Department of Pharmaceutical Sciences, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Department of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
J Control Release. 2021 Jan 10;329:585-597. doi: 10.1016/j.jconrel.2020.09.052. Epub 2020 Sep 30.
Successful treatment of pancreatic cancer remains a challenge due to desmoplasia, development of chemoresistance, and systemic toxicity. Herein, we synthesized (6-(3-hydroxy-4-methoxylphenyl)pyridin-2-yl) (3,4,5-trimethoxyphenyl)methanone (CH-3-8), a novel microtubule polymerization inhibitor with little susceptible to transporter-mediated chemoresistance. CH-3-8 binding to the colchicine-binding site in tubulin protein was confirmed by tubulin polymerization assay and molecular modeling. CH-3-8 disrupted microtubule dynamics at the nanomolar concentration in MIA PaCa-2 and PANC-1 pancreatic cancer cell lines. CH-3-8 significantly inhibited the proliferation of these cells, induced G2/M cell cycle arrest, and led to apoptosis. CH-3-8 is hydrophobic with an aqueous solubility of 0.97 ± 0.16 μg/mL at pH 7.4. We further conjugated it with dodecanol through diglycolate linker to increase hydrophobicity and thus loading in lipid-based delivery systems. Hence, we encapsulated CH-3-8 lipid conjugate (LDC) into methoxy poly(ethylene glycol)-block-poly(2-methyl-2-carboxyl-propylene carbonate-graft-dodecanol) (mPEG-b-PCC-g-DC) polymeric nanoparticles (NPs) by solvent evaporation, resulting in a mean particle size of 125.6 ± 2.3 nm and drug loading of 10 ± 1.0% (w/w) while the same polymer could only load 1.6 ± 0.4 (w/w) CH-3-8 using the same method. Systemic administration of 6 doses of CH-3-8 and LDC loaded NPs at the dose of 20 mg/kg into orthotopic pancreatic tumor-bearing NSG mice every alternate day resulted in significant tumor regression. Systemic toxicity was negligible, as evidenced by histological evaluations. In conclusion, CH-3-8 LDC loaded NPs have the potential to improve outcomes of pancreatic cancer by overcoming transporter-mediated chemoresistance and reducing systemic toxicity.
由于细胞外基质形成、化学抗性的发展和全身毒性,成功治疗胰腺癌仍然是一个挑战。在此,我们合成了(6-(3-羟基-4-甲氧基苯基)吡啶-2-基)(3,4,5-三甲氧基苯基)甲酮(CH-3-8),这是一种新型的微管聚合抑制剂,不易受到转运体介导的化学抗性的影响。通过微管聚合测定和分子建模证实,CH-3-8 结合到微管蛋白中的秋水仙碱结合位点。CH-3-8 在纳摩尔浓度下破坏了 MIA PaCa-2 和 PANC-1 胰腺癌细胞系中的微管动力学。CH-3-8 显著抑制这些细胞的增殖,诱导 G2/M 细胞周期停滞,并导致细胞凋亡。CH-3-8 具有疏水性,在 pH 7.4 时的水溶解度为 0.97±0.16μg/mL。我们进一步通过二甘醇将其与十二醇偶联,以增加疏水性,从而在基于脂质的递药系统中增加载药量。因此,我们通过溶剂蒸发将 CH-3-8 脂质偶联物(LDC)包封到甲氧基聚乙二醇-嵌段-聚(2-甲基-2-羧基-丙交酯-接枝-十二醇)(mPEG-b-PCC-g-DC)聚合物纳米粒(NPs)中,得到平均粒径为 125.6±2.3nm,药物载量为 10±1.0%(w/w),而相同的聚合物通过相同的方法只能载 1.6±0.4(w/w)CH-3-8。在荷瘤 NSG 小鼠中,每天交替给予 6 次 20mg/kg 的 CH-3-8 和 LDC 负载 NPs,系统给药,结果肿瘤明显消退。组织学评价表明,全身毒性可忽略不计。总之,CH-3-8 LDC 负载 NPs 具有通过克服转运体介导的化学抗性和降低全身毒性来改善胰腺癌治疗效果的潜力。