In vitro GRPR-binding affinities were determined with competitive binding assays on PC3 human prostate cancer cells.
We further performed saturating (3H -spiroperidol (SPI) binding assays on striatal P2 membrane fractions 2 months later.
The Ki values of all compounds were determined by competitive binding assays on PSMA-positive LNCaP cells against 68Ga-PSMA-10 68Ga-PSMA-10 68Ga-PSMA-10cold reference compounds.
The affinity towards ETAR was confirmed in vitro by cell binding assays on human fibrosarcoma cells HT-10800) and in vivo by murine xenograft imaging studies.
Depending on the preferred metals for each chelator, reference Ga3+, complexes with AlF2+, Zr4+, Cu2+, In3+, Lu3+, Y3+, and Bi3+ were prepared and evaluated in competitive binding assays on Jurkat T - cells with [125I]FC131 as the radioactive reference (Table 1).
The difference between the K d of [125I]-AB-MECA obtained from our kinetic binding approach and the binding data as previously reported in the literature with traditional saturation binding assays on membranes from human A3R-transfected HEK-293 cells [29] was proved to be statistically not significant (P > 0.05) using two-tailed, unpaired Student's t test with Welch's correction (Fig. 6d).
The new compounds 2 8 and, in addition, the two enantiomers of 1 were tested in binding assays on the α1a-AR, α1b-AR, α1d-AR, and the 5-HT1A receptor.
On the basis of the affinities at the α1a-, α1b- and α1d-adrenoceptors and the 5-HT1A receptof of a previous series of sixteen 2-[ 2-phenoxyethyl)aminomethyl]-1,4-benzodioxanes ortho monosubstituted at the phenoxy moiety, a number of ortho disubstituted analogues were designed, synthesized in both the enantiomeric forms and tested in binding assays on the same receptors.
To determine whether STAT3 or STAT5 signalling are functional in CLTC-ALK in DLBCL, we performed DNA binding assays on lysates of LM1 and Karpas422 cells treated with DMSO or TAE-684 10 nM for 4 h.
To further investigate this, we performed radioligand binding assays on selected mutants.
