MedPath

LGX818 and MEK162 in Combination With a Third Agent (BKM120, LEE011, BGJ398 or INC280) in Advanced BRAF Melanoma

Phase 2
Completed
Conditions
Melanoma
Interventions
Registration Number
NCT02159066
Lead Sponsor
Pfizer
Brief Summary

The primary purpose of this study is to assess the anti-tumor activity of LGX818/MEK162 in combination with targeted agents after progression on LGX818/MEK162 combination therapy, as well as the safety and tolerability of the novel triple combinations.

Detailed Description

This study consists of two parts: in Part I/Run-In, patients naïve to selective BRAF and MEK inhibitors will be treated with the LGX818/MEK162 combination until disease progression (as defined per RECIST v1.1). Based on the genetic analysis of a tumor biopsy obtained at that time, patients will enter Part II of the study for tailored combination treatment in one of four arms of LGX818/MEK162 + either BKM120, BGJ398, INC280 or LEE011 Patients with BRAF mutant melanoma treated by LGX818/MEK162 combination in other studies can be enrolled directly in Part II of CLGX818X2109 after relapse.

Dose-escalations in the combination arms for which no MTD has been established will be based on the recommendations of a Bayesian logistic regression model guided by an escalation with overdose control criterion

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
158
Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
LGX818 + MEK162 + BGJ398BGJ398-
LGX818 + MEK162 + BKM120BKM120-
LGX818 + MEK162LGX818-
LGX818 + MEK162MEK162-
LGX818 + MEK162 + LEE011LEE011-
LGX818 + MEK162 + INC280INC280-
Primary Outcome Measures
NameTimeMethod
Overall Response Rate (ORR): Part IIFrom the start of the treatment until disease/clinical progression or death or early study discontinuation, whichever happened earlier (maximum treatment exposure for Part II was 97.0 weeks)

ORR: percentage of participants with confirmed complete response (CR) and partial response (PR). Response evaluation criteria in solid tumors (RECIST) v1.1: a) CR = disappearance of all non-nodal target lesions. In addition, any pathological lymph nodes assigned as target lesions that had a reduction in short axis to less than (\<) 10 millimeter (mm). Disappearance of all non-target lesions. In addition, all lymph nodes assigned a non-target lesion must be non-pathological in size (\<10 mm short axis) and b) PR = at least a 30 percent (%) decrease in the sum of diameter of all target lesions, taking as reference the baseline sum of diameters. Any radiological assessments taken more than 30 days after the last dose of study therapy or after antineoplastic agents other than study treatments taken by the participants was excluded from the best overall response derivation. Confirmation of CR or PR was to be at least 4 weeks apart from the previous radiological assessment.

Secondary Outcome Measures
NameTimeMethod
Number of Participants With Worst Post-baseline Hematology Results Based on Common Terminology Criteria for Adverse Events (CTCAE) v4.03 Grade: Part IBaseline up to last dose (maximum treatment exposure for Part I was 403.7 weeks)

Parameters evaluated were: Activated partial thromboplastin time (APTT) (seconds \[sec\]) - CTCAE graded high, fibrinogen (gram per liter \[g/L\]) - CTCAE graded low, hemoglobin (g/L) - CTCAE graded low, hemoglobin (g/L) - CTCAE graded high, prothrombin international normalized ratio (PINR) - CTCAE graded high, lymphocytes (10\^9 cells/L) - CTCAE graded low, lymphocytes (10\^9 cells/L) - CTCAE graded high, neutrophils (10\^9 cells/L) - CTCAE graded low, platelets (10\^9 cells/L) - CTCAE graded low, leukocytes (10\^9 cells/L) - CTCAE graded low, leukocytes (10\^9 cells/L) - CTCAE graded high. CTCAE version 4.03 was used: grade 1 = mild, grade 2 = moderate, grade 3 = severe, grade 4 = life-threatening consequences; grade 0 = values not meeting any of the criteria for grade 1 or higher. Baseline = last non-missing value prior to the first dose of study treatment.

Number of Participants With Worst Post-baseline Hematology Results Based on CTCAE v4.03 Grade: Part IIBaseline up to last dose (maximum treatment exposure for Part II was 97.0 weeks)

Parameters evaluated were: APTT (sec) - CTCAE graded high, fibrinogen (g/L) - CTCAE graded low, hemoglobin (g/L) - CTCAE graded low, hemoglobin (g/L) - CTCAE graded high, PINR - CTCAE graded high, lymphocytes (10\^9 cells/L) - CTCAE graded low, lymphocytes (10\^9 cells/L) - CTCAE graded high, neutrophils (10\^9 cells/L) - CTCAE graded low, platelets (10\^9 cells/L) - CTCAE graded low, leukocytes (10\^9 cells/L) - CTCAE graded low, leukocytes (10\^9 cells/L) - CTCAE graded high. CTCAE version 4.03 was used: grade 1 = mild, grade 2 = moderate, grade 3 = severe, grade 4 = life-threatening consequences; grade 0 = values not meeting any of the criteria for grade 1 or higher. Baseline = last non-missing value prior to the first dose of study treatment in Part II.

Number of Participants With Worst Post-baseline Serum Chemistry Results Based on CTCAE v4.03 Grade: Part IIBaseline up to last dose (maximum treatment exposure for Part II was 97.0 weeks)

Parameters evaluated were: albumin (g/L)- CTCAE graded low, alkaline phosphatase (U/L)- CTCAE graded high, alanine aminotransferase (U/L)- CTCAE graded high, amylase (U/L) - CTCAE graded high, aspartate aminotransferase(U/L)- CTCAE graded high, bilirubin (umol/L)- CTCAE graded high, creatinine (umol/L) - CTCAE graded high, creatine kinase (U/L)- CTCAE graded high, gamma glutamyl transferase (U/L)- CTCAE graded high, glucose (mmol/L)- CTCAE graded low, high, potassium (mmol/L)- CTCAE graded low, potassium (mmol/L)- CTCAE graded high, magnesium (mmol/L)- CTCAE graded low, high, phosphate (mmol/L)- CTCAE graded low, sodium (mmol/L)- CTCAE graded low, sodium (mmol/L)- CTCAE graded high, urate (umol/L)- CTCAE graded high. CTCAE version 4.03 was used: grade 1 = mild, grade 2 = moderate, grade 3 = severe, grade 4 = life-threatening consequences; grade 0 = values not meeting any of the criteria for grade 1 or higher.

Number of Participants With At Least One Dose Reduction: Part IIDuring study treatment (maximum treatment exposure for Part II was 97.0 weeks)

In this outcome measure number of participants with at least 1 dose reduction for encorafenib, binimetinib, and each third combination agent were reported.

Actual Dose Intensity: Part IDuring study treatment (maximum treatment exposure for Part I was 403.7 weeks)

Dose intensity across all cycles = cumulative dose/duration of exposure. Treatment cycle for encorafenib and binimetinib =21 days.

Last Measurable Plasma Concentration at Steady State (Clast, ss) of Encorafenib, Binimetinib, Binimetinib Metabolite, Ribociclib, Ribociclib Metabolite, Infigratinib, Infigratinib Metabolites, Capmatinib, and Buparlisib: Part IIC1 D15: 0.5 hour ± 10 min; 1 hour ± 10 min; 1.5 hour ± 15 min; 2 hour ± 15 min; 2.5 hour ± 15 min; 4 hour ± 30 min; 6 hour ± 30 min; 8 hour ± 60 min; 24 hour ± 2 hour
Measured Concentration at the End of a Dosing Interval at Steady State (Ctrough, ss) of Encorafenib, Binimetinib, Binimetinib Metabolite, Ribociclib, Ribociclib Metabolite, Infigratinib, Infigratinib Metabolites, Capmatinib, and Buparlisib: Part IIC1 D15: at the end of a dosing interval at steady-state (24 hour ± 2 hour), taken directly before next administration
Number of Participants With Dose Limiting Toxicities (DLTs) in Cycle 1: Part IICycle 1 (21 days following the first dose of the combination treatment with buparlisib and capmatinib; 28 days for the combination with ribociclib and infigratinib)

DLT was defined as an adverse event or abnormal laboratory value assessed as unrelated to disease, disease progression, inter-current illness, or concomitant medications that occurred within the first cycle (first 21 days for infigratinib and capmatinib; 28 days for ribociclib and buparlisib) of treatment initiation and met the defined criteria for study.

Number of Participants With Adverse Events (AEs) and Serious AEs (SAEs): Part IDay 1 up to 30 days after last dose (maximum treatment exposure for Part I was 403.7 weeks)

An AE was defined as the appearance of (or worsening of any pre-existing) undesirable sign(s), symptom(s), or medical condition(s) that occurred after participants' signed informed consent has been obtained. An SAE was an AE resulting in any of the following outcomes: was fatal or life-threatening; resulted in persistent or significant disability/incapacity; constituted a congenital anomaly/birth defect; was medically significant; required inpatient hospitalization or prolongation of existing hospitalization. AEs included both SAEs and all Non-SAEs.

Number of Participants With AEs and SAEs: Part IIDay 1 up to 30 days after last dose (maximum treatment exposure for Part II was 97.0 weeks)

An AE was defined as the appearance of (or worsening of any pre-existing) undesirable sign(s), symptom(s), or medical condition(s) that occurred after participants' signed informed consent has been obtained. An SAE was an AE resulting in any of the following outcomes: was fatal or life-threatening; resulted in persistent or significant disability/incapacity; constituted a congenital anomaly/birth defect; was medically significant; required inpatient hospitalization or prolongation of existing hospitalization. AEs included both SAEs and all Non-SAEs.

Number of Participants With At Least One Dose Interruption: Part IIDuring study treatment (maximum treatment exposure for Part II was 97.0 weeks)

In this outcome measure number of participants with at least 1 dose interruption for encorafenib, binimetinib, and each third combination agent were reported.

Number of Participants With At Least One Dose Reduction: Part IDuring study treatment (maximum treatment exposure for Part I was 403.7 weeks)

In this outcome measure number of participants with at least 1 dose reduction for encorafenib and binimetinib were reported.

Actual Dose Intensity: Part IIDuring study treatment (maximum treatment exposure for Part II was 97.0 weeks)

Dose intensity = cumulative dose/ duration of exposure. Treatment cycle = 21days for the combination treatment with buparlisib and capmatinib and 28 days for the combination treatment with ribociclib and infigratinib.

Duration of Response (DOR): Part IFrom date of first documented response (CR or PR) till the date of first documented progression or death due to underlying cancer or censoring date (maximum treatment exposure for Part I was 403.7 weeks)

DOR: time between date of first documented response (CR or PR) and date of first documented progression or death due to underlying cancer. If there was no progression or death due to underlying cancer, then the participant was censored at the date of last tumor assessment other than unknown. RECIST v1.1: CR = disappearance of all non-nodal target lesions. Any pathological lymph nodes assigned as target lesions must had a reduction in short axis to \<10 mm. Disappearance of all non-target lesions. All lymph nodes assigned a non-target lesion must be non-pathological in size (\<10 mm short axis); b) PR = at least a 30% decrease in sum of diameter of all target lesions, taking as reference baseline sum of diameters; c) PD= At least a 20% increase in sum of diameter of all measured target lesions, taking as reference the smallest sum of diameter of all target lesions recorded at or after baseline. In addition, sum must also demonstrate an absolute increase of at least 5 mm.

Number of Participants With Worst Post-baseline Serum Chemistry Results Based on CTCAE v4.03 Grade: Part IBaseline up to last dose (maximum treatment exposure for Part I was 403.7 weeks)

Parameters evaluated were: albumin (g/L)- CTCAE graded low, alkaline phosphatase (units per liter \[U/L\])- CTCAE graded high, alanine aminotransferase (U/L)- CTCAE graded high, amylase (U/L - CTCAE graded high, aspartate aminotransferase(U/L)- CTCAE graded high, bilirubin (micromole per liter \[umol/L\])- CTCAE graded high, creatinine (umol/L) - CTCAE graded high, creatine kinase (U/L)- CTCAE graded high, gamma glutamyl transferase (U/L)- CTCAE graded high, glucose (millimole per liter \[mmol/L\])- CTCAE graded low, high, potassium (mmol/L)- CTCAE graded low, potassium (mmol/L)- CTCAE graded high, magnesium (mmol/L)- CTCAE graded low, high, phosphate (mmol/L)- CTCAE graded low, sodium (mmol/L)- CTCAE graded low, sodium (mmol/L)- CTCAE graded high, urate (umol/L)- CTCAE graded high. CTCAE version 4.03 was used: grade 1 = mild, grade 2 = moderate, grade 3 = severe, grade 4 = life-threatening consequences; grade 0 = values not meeting any of the criteria for grade 1 or higher.

Number of Participants With Newly Occurring Notably Abnormal Vital Signs: Part IDuring study treatment (maximum treatment exposure for Part I was 403.7 weeks)

Vital signs evaluated were: Low/high systolic blood pressure (BP) (millimeter of Mercury \[mmHg\]): less than or equal to (\<=) 90 mmHg with decrease from baseline of \>=20 mmHg / \>=160 mmHg with increase from baseline of \>=20 mmHg; low/high diastolic BP \[mmHg\]: \<=50 mmHg with decrease from baseline of \>=15 mmHg / \>=100 mmHg with increase from baseline of \>=15 mmHg; low/high pulse rate (beats per minute \[bpm\]): \<=50 bpm with decrease from baseline of \>=15 bpm / \>=120 bpm with increase from baseline of \>=15 bpm; low/high weight (kilogram \[kg\]): \>=20% decrease/increase from baseline; and low/high body temperature (degree Celsius \[C\]): \<=36 C / \>= 37.5 C.

Number of Participants With Newly Occurring Notably Abnormal Vital Signs: Part IIDuring study treatment (maximum treatment exposure for Part II was 97.0 weeks)

Vital signs evaluated were: Low/high systolic BP (mmHg): \<=90 mmHg with decrease from baseline of \>=20 mmHg / \>=160 mmHg with increase from baseline of \>=20 mmHg; low/high diastolic BP \[mmHg\]: \<=50 mmHg with decrease from baseline of \>=15 mmHg / \>=100 mmHg with increase from baseline of \>=15 mmHg; low/high pulse rate (bpm): \<=50 bpm with decrease from baseline of \>=15 bpm / \>=120 bpm with increase from baseline of \>=15 bpm; low/high weight (kg): \>=20% decrease/increase from baseline; and low/high body temperature (C): \<=36 C / \>= 37.5 C.

Number of Participants With Notable Electrocardiograms (ECG) Values: Part IDuring study treatment (maximum treatment exposure for Part I was 403.7 weeks)

Number of participants with notable ECG values were reported in this outcome measure. Abnormality categories were: Heart rate (HR): increase from baseline \>25% and to a value \>100 bpm, decrease from baseline \>25% and to a value \<60 bpm; PR: increase from baseline \>25% and to a value \>200 millisecond (ms); QRS: increase from baseline \>25% and to a value \>110 ms; QT: increase from baseline \>30 ms, increase from baseline \>60 ms, new interval \>450 ms, new interval \>480 ms, new interval \>500 ms; and Corrected QT interval by Fridericia (QTcF): increase from baseline \>30 ms, increase from baseline \>60 ms, new interval \>450 ms, new interval \>480 ms, new interval \>500 ms. New = newly occurred post-baseline value.

Number of Participants With Notable ECG Values: Part IIDuring study treatment (maximum treatment exposure for Part II was 97.0 weeks)

Number of participants with notable ECG values were reported in this outcome measure. Abnormality categories were: HR: increase from baseline \>25% and to a value \>100 bpm, decrease from baseline \>25% and to a value \<60 bpm; PR: increase from baseline \>25% and to a value \>200 ms; QRS: increase from baseline \>25% and to a value \>110 ms; QT: increase from baseline \>30 ms, increase from baseline \>60 ms, new interval \>450 ms, new interval \>480 ms, new interval \>500 ms; and QTcF: increase from baseline \>30 ms, increase from baseline \>60 ms, new interval \>450 ms, new interval \>480 ms, new interval \>500 ms. New = newly occurred post-baseline value.

Number of Participants With At Least One Dose Interruption: Part IDuring study treatment (maximum treatment exposure for Part I was 403.7 weeks)

In this outcome measure number of participants with at least 1 dose interruption for encorafenib and binimetinib were reported.

Progression-Free Survival (PFS): Part IFrom start of study drug until documented PD or death due to any cause or censoring date (maximum treatment exposure for Part I was 403.7 weeks)

PFS was defined as the time from the start date of study drug in Part I until documented PD or death due to any cause. All participants who had not progressed or died at the time of the data cut-off were censored at the date of last tumor assessment (other than those who were unknown or missing) prior to cut-off date or start date of new anti-neoplastic therapy, whichever is earlier. Per RECIST 1.1, PD= At least a 20% increase in the sum of diameter of all measured target lesions, taking as reference the smallest sum of diameter of all target lesions recorded at or after baseline. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. Kaplan Meier method used for estimation.

PFS: Part IIFrom start of study drug until documented PD or death due to any cause or censoring date (maximum treatment exposure for Part II was 97.0 weeks)

PFS was defined as the time from the start date of study drug in Part II until documented PD or death due to any cause. All participants who had not progressed or died at the time of the data cut-off were censored at the date of last tumor assessment (other than those who were unknown or missing) prior to cut-off date or start date of new anti-neoplastic therapy, whichever is earlier. Per RECIST 1.1, PD= At least a 20% increase in the sum of diameter of all measured target lesions, taking as reference the smallest sum of diameter of all target lesions recorded at or after baseline. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. Kaplan Meier method used for estimation.

TTR: Part IIFrom start date of study drug till first documented response (CR or PR) (maximum treatment exposure for Part II was 97.0 weeks)

TTR was defined as the time between the start date of study drug in Part II and first documented response (CR or PR). RECIST v1.1: a) CR = disappearance of all non-nodal target lesions. In addition, any pathological lymph nodes assigned as target lesions must had a reduction in short axis to \<10 mm. Disappearance of all non-target lesions. In addition, all lymph nodes assigned a non-target lesion must be non-pathological in size (\<10 mm short axis) and b) PR = at least a 30% decrease in the sum of diameter of all target lesions, taking as reference the baseline sum of diameters. Kaplan Meier method used for estimation.

Summary of Genomic Biomarkers From Tumor Samples: Part IBaseline up to end of treatment (EOT) (maximum treatment exposure for Part I was 403.7 weeks)

Number of participants with multiple alterations in genomic biomarkers like biomarker BRAF, CCND1, CDK4, EGFR, FGFR1, FGFR4, KRAS, MET, NRAS, PIK3CA, and PTEN were reported and alterations included copy number variant/copy number ratio (CNV/CNR), rearrangement, short variant. It was not necessary that all biomarkers had all alterations. Baseline = last non-missing value prior to the first dose of study treatment.

Plasma Concentration for Encorafenib (LGX): Part IIC1 (1.5, 4 hrs post-dose on D1; pre-dose on D8; pre-dose, 0.5, 1.5, 2.5, 4, 6, 8 hrs post-dose on D15; 24 hrs post-dose on D16; pre-dose on D21); C2 (pre-dose on D1 and D15); C3 pre-dose on D1; C4 pre-dose on D1; C5 pre-dose on D1; EOT

In results reported below, following abbreviation have been used: Cycle 1 (C1), Day 1 (D1), Day 8 (D8), Day 15 (D15), Day 16 (D16), Day 21 (D21), Cycle 2 (C2), Cycle 3 (C3), Cycle 4 (C4), Cycle 5 (C5). Maximum treatment exposure for Part II was of 97.0 weeks.

Plasma Concentration for Binimetinib (MEK) and Its Metabolite: Part IC1 (1.5 hrs post-dose on D1; pre-dose, 1.5 hrs post-dose on D15); C2 (pre-dose on D8 and D21); C3 pre-dose on D15; C4 pre-dose on D15; C5 pre-dose on D15; EOT

AR00426032 is metabolite of binimetinib. Maximum treatment exposure for Part I was of 403.7 weeks.

DOR: Part IIFrom date of first documented response (CR or PR) till the date of first documented progression or death due to underlying cancer or censoring date (maximum treatment exposure for Part II was 97.0 weeks)

DOR: time between date of first documented response (CR or PR) and date of first documented progression or death due to underlying cancer. If there was no progression or death due to underlying cancer, then the participant was censored at the date of last tumor assessment other than unknown. RECIST v1.1: CR = disappearance of all non-nodal target lesions. Any pathological lymph nodes assigned as target lesions must had a reduction in short axis to \<10 mm. Disappearance of all non-target lesions. All lymph nodes assigned a non-target lesion must be non-pathological in size (\<10 mm short axis); b) PR = at least a 30% decrease in sum of diameter of all target lesions, taking as reference baseline sum of diameters; c) PD= At least a 20% increase in sum of diameter of all measured target lesions, taking as reference the smallest sum of diameter of all target lesions recorded at or after baseline. In addition, sum must also demonstrate an absolute increase of at least 5 mm.

Time to Response (TTR): Part IFrom start date of study drug till first documented response (CR or PR) (maximum treatment exposure for Part I was 403.7 weeks)

TTR was defined as the time between the start date of study drug in Part I and first documented response (CR or PR). RECIST v1.1: a) CR = disappearance of all non-nodal target lesions. In addition, any pathological lymph nodes assigned as target lesions must had a reduction in short axis to \<10 mm. Disappearance of all non-target lesions. In addition, all lymph nodes assigned a non-target lesion must be non-pathological in size (\<10 mm short axis) and b) PR = at least a 30% decrease in the sum of diameter of all target lesions, taking as reference the baseline sum of diameters. Kaplan Meier method used for estimation.

Apparent Volume of Distribution at Steady State (Vz, ss/F) of Encorafenib, Binimetinib, Ribociclib, Capmatinib, and Buparlisib: Part IIC1 D15: 0.5 hour ± 10 min; 1 hour ± 10 min; 1.5 hour ± 15 min; 2 hour ± 15 min; 2.5 hour ± 15 min; 4 hour ± 30 min; 6 hour ± 30 min; 8 hour ± 60 min; 24 hour ± 2 hour

Volume of distribution is defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired blood concentration of a drug. Steady state volume of distribution is the apparent volume of distribution at steady-state.

Disease Control Rate (DCR): Part IFrom start date of study drug till first documented response (CR or PR or SD) (maximum treatment exposure for Part I was 403.7 weeks)

DCR was defined as percentage of participants with a best overall response of CR or PR or SD. RECIST v1.1: a) CR = disappearance of all non-nodal target lesions. In addition, any pathological lymph nodes assigned as target lesions must had a reduction in short axis to \<10 mm. Disappearance of all non-target lesions. In addition, all lymph nodes assigned a non-target lesion must be non-pathological in size (\<10 mm short axis); b) PR = at least a 30% decrease in the sum of diameter of all target lesions, taking as reference the baseline sum of diameters and c) SD = neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for PD. PD= At least a 20% increase in the sum of diameter of all measured target lesions, taking as reference the smallest sum of diameter of all target lesions recorded at or after baseline. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm.

DCR: Part IIFrom start date of study drug till first documented response (CR or PR or SD) (maximum treatment exposure for Part II was 97.0 weeks)

DCR was defined as percentage of participants with a best overall response of CR or PR or SD. RECIST v1.1: a) CR = disappearance of all non-nodal target lesions. In addition, any pathological lymph nodes assigned as target lesions must had a reduction in short axis to \<10 mm. Disappearance of all non-target lesions. In addition, all lymph nodes assigned a non-target lesion must be non-pathological in size (\<10 mm short axis); b) PR = at least a 30% decrease in the sum of diameter of all target lesions, taking as reference the baseline sum of diameters and c) SD = neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for PD. PD= At least a 20% increase in the sum of diameter of all measured target lesions, taking as reference the smallest sum of diameter of all target lesions recorded at or after baseline. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm.

Overall Survival (OS): Part IIFrom date of start of treatment to date of death due to any cause or censoring date (maximum treatment exposure for Part II was 97.0 weeks)

OS was defined as the time from the start date of study treatment (3rd agent combined with encorafenib and binimetinib) to date of death due to any cause. If a participant was not known to have died, survival was censored at the date of last known date participant alive. Kaplan Meier method used for estimation.

Plasma Concentration for Encorafenib (LGX): Part IC1 (1.5 hrs post-dose on D1; pre-dose, 1.5 hrs post-dose on D15); C2 (pre-dose on D8 and D21); C3 pre-dose on D15; C4 pre-dose on D15; C5 pre-dose on D15; EOT

In results reported below, following abbreviation have been used: Cycle 1 (C1), Day 1 (D1), Day 8 (D8), Day 15 (D15), Day 21 (D21), Cycle 2 (C2), Cycle 3 (C3), Cycle 4 (C4), Cycle 5 (C5) and end of treatment (EOT). Maximum treatment exposure for Part I was of 403.7 weeks.

Plasma Concentration for Binimetinib (MEK) and Its Metabolite: Part IIC1 (1.5, 4 hrs post-dose on D1; pre-dose on D8; pre-dose, 0.5, 1.5, 2.5, 4, 6, 8 hrs post-dose on D15; 24 hrs post-dose on D16; pre-dose on D21); C2 (pre-dose on D1 and D15); C3 pre-dose on D1; C4 pre-dose on D1; C5 pre-dose on D1; EOT

AR00426032 is metabolite of binimetinib. Maximum treatment exposure for Part II was of 97.0 weeks.

Plasma Concentration for Ribociclib (LEE) and Its Metabolite: Part IIC1 (1.5, 4 hrs post-dose on D1; pre-dose on D8; pre-dose, 0.5, 1.5, 2.5, 4, 6, 8 hrs post-dose on D15; 24 hrs post-dose on D16; pre-dose on D21); C2 (pre-dose on D1 and D15); C3 pre-dose on D1; C4 pre-dose on D1; C5 pre-dose on D1; EOT

LEQ803 is metabolite of ribociclib. Maximum treatment exposure for Part II was of 97.0 weeks.

Plasma Concentration for Infigratinib (BGJ) and Its Metabolites: Part IIC1 (1.5 hrs post-dose on D1; pre-dose on D8; pre-dose, 0.5, 1.5, 2.5, 4, 6 hrs post-dose on D15; 24 hrs post-dose on D16; pre-dose on D21); C2 (pre-dose on D1 and D15); C3 pre-dose on D1; EOT

BHS697 and CQM157 are metabolites of infigratinib. Maximum treatment exposure for Part II was of 97.0 weeks.

Plasma Concentration for Capmatinib (INC): Part IIC1 (1.5 hrs post-dose on D1; pre-dose on D8; pre-dose, 0.5, 1.5, 2.5, 4, 6, 8 hrs post-dose on D15; 24 hrs post-dose on D16); C2 (pre-dose on D1 and D15); C3 pre-dose on D1; C4 pre-dose on D1; C5 pre-dose on D1; EOT

Maximum treatment exposure for Part II was of 97.0 weeks.

Plasma Concentration for Buparlisib (BKM): Part IIC1 (1.5 hrs post-dose on D1; pre-dose on D8; pre-dose, 0.5, 1.5, 2.5, 4, 6, 8 hrs post-dose on D15; 24 hrs post-dose on D16); C2 (pre-dose on D1 and D15); C3 pre-dose on D1; C4 pre-dose on D1; C5 pre-dose on D1; EOT

Maximum treatment exposure for Part II was of 97.0 weeks.

Maximum Observed Plasma Concentration at Steady State (Cmax,ss) for Encorafenib, Binimetinib, Binimetinib Metabolite, Ribociclib, Ribociclib Metabolite, Infigratinib, Infigratinib Metabolites, Capmatinib, and Buparlisib: Part IIC1 D15: 0.5 hour ± 10 (minutes) min; 1 hour ± 10 min; 1.5 hour ± 15 min; 2 hour ± 15 min; 2.5 hour ± 15 min; 4 hour ± 30 min; 6 hour ± 30 min; 8 hour ± 60 min; 24 hour ± 2 hour
Apparent Total Plasma Clearance at Steady State (Cl, ss/F) of Encorafenib, Binimetinib, Ribociclib, Capmatinib, and Buparlisib: Part IIC1 D15: 0.5 hour ± 10 min; 1 hour ± 10 min; 1.5 hour ± 15 min; 2 hour ± 15 min; 2.5 hour ± 15 min; 4 hour ± 30 min; 6 hour ± 30 min; 8 hour ± 60 min; 24 hour ± 2 hour

Clearance of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes.

Time to Reach Cmax at Steady State (Tmax, ss) for Encorafenib, Binimetinib, Binimetinib Metabolite, Ribociclib, Ribociclib Metabolite, Infigratinib, Infigratinib Metabolites, Capmatinib, and Buparlisib: Part IIC1 D15: 0.5 hour ± 10 min; 1 hour ± 10 min; 1.5 hour ± 15 min; 2 hour ± 15 min; 2.5 hour ± 15 min; 4 hour ± 30 min; 6 hour ± 30 min; 8 hour ± 60 min; 24 hour ± 2 hour
Area Under the Concentration-time Curve From Time Zero to Time Tau at Steady-State (AUCtau,ss) for Encorafenib, Binimetinib, Binimetinib Metabolite, Ribociclib, Ribociclib Metabolite, Capmatinib, and Buparlisib: Part IIC1 D15: 0.5 hour ± 10 min; 1 hour ± 10 min; 1.5 hour ± 15 min; 2 hour ± 15 min; 2.5 hour ± 15 min; 4 hour ± 30 min; 6 hour ± 30 min; 8 hour ± 60 min; 24 hour ± 2 hour
Elimination Half-life at Steady State (t1/2, ss) of Encorafenib, Binimetinib, Binimetinib Metabolite, Ribociclib, Ribociclib Metabolite, Capmatinib, and Buparlisib: Part IIC1 D15: 0.5 hour ± 10 min; 1 hour ± 10 min; 1.5 hour ± 15 min; 2 hour ± 15 min; 2.5 hour ± 15 min; 4 hour ± 30 min; 6 hour ± 30 min; 8 hour ± 60 min; 24 hour ± 2 hour

Elimination half-life means the time required for the plasma concentration to decline by 50% during the elimination phase.

Trial Locations

Locations (31)

Doris Stein Research Center Building

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Los Angeles, California, United States

OHSU Center for Health and Healing 2

🇺🇸

Portland, Oregon, United States

University of California Los Angeles

🇺🇸

Los Angeles, California, United States

UCLA Dermatology Clinic

🇺🇸

Los Angeles, California, United States

UCLA Oncology Center

🇺🇸

Los Angeles, California, United States

Cancer Care Center

🇺🇸

Los Angeles, California, United States

Ronald Reagan UCLA Medical Center Drug Information Center Department of Pharmaceutical Services

🇺🇸

Los Angeles, California, United States

Oregon Health and Science University

🇺🇸

Portland, Oregon, United States

Sarah Cannon Research Institute

🇺🇸

Nashville, Tennessee, United States

Tennessee Oncology, PLLC

🇺🇸

Nashville, Tennessee, United States

UCLA Radiology

🇺🇸

Los Angeles, California, United States

Memorial Sloan Kettering Cancer Center Attn: Geny O'neill

🇺🇸

New York, New York, United States

Memorial Sloan Kettering Cancer Center Inpatient Hospital & Main Campus

🇺🇸

New York, New York, United States

Memorial Sloan Kettering Cancer Center- Outpatient Clinic

🇺🇸

New York, New York, United States

OHSU Knight Cancer Institute

🇺🇸

Portland, Oregon, United States

OHSU Research Pharmacy Services

🇺🇸

Portland, Oregon, United States

OHSU Center for Health and Healing

🇺🇸

Portland, Oregon, United States

Peter MacCallum Cancer Centre

🇦🇺

Melbourne, Victoria, Australia

East St Kilda Eye Clinic

🇦🇺

Melbourne, Victoria, Australia

Princess Margaret Cancer Center

🇨🇦

Toronto, Ontario, Canada

Sir Mortimer B. Davis-Jewish General Hospital

🇨🇦

Monteral, Quebec, Canada

University Clinic Heidelberg PPDS

🇩🇪

Heidelberg, Baden-württemberg, Germany

Uniklinik Köln

🇩🇪

Köln, Germany

Universitätsklinikum Würzburg

🇩🇪

Wuerzburg, Germany

Städtisches Klinikum München

🇩🇪

Muenchen, Germany

Het Nederlands Kanker Instituut Antoni Van Leeuwenhoek Ziekenhuis

🇳🇱

Amsterdam, Netherlands

Azienda Ospedaliera Monaldi

🇮🇹

Napoli, Campania, Italy

U.O.C. Oncologia Medica e Terapie Innovative Dipartimento di Melanoma IRCCS Fondazione G. Pascale

🇮🇹

Napoli, Italy

Churchill Hospital

🇬🇧

Oxford, United Kingdom

Hospital Universitario Vall d'Hebrón - PPDS

🇪🇸

Barcelona Cataluna, Barcelona, Spain

Universitätsspital Zürich

🇨🇭

Zurich Flughafen, Switzerland

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