Participants were asked to rate their migraine headache severity with ratings of 0=No pain, 1=Mild pain, 2=Moderate pain, and 3=Severe pain. PF at 2 hours post-dose is defined as a decrease from a moderate or severe migraine headache (Grade 2 or 3) at baseline to no pain (Grade 0) at 2 hours post-dose.

Participants were asked to rate their migraine headache severity with ratings of 0=No pain, 1=Mild pain, 2=Moderate pain, and 3=Severe pain. PR at 2 hours post-dose is defined as a shift from a moderate or severe migraine headache (Grade 2 or 3) at baseline to mild or no pain (Grade 1 or 0) at 2 hours post-dose.

Participants were asked if they experienced any sensitivity to light. The number of participants who experienced no photophobia (sensitivity to light) at 2 hours post-dose was determined.

Participants were asked if they experienced any sensitivity to sound. The number of participants who experienced no phonophobia (sensitivity to sound) at 2 hours post-dose was determined.

Participants were asked if they experienced any nausea. The number of participants who experienced no nausea at 2 hours post-dose was determined.

An AE is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the study drug, whether or not considered related to the use of the product. Participants were monitored for occurrence AEs for up to 14 days after last dose study drug. Participants who took both active and placebo study drug were counted in the active group.

An AE is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the study drug, whether or not considered related to the use of the product. Participants who took both active and placebo study drug were counted in the active group.

An AE is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the study drug, whether or not considered related to the use of the study drug. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the study drug, is also an AE. A clinical AE is an AE reported as a result of a clinical examination or reported by the participant.

An AE is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the study drug, whether or not considered related to the use of the study drug. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the study drug, is also an AE. A clinical AE is an AE reported as a result of a clinical examination or reported by the participant.

An AE is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the study drug, whether or not considered related to the use of the study drug. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the study drug, is also an AE. A laboratory AE is an AE reported as a result of a laboratory assessment or test.

An AE is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the study drug, whether or not considered related to the use of the study drug. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the study drug, is also an AE. A laboratory AE is an AE reported as a result of a laboratory assessment or test.

Participants completed a headache diary each evening at bedtime, including recording headache duration and acute headache medication use. Mean monthly headache days was calculated from diary data. A headache day was defined as a day in which a headache (defined as headache pain ≥30 minute duration or requiring acute treatment) started, ended, or recurred. Headache pain persisting for more than 1 calendar day after initial onset was considered an occurrence of additional headache days. Mean monthly rate was adjusted to 28 days. Participant subgroups (based on symptoms over the 3 menstrual cycles prior to study): PMM - In ≥2 out of 3 cycles attacks occur exclusively on Day 1 ± 2 of menstruation and at no other times of the cycle; MRM - In ≥2 out of 3 cycles attacks occur on Day 1 ± 2 of menstruation and additionally at other times of the cycle.

Any AEs occurring among participants (all were healthy subjects) in Part I of study were recorded. An AE was defined as any unfavorable and unintended change in the structure, function or chemistry of the body temporally associated with study drug administration, whether or not considered related to the study drug. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which was temporally associated with the administration of the study drug, was also an AE.

Any AEs occurring among participants (all were migraine patients) in Part III of study were recorded. An AE was defined as any unfavorable and unintended change in the structure, function or chemistry of the body temporally associated with study drug administration, whether or not considered related to the study drug. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which was temporally associated with the administration of the study drug, was also an AE.

Brain CGRP RO post telcagepant was determined by change in \[11C\]MK-4232 PET tracer biokinetics at baseline and post telcagepant administration. Using PET brain images acquired over \~0-90 minutes after \[11C\]MK-4232 dose, regions of interest (ROIs) were drawn throughout cerebral cortex and white matter, striatum, thalamus, cerebellum and pons. The ROIs were projected onto all frames of the dynamic PET scans in order to generate \[11C\]MK-4232 tissue time-activity curves (TACs). Serial arterial blood samples for measurement of plasma radioactivity and \[11C\]MK-4232 concentrations were collected during the PET scans. These samples provided the arterial input function for a two-tissue compartmental model of \[11C\]MK-4232 tracer biokinetics. Total volume of distribution (VT), an index of receptor density, was estimated by fitting the two-tissue compartmental model to the PET \[11C\]MK-4232 TACs. Change in VT between baseline and post telcagepant PET studies was used to quantify the brain CGRP RO.

In Part I, Period 1 blood samples for determination of plasma telcagepant concentrations were obtained prior to the telcagepant dose (time 0) and at 2, 3, 4 and 5 hours post telcagepant dose. The average plasma telcagepant concentration during the PET scan was determined, calculated as the area under the plasma telcagepant concentration versus time curve during the PET scanning interval divided by the duration of the PET scanning interval.

Brain CGRP RO post telcagepant was determined by change in \[11C\]MK-4232 PET tracer biokinetics at baseline and post telcagepant administration. Using PET brain images acquired over \~0-90 miniutes after \[11C\]MK-4232 dose, ROIs were drawn throughout the cerebral cortex and white matter, striatum, thalamus, cerebellum and pons. The ROIs were projected onto all frames of the dynamic PET scans in order to generate \[11C\]MK-4232 tissue TACs. Serial arterial blood samples for measurement of plasma radioactivity and \[11C\]MK-4232 concentrations were collected during the PET scans. These samples provided the arterial input function for a two-tissue compartmental model of \[11C\]MK-4232 tracer biokinetics. VT, an index of receptor density, was estimated by fitting the two-tissue compartmental model to the PET \[11C\]MK-4232 TACs. The change in VT between the baseline and post telcagepant PET studies was used to quantify the brain CGRP RO.

In Part I, Period 2 blood samples for determination of plasma telcagepant concentrations were obtained prior to the telcagepant dose (time 0) and at 1, 2, 3 and 4 hours post telcagepant dose. The average plasma telcagepant concentration during the PET scan was determined, calculated as the area under the plasma telcagepant concentration versus time curve during the PET scanning interval divided by the duration of the PET scanning interval.

Brain CGRP RO post telcagepant was determined by change in \[11C\]MK-4232 PET tracer biokinetics at baseline and post telcagepant administration. Using PET brain images acquired over \~0-90 minutes after \[11C\]MK-4232 dose, ROIs were drawn throughout the cerebral cortex and white matter, striatum, thalamus, cerebellum and pons. The ROIs were projected onto all frames of the dynamic PET scans in order to generate \[11C\]MK-4232 tissue TACs. Serial arterial blood samples for measurement of plasma radioactivity and \[11C\]MK-4232 concentrations were collected during the PET scans. These samples provided the arterial input function for a two-tissue compartmental model of \[11C\]MK-4232 tracer biokinetics. VT, an index of receptor density, was estimated by fitting the two-tissue compartmental model to the PET \[11C\]MK-4232 TACs. The change in VT between the baseline and post telcagepant PET studies was used to quantify the brain CGRP RO.

Brain CGRP RO post telcagepant was determined by change in \[11C\]MK-4232 PET tracer biokinetics at baseline and post telcagepant administration. Using PET brain images acquired over \~0-90 minutes after \[11C\]MK-4232 dose, ROIs were drawn throughout the cerebral cortex and white matter, striatum, thalamus, cerebellum and pons. The ROIs were projected onto all frames of the dynamic PET scans in order to generate \[11C\]MK-4232 tissue TACs. Serial arterial blood samples for measurement of plasma radioactivity and \[11C\]MK-4232 concentrations were collected during the PET scans. These samples provided the arterial input function for a two-tissue compartmental model of \[11C\]MK-4232 tracer biokinetics. VT, an index of receptor density, was estimated by fitting the two-tissue compartmental model to the PET \[11C\]MK-4232 TACs. The change in VT between the baseline and post telcagepant PET studies was used to quantify the brain CGRP RO.