Organisms ranging from cyanobacteria to humans use circadian rhythmicity to adapt to the daily changes in their environment. In humans, the malfunction of this rhythmicity (e.g. familial advanced sleep phase syndrome) or the conflict of these rhythms with either clinical treatments (e.g. chemotherapy) or atypical environments (e.g. plane travel or shift work) may lead to social and health consequences. The mammalian gene network responsible for circadian rhythms shares a high degree of homology with the network found in the fruit fly, Drosophila. In Drosophila, the interaction and nuclear transport of two proteins, PERIOD and TIMELESS, is a key regulatory point within the circadian cycle where factors including light adjust the phase of rhythmicity. Recent experimental observations have suggested this cytoplasmic association remains stable over a long duration with a precipitous dissociation immediately prior to nuclear transport, forming an interval “timer” within the context of the larger circadian cycle. Refining our previously constructed mathematical model of circadian rhythmicity in Drosophila, we investigate several mechanisms through which this timer may be created. Potential mechanisms are compared based on consistency with available experimental observations. Elucidating the regulatory mechanism responsible for this interval timer may lead to possible therapeutic targets for malfunctioning clocks, or enhance the ability to control internal clocks.