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Ceruletide, an analog of cholecystokinin octapeptide: New perspectives on its efficacy

Ceruletide is the international nonproprietary name of caerulein, a decapeptide originally isolated from the skin of the Australian frog Hyla caerulea more than 30 years ago (2). Although caerulein does not exist in mammals, including humans, it closely resembles cholecystokinin octapeptide (CCK-8) in the C-terminal amino acid sequence (Fig. 1) and possesses a virtually identical spectrum of biological activities. Because ceruletide induces a variety of CCK-8-like effects on the digestive organs (e.g., stimulation of gallbladder contraction, pancreatic enzyme secretion, and intestinal motility), it was initially thought to be potentially useful for examining digestive functions and treating intestinal disease (100). Actually, ceruletide has been clinically used in cholecystography (80). Since the discovery of CCK-containing neurons in the brain by Vanderhaeghen et al. (95) in the mid-1970s, the interest in CCK has primarily focused on its physiological roles in the CNS. Evidence for the coexistence of CCK and dopamine in the midbrain neurons, as demonstrated by Hökfelt et al. (33,34), had a striking influence on the subsequent investigations in this field. This evidence led to an intriguing hypothesis that CCK may be a neuromodulator of dopaminergic functions in the mesolimbic systems. Numerous studies have focused on the interaction between CCK and dopamine, which suggested that exogenously administered CCK and its related compounds might possibly modulate dopaminergic activity (85,94). Accordingly, ceruletide has been considered to be a candidate as a new treatment of neuropsychiatric disease, in which pathophysiological dopaminergic dysfunction has been assumed to exist. Moreover, in the early 1980s, Zetler (103,104) reported a variety of behavioral effects of ceruletide in mice (e.g., the induction of sedation, catalepsy, ptosis, and hypothermia, and the antagonism of nociception, methylphenidate-induced stereotypy, picrotoxin-induced convulsions and indole alkaloids-