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Table 1.

Reaction conditions for measurement of DPP-2, DPP-8, DPP-9, PEP, and FAPα activities.

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Table 1 Expand

Fig 1.

Two-step inhibition model.

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Fig 1 Expand

Fig 2.

Concentration response curves of DPP-4 inhibitory activities by trelagliptin, alogliptin and sitagliptin.

Concentration response curves of DPP-4 inhibitory activities by trelagliptin, alogliptin and sitagliptin. Activity was measured as described under Materials and Methods.

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Fig 2 Expand

Table 2.

Inhibitory activity of trelagliptin in human, dog, and rat plasma.

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Table 2 Expand

Table 3.

Inhibitory activity of trelagliptin against DPP-4-related proteases.

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Table 3 Expand

Fig 3.

Double-reciprocal plot showing competitive inhibition of DPP-4 by trelagliptin.

Initial rate (first 40 seconds only) was measured as described under Materials and Methods using a range of GP-pNA substrate concentrations bracketing the apparent Km value at several fixed trelagliptin concentrations.

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Fig 3 Expand

Fig 4.

Time course of the reaction of DPP-4 in the absence or presence of different concentrations of trelagliptin.

Progress curves at 405 nm for pNA generation were recorded over 2000 sec using a 10 sec interval. Reaction was initiated with 1 nmol/L DPP-4 in the presence of 400 μmol/L GP-pNA substrate (approximately 4x Km) and varying concentrations of trelagliptin. Inset: Replot of apparent association rate constant, k’, against trelagliptin concentration used to estimate kon’ from the slope according to Eq 7.

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Fig 4 Expand

Fig 5.

Time course of the recovery of DPP-4 activity following dissociation of trelagliptin from the preformed DPP-4-inhibitor complex.

A preformed enzyme-inhibitor complex (where [DPP-4] = 50 nmol/L and trelagliptin concentration is as shown in the plot) was diluted 50-fold into a solution containing 2 mmol/L GP-pNA substrate (approximately 17x Km). Absorbance readings were taken every 10 seconds. Inset: Replot of the apparent dissociation rate constant, k’, against trelagliptin concentration used to estimate koff from the Y-intercept according to Eq 7.

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Fig 5 Expand

Table 4.

Kinetic constants for trelagliptin determined from association progress curves.

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Table 4 Expand

Table 5.

Kinetic constants for trelagliptin determined from dissociation progress curves.

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Table 5 Expand

Fig 6.

Comparison of x-ray crystal structures of inhibitors bound to DPP-4.

Comparison of x-ray crystal structure of inhibitors bound to DPP-4 for alogliptin (left panel) and trelagliptin (right panel).

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Fig 6 Expand

Fig 7.

Potential fluorine atom interactions in trelagliptin x-ray crystal structure.

Close-up showing potential differential interaction of F-atom of trelagliptin (right panel) with Trp659 residue in DPP-4 crystal structure as compared to H-atom of alogliptin (left panel).

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Fig 7 Expand

Fig 8.

Relationship between trelagliptin pharmacokinetics and pharmacodynamics in T2DM patients in phase 2 dose-ranging study.

Observed value plotted in “X” and predicted relationship between pharmacokinetics and pharmacodynamics by sigmoid Emax model is indicated by solid line. The plasma trelagliptin concentration estimated to yield 70% and 80% inhibition of human plasma DPP-4 activity was 2.31 ng/mL and 3.13 ng/mL, respectively.

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Fig 8 Expand