likelihoods of pharynx reactions (OR: 0.37, CI: 0.13-1.00), particularly with doses between 2801 and 4800 cGy (OR: 0.45, CI: 0.96-21.6). CONCLUSION:This study identified a few significant predictors for the occurrence of various types of MDAEs among patients undergoing radiotherapy. Reporting MDAEs can prevent adverse effects caused by medical devices and enhance radiotherapy safety.

The most common type of blood cancer, leukemia, presents global therapeutic challenges like heterogeneity regarding age, sex, race, and a multiple pool of oncogenes and their complex network. In the last few years, nanotechnology has become the potential solution in leukemic resistance, chemotherapeutic failure, and disease-remission risk. Interestingly, the nanocarriers alone sometimes cannot overcome leukemia's obstacles, which demands a more advanced flagship in the nanocarrier segment like modification of the nanocarrier system, external stimuli for synergistic antileukemic effect, etc. This review has highlighted the need for emerging nanocarriers like exosome-like vesicles, nanodiamonds, nanoflower, etc. and biomimetic nanocarriers that reach the bone marrow niche. Notably, the role of nanoparticle-based vaccines in a disease-remission-free life and novel technology for nanocarrier delivery (microfluidics and plasmonic nanobubbles) have been discussed. This review also focuses on the clinical transition barriers of nanocarriers from the research laboratory. The continual research on novel nanocarriers and integration of new technologies to deliver the nanocarriers in the right way is paving the path for enhanced selectivity and efficacy in leukemia. The promising results in precise drug delivery and leukemic cell destruction are showing its great clinical prospects.