SLLN-15 is an oral active, selective and potent enhancer of autophagy. SLLN-15 activates cytostatic macroautophagy/autophagy in triple-negative breast cancer (TNBC) [1].

SLLN-15 (0, 1, 5, 10, 25 μM) treatment for 24 h significantly decreases overall cell viability of breast cancer cells in a dose-dependent manner [1]. SLLN-15 (100 nM and 1000 nM, 7 days) is able to equally inhibit the colony formation abilities of several breast cancer cell lines [1]. Overall, SLLN-15 induces a dose-dependent anti-proliferative activity in the TNBC cell lines MDA-MB-231 and BT-20 via induction of autophagy and autophagic flux. This induction is associated with a selective inhibition of AKT-MTOR signaling. Cell Viability Assay [1] Cell Line: TNBC cell lines BT-20 and MDA-MB-231. Concentration: 0, 1, 5, 10, 25 μM. Incubation Time: 24 hours. Result: Inhibited the proliferation of two TNBC cell lines, BT-20 and MDA-MB-231. Cell Viability Assay [1] Cell Line: TNBC cell lines (MDA-MB-231, BT-20, 4T1, MDA-MB-468), MCF-7 ( ERBB2 - ), SKBR-3 ( ERBB2 + ) and HEK293T. Concentration: 100 nM and 1000 nM. Incubation Time: 7 days. Result: Equally inhibited the colony formation abilities of several breast cancer cell lines.

SLLN-15 (30mg/kg, PO, 3 times a week) not only inhibits the growth of TNBC in animal model, but also TNBC cell progression to metastases [1]. In general, oral SLLN-15 reveals a potent anticancer and anti-metastatic activity in mice bearing TNBC [1]. Animal Model: BALB/c mice or SCID mice transplanted with mouse mammary carcinoma 4T1 cells and human breast adenocarcinoma MDA-MB-231 cells (1 X 10 6 cells/ each mouse) [1] Dosage: 30mg/kg. Administration: PO, 3 times a week for 40 days. Result: Tumor allografts grew at a slower rate compared to control groups. Significant inhibition of the number of lung metastases as visualized.