Chemical structures. (a) N-acyl amides. (b) N-acyl ethanolamides. (c) N-acyl amino acids (elmiric acids) R′ = H, CH₃, (d) N-acyl dopamine. (e) N-acyl GABA (γ-aminobutyric acid).

Time course in HTB-126 breast cancer cells. Cells derived from a human tumor were obtained from ATCC and seeded in 18 wells of four 24 well plates at 2000 cells/well under the conditions described in Section 6.1.1. Following a 24 h incubation period, each plate was treated with vehicle, N-palmitoyl tyrosine and AJA (N = 6). After 60 min, one plate was subjected to the cell proliferation assay (see Section 6.1.1), a second plate was assayed after 24 h, a third after 48 h and the last after 72 h. Both agents were given at a final concentration of 10 μM from a 100× stock solution in DMSO. Values shown are in relative fluorescence units.

Selective inhibition of human breast cancer cells (HTB-126) versus normal (HTB-125) cells by acylamido analogs. Cells were grown and treated under conditions similar to those described in Figure 2 except that 96 well plates were used and four replicates were done for each point. The cell proliferation assay was performed at 48 h following drug treatment and the values in (A–E) are expressed as a percentage of the vehicle treated wells. In (F), the antagonist rimonabant (10 μM) was added 30 min prior to the treatment with N-palmitoyl tyrosine (10 μM) and the assay performed 48 h later. Here the values are shown as fluorescence units since there are two control treatments.

Effects of acyl dopamide analogs on proliferation of cervical cancer (HeLa) Cells. The cells were seeded in 96 well plates and cultured as described in Section 6.1.1. Treatments were made at 24 h after seeding and the assays performed at 48 h post treatment. Four replicates were done for each and the concentrations are shown as the numbers in brackets in μM units. DH = dihomo. Values are mean ± SEM.