eCF506 is a potent, orally active inhibitor of the non-receptor tyrosine kinase Src, with an IC50 value of <0.5 nM. eCF506 inhibits the phosphorylation of SRC and FAK at low nanomolar levels, with complete inhibition of phosphorylation at 100 nM. eCF506 inhibits only SFK, with sub-nanomolar IC50 values for SRC and YES (IC50=0.5, 2.1 nM). It is noted that eCF506 shows a large difference in activity between ABL and its primary target, SRC (>950-fold difference)[1].
eCF506 细胞实验
Cell Line
Concentration
Treated Time
Description
References
5637 cells
100 nM
72 hours
To evaluate the enhanced effect of eCF506 combined with cisplatin on apoptosis and cell death rates in 5637 cells. Results showed that eCF506 synergized with cisplatin to significantly increase apoptosis and cell death rates in 5637 cells.
Commun Biol. 2025 Jan 10;8(1):36
T24 cells
100 nM
24 hours
To evaluate the inhibitory effect of eCF506 on the proliferation, migration, and invasion of bladder cancer cells. Results showed that eCF506 significantly inhibited the proliferation, colony formation, migration, and invasion of T24 cells and arrested the cell cycle in the G0/G1 phase.
Commun Biol. 2025 Jan 10;8(1):36
MCF7
0.1 µmol/L
5 days
To evaluate the effect of eCF506 on proliferation of ER+ breast cancer cells, results showed eCF506 exhibited higher anti-proliferative activity in ER+ cell lines.
Cancer Res. 2021 Nov 1;81(21):5438-5450
MDA-MB-231
0.1 µmol/L
6 hours
To study the effect of eCF506 on SRC-FAK complex formation, results showed eCF506 decreased the recovery of FAK protein by 50%.
Cancer Res. 2021 Nov 1;81(21):5438-5450
MDA-MB-231
40 nmol/L
72 hours
To evaluate the sensitivity of ILK knockout cells to eCF506, results showed that ILK knockout enhanced the inhibitory effect of eCF506.
Cancer Res. 2022 Feb 15;82(4):632-647
MDA-MB-231 cells
1-10,000 nM
5 days
Evaluate the inhibitory effect of compounds on MDA-MB-231 cell proliferation
J Med Chem. 2016 May 26;59(10):4697-710
MCF7 cells
100 μM
5 days
Evaluate the inhibitory effect of compounds on MCF7 cell proliferation
J Med Chem. 2016 May 26;59(10):4697-710
eCF506 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
HCT116 xenograft model
Oral
50 mg/kg
Once daily for 3 days
Evaluate the inhibitory effect of eCF506 on SRC phosphorylation in vivo
J Med Chem. 2016 May 26;59(10):4697-710
C57BL/6 mice
Cell-derived xenograft model (CDX)
Intraperitoneal injection
20 mg/kg
Every 2 days until the end of the experiment
To evaluate the anti-tumor effect of eCF506 in the CDX model. Results showed that eCF506 significantly inhibited tumor growth, and no obvious adverse effects were observed.
To evaluate the antitumor effect of eCF506 in immunocompetent mice, results showed potent antitumor activity during the treatment phase and delayed tumor relapse post-treatment.
Cancer Res. 2021 Nov 1;81(21):5438-5450
Immunodeficient Rag2-Il2rg double knockout mice
MDA-MB-231 xenograft model
Oral gavage
40 mg/kg body weight
Once daily for 35 days
To evaluate the growth inhibitory effect of eCF506 on ILK knockout tumors, results showed that eCF506 completely blocked the growth of ILK knockout tumors.
Cancer Res. 2022 Feb 15;82(4):632-647
eCF506 动物研究
Animal study
The oral bioavailability of eCF506 was moderate (25.3%). Phosphorylated-SRCY416 was significantly reduced in xenograft sections of mice treated with eCF506 compared to untreated animal controls[1].
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