conclusions an appreciable dose-concentration-response relationship between nn1731 and f 1+2 was...

1
Conclusions An appreciable dose-concentration-response relationship between NN1731 and F 1+2 was expressed in a population PK/PD model. Since F 1+2 appearance traces the formation of thrombin, this relationship supports the possibility of using F 1+2 as a biomarker for haemostatic agents. Aims To explore the potential of prothrombin fragments 1&2 (F 1+2 ) as a biomarker for haemostatic agents with a model of the effects of the FVIIa analogue NN1731. Background Haemophilic patients suffer a defect in blood coagulation due to lack of either coagulation factor VIII or IX. In some patients, replacement therapy with the lacking coagulation factor eventually results in the formation of antibodies (inhibitors). Inhibitor patients may be treated with by-passing agents such as activated human coagulation factor FVII (FVIIa, NovoSeven). NN1731 is a FVIIa analogue that in vitro has shown increased activity in stimulating the cleavage of prothrombin to thrombin and F 1+2 , a key step in the coagulatory pathway 1 . F 1+2 was measured in the first clinical trial with NN1731, a dose escalation trial with 4 dosing arms. NN1731 and F 1+2 plasma concentrations were related to NN1731 doses to establish a population PK/PD model treating F 1+2 as a PD biomarker. A Population PK/PD Model Assessing the Pharmacodynamics of a Rapid-acting Recombinant FVIIa Analogue, NN1731, in Healthy Male Subjects . Andreas Groth 1 , Judi Møss 2 , Tine Møller 3 , Steen H. Ingwersen 1 1 Biomodelling, 2 Medical and Science, NovoSeven Key Projects, 3 Biostatistics, Novo Nordisk A/S, Copenhagen, Denmark [email protected] Results Figure 3. Dose-independence check of PK model Post-hoc parameter estimates of CL and V 2 were checked for dose independence. Such a dependence appears to be absent for both parameters, indicating that the PK model is valid over the studied dose-range. Strategy: i. Develop PK-model from NN1731 plasma concentration data. ii.Develop PD-model from individual post-hoc PK model parameters and F 1+2 plasma concentration data. Data source: (3 pre- and 10 post-dose PK samples + 1 pre- and 5 post-dose PD samples) 6 healthy subjects 4 active (non-zero) dose levels. Dose range 5 µg/kg-30 µg/kg Modelling: PK and PD in man was modelled sequentially using NONMEM V with FOCE. Regarding inter-individual variability (i.i.v.) on model parameters, log-normal distributions were tested for significance against the hypotheses of zero i.i.v on that parameter (which is why the geometric, rather than the arithmetic, post-hoc estimate means are displayed on fig. 4). Methods Figure 4. Dose-independence check of PD model Figure 1. Structure of PK/PD model The resulting PK model was a standard two-compartment model with inter-individual variability (i.i.v.) on CL and V 2 . The PD model was a linear indirect response model with the plasma concentration of NN1731 affecting the formation of F 1+2 , incorporating i.i.v. on baseline F 1+2 levels (B) and the efficacy parameter (E) . The F 1+2 formation rate at the baseline state C p =0 equals B k out . F 1+2 B k out (1+ E C p ) k out CL V 1 V 2 NN1731 dose Q C p NN1731 effect 0 50 100 150 5 10 15 20 25 30 DOSE CL Indv C L vs D ose 0 20 40 60 80 100 5 10 15 20 25 30 DOSE V2 Indv V2 vs D ose 0.0 0.1 0.2 0.3 0.4 5 10 15 20 25 30 DOSE EFF Indv EFF vs D ose The individual post-hoc parameter estimates in the PD model were also checked for dependence on NN1731 dose. The result is less clear-cut than that of the PK parameters (fig. 3), but since the ranges of values for the lowest and the highest dose are quite similar for the efficacy parameter E, it is concluded that the NN1731 concentration-PD response relationship is well described. 0 50 100 150 200 5 10 15 20 25 30 DOSE BAS Indv BAS vs D ose o Individual post-hoc estimates + Geometric mean of individual post-hoc estimates o Individual post-hoc estimates + Geometric mean of individual post-hoc estimates Figure 2. Fit of PK/PD model PK/PD model parameters V 1 , V 2 : central & peripheral volumes of distribution, CL: clearance, Q: intercompartmental clearance, B: baseline F 1+2 level, k out : rate constant for F 1+2 , E: NN1731 efficacy Values in parenthesis: Coefficients of Variation (CV’s) regarding i.i.v. for each parameter. 845 C oncentration [pM ] 0 5 10 15 20 100 200 300 400 C oncentration [pM ] 1690 0 5 10 15 20 100 200 300 400 3380 Tim e [h] C oncentration [pM ] 0 5 10 15 20 100 200 300 400 5070 Tim e [h] 0 5 10 15 20 100 200 300 400 The PK/PD model predictions of the F 1+2 time profiles for each trial subject as well as for the typical subject are shown along with the observations and their means for each dose level. , ,.. Model predictions (individual) Model predictions (typical subject) o,o,.. Observations + Mean of observations at time point 5 g/kg 10 g/kg 20 g/kg 30 g/kg References 1 E. Persson et al, Proc Natl Acad Sci U S A, 96;13583,2001 NN1731 dose (µg/kg) NN1731 dose (µg/kg) NN1731 dose (µg/kg) NN1731 dose (µg/kg) E pM/h/(IU/ml ) V 2 (ml/kg) CL ml/kg//h B (pM) Model paramete r V1 V2 CL Q B kout E Unit ml/kg ml/kg ml/kg/h ml/kg/h pM 1/h pM/h/IU/ ml) Estimate 59.6 78.0 (14%) 120 (14%) 38.6 132 (29%) 0.346 0.164 (46%) S.E. of estimate 2.2 4.0 4.5 2.0 11 0.048 0.042 A sketch of the pro-coagulatory actions of thrombin, also known as coagulation factor IIa. Thrombin activates several coagulatory proteins and these actions cascade down eventually leading to the formation of cross-linked fibrin (CLIa) which forms the actual blood clot.

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Page 1: Conclusions An appreciable dose-concentration-response relationship between NN1731 and F 1+2 was expressed in a population PK/PD model. Since F 1+2 appearance

ConclusionsAn appreciable dose-concentration-response relationship between NN1731 and F1+2 was expressed in a population PK/PD model. Since F1+2 appearance traces the formation of thrombin, this relationship supports the possibility of using F1+2 as a biomarker for haemostatic agents.

Aims To explore the potential of prothrombin fragments 1&2 (F1+2) as a biomarker for haemostatic agents with a model of the effects of the FVIIa analogue NN1731.

BackgroundHaemophilic patients suffer a defect in blood coagulation due to lack of either coagulation factor VIII or IX. In some patients, replacement therapy with the lacking coagulation factor eventually results in the formation of antibodies (inhibitors). Inhibitor patients may be treated with by-passing agents such as activated human coagulation factor FVII (FVIIa, NovoSeven). NN1731 is a FVIIa analogue that in vitro has shown increased activity in stimulating the cleavage of prothrombin to thrombin and F1+2, a key step in the coagulatory

pathway1. F1+2 was measured in the first clinical trial with NN1731, a

dose escalation trial with 4 dosing arms. NN1731 and F1+2 plasma

concentrations were related to NN1731 doses to establish a population PK/PD model treating F1+2 as a PD biomarker.

A Population PK/PD Model Assessing the Pharmacodynamics of a Rapid-acting Recombinant FVIIa Analogue, NN1731, in Healthy Male Subjects .

Andreas Groth1, Judi Møss2, Tine Møller3, Steen H. Ingwersen1

1Biomodelling, 2Medical and Science, NovoSeven Key Projects, 3Biostatistics, Novo Nordisk A/S, Copenhagen, Denmark [email protected]

Results

Figure 3. Dose-independence check of PK model

Post-hoc parameter estimates of CL and V2 were checked for dose independence. Such a dependence appears to be absent for both parameters, indicating that the PK model is valid over the studied dose-range.

• Strategy:i. Develop PK-model from NN1731 plasma concentration data.

ii. Develop PD-model from individual post-hoc PK model parameters and F1+2 plasma concentration data.

• Data source: (3 pre- and 10 post-dose PK samples + 1 pre- and 5 post-dose PD samples) 6 healthy subjects 4 active (non-zero) dose levels. Dose range 5 µg/kg-30 µg/kg

• Modelling: PK and PD in man was modelled sequentially using NONMEM V with FOCE. Regarding inter-individual variability (i.i.v.) on model parameters, log-normal distributions were tested for significance against the hypotheses of zero i.i.v on that parameter (which is why the geometric, rather than the arithmetic, post-hoc estimate means are displayed on fig. 4).

Methods

Figure 4. Dose-independence check of PD model

Figure 1. Structure of PK/PD model

The resulting PK model was a standard two-compartment model with inter-individual variability (i.i.v.) on CL and V2. The PD model was a linear indirect response model withthe plasma concentration of NN1731 affecting the formation of F1+2 , incorporating i.i.v. on baseline F1+2 levels (B) and the efficacy parameter (E) . The F1+2 formation rate at the baseline state Cp=0 equals B kout .

F1+2

B kout (1+ E Cp)

koutCL

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V2

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NN1731 effect

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Indv EFF vs Dose

The individual post-hoc parameter estimates in the PD model were also checked for dependence on NN1731 dose. The result is less clear-cut than that of the PK parameters (fig. 3), but since the ranges of values for the lowest and the highest dose are quite similar for the efficacy parameter E, it is concluded that the NN1731 concentration-PD response relationship is well described.

0

50

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DOSE

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S

Indv BAS vs Dose

o Individual post-hoc estimates

+ Geometric mean of individual post-hoc estimates

o Individual post-hoc estimates

+ Geometric mean of individual post-hoc estimates

Figure 2. Fit of PK/PD model

PK/PD model parameters

V1, V2: central & peripheral volumes of distribution, CL: clearance, Q: intercompartmental clearance, B: baseline F1+2 level, kout: rate constant for F1+2, E: NN1731 efficacyValues in parenthesis: Coefficients of Variation (CV’s) regarding i.i.v. for each parameter.

845

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The PK/PD model predictions of the F1+2 time profiles for each trial subject as well as for the typical subject are shown along with the observations and their means for each dose level.

, ,.. Model predictions

(individual)

Model predictions (typical

subject)

o,o,.. Observations

+ Mean of observations at time

point

5 g/kg 10 g/kg

20 g/kg 30 g/kg

References1 E. Persson et al, Proc Natl Acad Sci U S A, 96;13583,2001

NN1731 dose(µg/kg)

NN1731 dose(µg/kg)

NN1731 dose(µg/kg)

NN1731 dose(µg/kg)

E

pM

/h/(

IU/m

l)

V2 (m

l/kg

)

CL m

l/kg

//h

B (

pM

)

Model parameter V1 V2 CL Q B kout E

Unit ml/kg ml/kg ml/kg/h ml/kg/h pM 1/h pM/h/IU/ml)

Estimate 59.6 78.0 (14%) 120 (14%) 38.6 132 (29%) 0.346 0.164 (46%)

S.E. of estimate 2.2 4.0 4.5 2.0 11 0.048 0.042

A sketch of the pro-coagulatory actions of thrombin, also known as coagulation factor IIa. Thrombin activates several coagulatory proteins and these actions cascade down eventually leading to the formation of cross-linked fibrin (CLIa) which forms the actual blood clot.