1. Analgesic activities of N-cyclopropylmethyl derivatives of (−)-6β-acetylthionormorphine, KT-89 and KT-90 and their interactions with opioid receptors were studied. 2. KT-89 and KT-90, as well as morphine inhibited the twitch response of the guinea-pig ileal preparation to electrical stimulation. Their pD 2 values indicated that KT-89 and KT-90 are about 6.5 and 10 times as potent as morphine, respectively. In guinea-pig ileal preparation KT-89 and KT-90 also behaved as a μ-antagonist. 3. In rabbit vas deferens which contains κ-receptors, these substances inhibited the twitch response to electrical stimulation and were about 6 times as potent as dynorphin. 4. Their effects on specific binding of [ 3H]naloxone (μ-selective ligand), [ 3H]ethylketocyclazocine (κ-selective ligand) and [ 3H] d-Ala 2- d-Leu 5-enkephalin (δ-selective ligand) to the synaptosomal fractions from rat brain were tested. Though both drugs had a nonselectively high affinity to μ-, κ- and δ-receptors, affinities of KT-89 and KT-90 to κ-receptors were about 6 and 13 times higher than that of morphine, respectively. 5. Analgesic activities of KT-89 and KT-90 were 6 and 10 times as potent as morphine in an acetic acid-induced writhing test, and 4 and 5 times as potent in a pressure test. 6. The present results suggest that KT-89 and KT-90 induced analgesic actions are mediated through an activation of κ-receptors. Both the drugs acted as δ-receptor antagonists. Further experiments are needed to study effects of their property as a δ-antagonist on analgesic action.