Table 1.
K1–BSA | K2–BSA | ||||||
---|---|---|---|---|---|---|---|
Immunogen | Ab1* clones | Isotype | Affinity (Ka)§ | Reactivity† | Inhibitor‡ | Reactivity† | Inhibitor‡ |
K1–KLH | Kl–1 | κγ1 | 5·9 × 106 | + | + | – | n/a |
K1–2 | κγ1 | 5·9 × 104 | + | + | + | + | |
K1–4 | κγ1 | 3·8 × 106 | + | + | – | n/a | |
K2–KLH | K2–1 | λγ1 | 1·0 × 106 | + | + | + | + |
K2–2 | κγ1 | 4·0 × 107 | – | n/a | + | + | |
K2–3 | κγ1 | 2·0 × 108 | – | n/a | + | + | |
K2–4 | κγ1 | 6·7 × 105 | + | + | + | + | |
K2–5 | λγ2a | 2·0 × 106 | + | + | + | + |
mAb1 are identified with the designation of the cocaine hapten precursor that elicited them (K1 or K2) followed by a number (K1–1, K1–2, etc., K2–1, K2–2, etc.).
Reactivity was determined by enzyme-linked immunosorbent assay (ELISA) on plates coated with K1–bovine serum albumin (BSA) or K2–BSA.
The inhibitor was soluble cocaine-HCl (1 mg/ml).
Affinity determination was performed with ELISA on plates coated with the homologous conjugate using, as inhibitor, a range of concentrations of cocaine-HCl between 500 μg/ml and 1 ng/ml.