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ASO
FUEL · 2022 · IF 8.035

Alkylation catalyzed by H2SO4: Promoting effects of ASO on the solubility of isobutane in acid phase

Yangyang Xin,Yufeng Hu,Yichuan Wang,Siqi Jiang,Mengchen Li,Kebin Chi,Shang Zhang,Fei Gao,Chunxiao Ren,Shuai Zhang,Chenglong Ma

For alkylation catalyzed by H 2 SO 4 , the promotion of solubility of isobutane in H 2 SO 4 is of major importance to the enhancement of quality of alkylates. ASO (acid-soluble oils or conjunct polymers or red oil) are the potential co-catalyst to improve the solubility of isobutane and to optimize the interfacial characteristics of acid/hydrocarbon dispersions. On the basis of the calculation results of COSMO-RS method, we found that the solubility of isobutane in H 2 SO 4 was obviously increased upon the addition of most ASO molecules. Moreover, a better dissolution of isobutane in H 2 SO 4 can be achieved by adding the hydrocarbons like paraffins and cycloparaffins into H 2 SO 4 . On the basis of these findings, two cycloparaffins were selected and used as the co-catalyst (the co-catalysts A and B) to improve the performance of the H 2 SO 4 catalyst. The alkylation results showed that these cycloparaffins enhanced the quality of alkylates. In particular, upon the addition of the co-catalyst B, the RON (research octane number) value, the TMP/DMH (trimethylpentane/dimethylhexane) ratio, and the contents of C8 and TMP (trimethylpentane) were increased significantly from 92.67 and 6.51, 68.25% and 59.10% to 94.38 and 6.97, 74.81% and 65.34%, and the consumption of the H 2 SO 4 catalyst was reduced by 38%.

CAS / MDL: 67-64-1
研究领域: 化学工程 · 催化科学
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Molecular Therapy-Nucleic Acids · 2023 · IF 8.8

Modified ASO conjugates encapsulated with cytidinyl/cationic lipids exhibit more potent and longer-lasting anti-HCC effects

Yufei Pan,Jing Guan,Yujing Gao,Yuejie Zhu,Huantong Li,Hua Guo,Qianyi He,Zhu Guan,Zhenjun Yang

Antisense oligonucleotides (ASOs) are a class of therapeutics targeting mRNAs or genes that have attracted much attention. However, effective delivery and optimal accumulation in target tissues in vivo are still challenging issues. CT102 is an ASO that targets IGF1R mRNA and induces cell apoptosis. Herein, a detailed exploration of the tissue distribution of ASOs delivered by liposomes was carried out. A formulation that resulted in increased hepatic accumulation was identified based on multiple intermolecular interactions between DCP (cytidinyl/cationic lipid DNCA/CLD and DSPE-PEG) and oligonucleotides, including hydrogen bonding, π-π stacking, and electrostatic interactions. The structurally optimized CT102s present a novel strategy for the treatment of hepatocellular carcinoma. The gapmer CT102 MOE5 and conjugate Glu-CT102 MOE5 showed superior antiproliferation and IGF1R mRNA suppression effects at 100 nM in vitro and achieved greater efficacy at a lower dose and administration frequency in vivo . Combined transcriptome and proteome analyses revealed that additional associated targets and functional regulations might simultaneously exist in ASO therapy. These results showed that a combination of lipid encapsulation and structural optimization in the delivery of oligonucleotide drugs has favorable prospects for clinical application.

CAS / MDL: 284461-73-0
研究领域: 分子生物学 · 肿瘤学 · 药物递送系统
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Advanced Healthcare Materials · 2025 · IF 9.6

A Galactose-Engineered Dual-Responsive Nanocarrier for ASO/CRISPR-Cas9 Delivery to Inhibit HBV Replication

Liuxian Chen,Qin Huang,Yongjie Liu,Ke Chen,Qing Yang,Hua Tang,Dan Wang,Zhenrong Tang

Complete hepatitis B virus (HBV) cure is hindered primarily by the stable persistence of covalently closed circular DNA (cccDNA). Gene editing approaches to eradicate HBV by targeting cccDNA face challenges and limitations due to suboptimal editing efficiency and substantial off-target effects. Herein, a combinatorial therapeutic strategy is developed that integrates CRISPR/Cas9-mediated cccDNA disruption with an antisense oligonucleotide (ASO)-targeted degradation of pregenomic RNA (pgRNA). To overcome delivery challenges, a hepatocyte-targeting nanocarrier (UACPG) is engineered, featuring low immunogenicity, high payload capacity, and dual-stimuli responsiveness. The UACPG platform enabled liver-specific delivery through surface-conjugated targeting ligands, followed by on-demand release of Cas9 ribonucleoprotein complexes and ASO via RNase H-dependent degradation and near-infrared (NIR) light activation. The results demonstrated that UACPG can effectively reduce HBV replication and viral antigen levels, while significantly lowering cccDNA in hydrodynamic HBV-infected mouse models, with no significant off-target effects observed. This nanocarrier achieved the spatiotemporally controlled release of gene-editing systems in vitro and in vivo, significantly inhibiting the replication of HBV, thereby establishing an innovative technological platform for developing curative HBV therapies.

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EUROPEAN POLYMER JOURNAL · 2026 · IF 6.8

Baclofen-functionalized glycogen nanoparticles for GABAB receptor-mediated lung cancer cell-targeted delivery of survivin ASO

Zhou Cheng,Honghui Huang,Shiying Li,Yefan Peng,Yehui Lu,Ming Huang,Huijie Zhang,Wei Sun

As an inhibitor of apoptosis protein, survivin attracts growing interest as a oncotarget because it is highly expressed in various cancers but lacks expression in normal tissues. Although silencing survivin mRNA using antisense oligonucleotides (ASO) presents a potential strategy for lung cancer treatment, the application of ASO is constrained by multiple barriers, including rapid enzymatic degradation, limited cellular internalization and non-specific tissue distribution. To overcome these challenges, we engineered a novel glyco-nanocarrier by chemically modifying glycogen. Glycogen was aminated (NG) and further conjugated with baclofen (Bac-NG), a ligand and agonist for GABAB receptors overexpressed in lung cancer cells. Bac-NG demonstrated excellent biocompatibility and efficiently complexed with survivin ASO through electrostatic interactions, protecting it from nuclease degradation. Bac-NG significantly improved the internalization of ASO in A549 cells via GABAB receptor-mediated endocytosis. Consequently, Bac-NG/ASO effectively inhibited A549 cell proliferation by triggering apoptosis. This study highlights the therapeutic promise of Bac-NG/ASO for targeted gene therapy in lung cancer

CAS / MDL: 25952-53-8 6066-82-6
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