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| As a proof of concept,a non-polar amino acid (valine) was attached to the C20position of SN38 via an ester bond to generate Val-SN38 (Fig. 6B). The exact solubility of the Val-SN38 in lipids was not reported. It was categorised as a lipophilic prodrug given the non-polarity of the attached valine moiety. Val-SN38 improved intracellular accumulation in MCF7 cells by more than 5-fold in comparison to SN38, without inducing significant multiple-drug resistance. Improved accumulation of ValSN38 has been suggested to be due to augmented uptakeviavarious amino acid transporters. The prodrug, however, showed poor stability and readily converted to the inactive carboxylate form in PBS, MCF 7 cell lines and plasma. Further optimisation of the prodrug to better control the conversion rate to the carboxylate form may result in more potent prodrugs. Alternatively, the prodrug may be incorporated into lipid-based formulations to stabilise the lactone form. |
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【答案】應(yīng)助回帖
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gundnir: 金幣+50, 翻譯EPI+1 2014-02-26 01:07:11
gundnir: 金幣+50, 翻譯EPI+1 2014-02-26 01:07:11
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As a proof of concept, a non-polar amino acid (valine) was attached to the C20position of SN38 via an ester bond to generate Val-SN38 (Fig. 6B). The exact solubility of the Val-SN38 in lipids was not reported. It was categorised as a lipophilic prodrug given the non-polarity of the attached valine moiety. 作為一個(gè)概念驗(yàn)證,非極性氨基酸(纈氨酸) 通過(guò)酯鍵附加成至SN38的C20位置生成Val-SN38(圖6 b)，Val-SN38在脂質(zhì)的溶解度未被報(bào)道。這種歸類為親脂性的藥物前體的具有非極性加成纈氨酸的成分。 Val-SN38 improved intracellular accumulation in MCF7 cells by more than 5-fold in comparison to SN38, without inducing significant multiple-drug resistance. Improved accumulation of Val-SN38 has been suggested to be due to augmented uptake via various amino acid transporters. 與SN38相比，Val-SN38 在MCF7細(xì)胞胞內(nèi)積累提高了5倍以上，沒(méi)有引起顯著的多藥耐藥性。Val-SN38的改進(jìn)積累一直被猜想是由于氨基酸轉(zhuǎn)運(yùn)蛋白的吸收增強(qiáng)。 The prodrug, however, showed poor stability and readily converted to the inactive carboxylate form in PBS, MCF 7 cell lines and plasma. Further optimisation of the prodrug to better control the conversion rate to the carboxylate form may result in more potent prodrugs. 然而,該前體藥物表現(xiàn)為穩(wěn)定性差，在PBS,MCF 7細(xì)胞系和細(xì)胞質(zhì)中容易轉(zhuǎn)化為不活躍的羧酸鹽形式。前體藥物的進(jìn)一步優(yōu)化,以更好地控制羧酸鹽形式轉(zhuǎn)化率可能導(dǎo)致更高活性化合物。 Alternatively, the prodrug may be incorporated into lipid-based formulations to stabilise the lactone form. 另外,前體藥物可能以穩(wěn)定的內(nèi)酯形式被納入基于脂質(zhì)的制劑。 作為一個(gè)概念驗(yàn)證，非極性氨基酸(纈氨酸) 通過(guò)酯鍵附加成至SN38的C20位置生成Val-SN38(圖6 b)，Val-SN38的脂溶度未被報(bào)道。這種歸類為親脂性的藥物前體的具有非極性加成纈氨酸的成分。與SN38相比，Val-SN38 在MCF7細(xì)胞胞內(nèi)積累提高了5倍以上，沒(méi)有引起顯著的多藥耐藥性。Val-SN38的改進(jìn)積累一直被猜想是由于氨基酸轉(zhuǎn)運(yùn)蛋白的吸收增強(qiáng)。然而，該前體藥物表現(xiàn)為穩(wěn)定性差，在PBS、MCF 7細(xì)胞系和細(xì)胞質(zhì)中容易轉(zhuǎn)化為不活躍的羧酸鹽形式。隨著前體藥物的進(jìn)一步優(yōu)化，以更好地控制羧酸鹽的轉(zhuǎn)化率可能導(dǎo)致更高活性化合物。另外，前體藥物可能以穩(wěn)定的內(nèi)酯形式被納入基于脂質(zhì)的制劑。 |
2樓2014-02-25 22:31:40
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