FTY720プロドラッグ(pro-FTY)がリンパ球減少を回避して乳がんの増殖を抑制することを明らかに~今後化学療法と併用することでさらなる相乗効果が生じる可能性にも期待~

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2025-06-19 兵庫医科大学,理化学研究所,東京科学大学,大阪国際大

兵庫医科大学らの共同研究チームは、FTY720のプロドラッグ型「pro‑FTY」を開発し、乳がんに選択的に作用しながら、リンパ球減少の副作用を回避することを実証しました。in vitroでは多剤耐性乳がん細胞株への生存阻害効果が確認され、正常乳腺細胞には影響なし。患者由来オルガノイドでもパクリタキセルやドキソルビシンに耐性を示す中、pro‑FTYは一致して効果を発揮。マウス実験では、静注後に腫瘍にFTY720が蓄積し、腫瘍増殖を抑制。リンパ球減少は観察されませんでした。アクロレイン応答性DDSにより、腫瘍選択的作用を実現しており、標準治療との併用による相乗効果も期待されます。本成果はS1P標的抗がん剤の臨床開発に基盤を築く重要な一歩です(掲載誌:Cancer Research Communications)。

<関連情報>

アクロレインをベースとした薬物送達システムにより、リンパ球減少を伴わない乳癌における腫瘍特異的スフィンゴシン-1-リン酸標的療法が可能になる An Acrolein-Based Drug Delivery System Enables Tumor-Specific Sphingosine-1-Phosphate Targeting in Breast Cancer without Lymphocytopenia

Masayuki Nagahashi;Miki Komatsu;Sayaka Urano;Mamiko Kuroiwa;Yuria Takahashi;Koji Morimoto;Ambara R. Pradipta;Katsunori Tanaka;Yasuo Miyoshi
Cancer Research Communications  Published:June 18 2025
DOI:https://doi.org/10.1158/2767-9764.CRC-25-0023

Pro-FTY, a novel anticancer prodrug that is converted to its active form (FTY720) after reacting with acrolein, which is overproduced in breast cancer cells. A, Synthesis of pro-FTY. FTY720 was reacted with compound 1 to synthesize pro-FTY. B, Schematic representation of the reaction of pro-FTY with acrolein in cancer cells to produce the active drug, FTY720, which can block S1P signaling. C, Acrolein expression in breast cancer tissue and normal breast tissue. Fluorescence microscopy images of acrolein expression in cancer (c) tissue and normal (n) breast tissue labeled with the CTS probe (red) and 4′,6-diamidino-2-phenylindole (DAPI; blue). Scale bars, 100 nm. D–G, Dose–response bar graphs for each drug in breast cancer and normal mammary cell lines. The IC50 values of FTY720 (D) and pro-FTY (E) were determined using the MDA-MB-468 breast cancer cell line by performing WST-8 assays, and the IC50 values of FTY720 (F) and pro-FTY (G) were determined in the noncancer, mammary epithelial cell line, MCF-10A.

Abstract

We developed a novel FTY720 prodrug (pro-FTY) that specifically inhibits sphingosine-1-phosphate signaling in cancer cells using a novel drug delivery system that reacts with acrolein. Our objective was to evaluate the efficacy and safety of pro-FTY in preclinical experiments. Ten breast cancer cell lines, two multidrug-resistant cell lines, and one normal mammary cell line were used to compare the IC50 values of pro-FTY with those of other drugs. Patient-derived organoids (PDO) were established and utilized for IC50 value comparisons. Drug efficacy was tested in mice bearing either syngeneic 4T1 cell tumors or patient-derived xenograft tumors, and blood analysis (including mass spectrometry) was performed. FTY720 and pro-FTY inhibited the survival of all breast cancer cell lines, including multidrug-resistant cells resistant to paclitaxel or doxorubicin. Unlike pro-FTY, FTY720 inhibited the survival of normal breast cell lines, suggesting that pro-FTY does not affect normal breast cells. Pro-FTY showed reproducible activity against multidrug-resistant PDOs, whereas paclitaxel and doxorubicin did not. Mass spectrometric analysis of pro-FTY–treated mice showed that FTY720 accumulated in tumors but was barely detectable in blood. Importantly, lymphocytopenia occurred in FTY720-treated mice but not in pro-FTY–treated mice. Furthermore, intravenous pro-FTY treatment significantly suppressed tumor growth in mice bearing patient-derived xenograft tumors generated from multidrug-resistant PDOs. In conclusion, pro-FTY inhibited breast cancer, including multidrug-resistant breast cancer, while avoiding lymphocytopenia, highlighting its clinical potential.

Significance:

Pro-FTY selectively inhibits sphingosine-1-phosphate signaling in cancer cells using a novel acrolein-responsive drug delivery system that reacts with acrolein. Pro-FTY does not inhibit normal cell growth, thus avoiding lymphocytopenia. Pro-FTY is effective against multidrug-resistant breast cancer with a unique mechanism of action, highlighting its translational and therapeutic potential.

医療・健康
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