Current Pharmaceutical Design - Volume 32, Issue 7, 2026

Sorafenib is a first-line treatment for patients with advanced hepatocellular carcinoma (HCC), but its clinical efficacy is often compromised by the acquisition of drug resistance. Various cancers, including HCC, are affected by long non-coding RNA (lncRNA), but the mechanisms underlying HCC sorafenib resistance have not been extensively studied. This article aims to summarize the recently reported pathways associated with sorafenib resistance and discusses potential applications for the treatment of HCC.

Relevant studies on the resistance of HCC to anti-tumor drugs were retrieved from PubMed. Given the compelling evidence that sorafenib is an effective treatment for advanced HCC, we analyzed the research papers on lncRNA and sorafenib resistance in HCC in the PubMed system in the past decade and found that lncRNA may be involved in sorafenib resistance in HCC through multiple pathways.

lncRNA is widely involved in the resistance mechanism of HCC to sorafenib. Recent studies have revealed that numerous lncRNAs, such as NEAT1, affect the sensitivity of HCC to sorafenib through various mechanisms, including autophagy and AKT signaling pathways.

lncRNAs play a pivotal role in modulating HCC resistance to sorafenib. And lncRNA is expected to become a new solution to the resistance of sorafenib and other targeted drugs.

Acne vulgaris is a prevalent dermatological condition resulting from inflammation, follicular hyperkeratinization, and bacterial growth. Standard treatments, whether topical or oral, frequently encounter challenges such as limited skin penetration, drug instability, and undesirable side effects. The report found that lipid-based nanocarriers have emerged as a promising alternative, demonstrating the potential for enhanced therapeutic effectiveness, better skin bioavailability, controlled drug release, and targeted delivery specifically to sebaceous glands, which help minimize systemic side effects.

This review article aims to explore the therapeutic potential of various lipid nanocarriers, including Solid Lipid Nanoparticles (SLNs), Nanostructured Lipid Carriers (NLCs), liposomes, microemulsions, niosomes, and ethosomes particularly by examining the mechanisms through which they penetrate the stratum corneum and deeper skin layers to enhance drug delivery.

This review comprehensively surveys lipid-based nanocarriers for acne vulgaris treatment, drawing from a systematic literature search across Google Scholar, Science Direct, Scopus, Web of Science, and PubMed for publications between 2015 and 2025. The search strategy employed keywords such as “lipid nanocarrier,” “acne vulgaris,” “animal models,” or “preclinical studies,” and “clinical trials” to capture the research landscape.

The review compiles evidence from multiple preclinical experiments and clinical trials regarding the effectiveness of lipid nanocarriers in managing acne. It explores the different pathways these lipid nanocarriers use to permeate the skin and reach target sites. Additionally, it also covers different patents filed by various researchers focusing on the application of lipid nanocarriers for acne management.

Lipid nanocarriers represent a significant advancement in dermatological drug delivery, particularly for acne management. By leveraging various skin penetration mechanisms to improve drug targeting to the pilosebaceous unit, they offer potential for more effective treatment compared to conventional methods. While promising, ongoing research and development are necessary to overcome current limitations and fully harness the potential of lipid nanocarriers in clinical practice.

This study aims to enhance the oral bioavailability of Nadolol (NDL), a β-blocker used in the management of hypertension, by incorporating it into a liposome-based delivery system. To improve the formulation’s stability, mucoadhesion, and permeability, chitosan coating was applied.

Liposomes were prepared via the ethanol injection method using soy phosphatidylcholine and diacetyl phosphate. Chitosan coating was applied by adding chitosan solution (1% v/v acetic acid) at different chitosan-to-lipid ratios (0.1-0.4 w/w). The optimal formulation was selected based on particle size, PDI, and zeta potential. Characterization included encapsulation efficiency, drug loading, enzymatic stability, drug release, and Caco-2-based cytotoxicity and permeability assays.

The particle size and polydispersity index of the optimized formulations, L1-NDL, L2-NDL, L1C-NDL, and L2C-NDL, were measured as 27.02 ± 0.18 nm, 24.55 ± 0.22 nm, 160.10 ± 3.17 nm, 161.00 ± 2.30 nm, 0.39 ± 0.01, 0.37 ± 0.01, 0.19 ± 0.01, and 0.18 ± 0.02. Encapsulation efficiencies of 56.01 ± 3.70% and 43.87 ± 1.24% were recorded for L1C-NDL and L2C-NDL, respectively, while drug loading capacities were 61.47 ± 2.03% and 67.80 ± 0.74%, respectively. In an enzymatic degradation study, it was found that chitosan coating increased the stability of liposomes in the gastric media. The in vitro release was higher at both pH 1.2 and 6.8. Caco-2 assays confirmed >95% cell viability and enhanced permeability in the apical-to-basolateral direction. In the permeability study, chitosan-coated liposomal formulations demonstrated enhanced transport in the apical-to-basolateral direction, indicating improved intestinal permeability.

Chitosan-coated liposomes improved NDL’s stability and permeability, showing promise as an effective oral delivery system.