7ACC1 (D 142) selectively affects a single part of the MCT symporter translocation cycle, leading to strict inhibition of lactate influx. This singular activity is associated with antitumor effects less prone to resistance and side effects.

7-(Diethylamino)coumarin-3-carboxylic acid对乳酸摄入的影响研究发现，在使用氧化癌细胞进行的实验中，这些细胞已知能够维持其体外乳酸作为能量燃料的摄取能力，而对于高度糖解的细胞，该化合物对乳酸排出没有影响。相应地，在表达MCT1和MCT4亚型的氧化人类宫颈癌细胞SiHa和Hela中，7-(Diethylamino)coumarin-3-carboxylic acid显著抑制了乳酸摄入和细胞增殖，而公认的MCT1/MCT2抑制剂AR-C155858未能如此。7-(Diethylamino)coumarin-3-carboxylic acid 在表达MCT1/4的咽部鳞状FaDu肿瘤细胞中的效果得到了确认。这些观察结果强烈表明，7-(Diethylamino)coumarin-3-carboxylic acid 通过MCT1和MCT4抑制乳酸的进入，抑制MCT1（乳酸摄取的主要途径），防止了任何补偿性效应。

7-(Diethylamino)coumarin-3-carboxylic acid被设计用于选择性干扰富含乳酸的肿瘤微环境中的乳酸流动。该化合物家族的两种化合物的药理特性，包括其对乳酸进出口和抗肿瘤活性的影响，通过使用人类癌症细胞系和小鼠异种移植模型进行了研究。7-(Diethylamino)coumarin-3-carboxylic acid意外地抑制了表达MCT1和MCT4转运蛋白的肿瘤细胞中的乳酸进口，但不抑制乳酸出口。7-(Diethylamino)coumarin-3-carboxylic acid延缓了宫颈SiHa肿瘤、结肠HCT116肿瘤和原位MCF-7乳腺肿瘤的生长。通过不表达功能性MCT的膀胱UM-UC-3癌细胞缺乏活性，确认了MCT目标的结合。7-(Diethylamino)coumarin-3-carboxylic acid还抑制了使用顺铂治疗后SiHa肿瘤的复发。最后，我们发现，与AR-C155858不同，7-(Diethylamino)coumarin-3-carboxylic acid没有阻止底物模拟药物3-溴丙酸（3BP）通过MCT1进入细胞，并有助于在3BP治疗后抑制肿瘤复发。

Cervix cancer cells(SiHa and HeLa) and mammary cancer cells (MDA-MB-231, MCF-7) were cultured in Dulbecco's Modified Eagle Medium (DMEM), and HCT-116 colorectal cancer cells in McCoy's 5A medium, UM-UC-3 bladder transitional cell carcinoma and pharynx squamous carcinoma FaDu cells in Eagle's MEM, HL-60 acute promyelocytic leukemia cells and K562 chronic myelogenous leukemia cells were cultured in suspension in RPMI-1640 medium. For treatments, SiHa, Hela, and MDA-MB231 cells were seeded in flat-bottom 96-well plates in DMEM. After overnight incubation, the culture medium was replaced by 100 μL of medium containing 7ACC1, 7ACC2, AR-C155858, or 3BP. Nonadherent HL-60 and K562 cells were directly treated in flat-bottom 96-well plates in RPMI medium. Antiproliferative effects were determined using MTT or Presto Blue assay for adherent cells or cell counting using a Cellometer Auto T4 for nonadherent cells.

Eight-week-old NMRI female nude mice (Elevage Janvier) were injected subcutaneously with 2 × 106 SiHa cells, 2 × 10^6 HCT-11^6 cells, or 5 × 10^6 UM-UC-3 cells. An orthotopic breast cancer model was also used with MCF-7 tumor cells injected into the mammary fat pad of mice; a 17β-estradiol pellet had first been subcutaneously implanted in these mice as previously described . When tumors reached a mean diameter of 5 mm, 7-(Diethylamino)coumarin-3-carboxylic acid compounds (3 mg/kg) or AR-C155858 (3 mg/kg) were daily injected intraperitoneally; in some experiments, 7-(Diethylamino)coumarin-3-carboxylic acid treatment was combined with cisplatin (5 mg/kg) injected intraperitoneally at days 0 and 7 (7-(Diethylamino)coumarin-3-carboxylic acid administered daily except at days 0 and 7) or 3BP(3 mg/kg) injected i.p. from day 0 to 4 and day 7 to 11 (7-(Diethylamino)coumarin-3-carboxylic acid administered together with 3BP). Cisplatin and 3BP were also administered alone and control mice were injected with vehicle (dimethyl sulfoxide). Tumor sizes were tracked with an electronic calliper and determined using the formula: (length × width^2 × π)/6.