An AE was defined as any untoward medical occurrence in a participant administered a study treatment and which does not necessarily have to have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the study treatment or protocol-specified procedure. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a pre-existing condition that is temporally associated with the use of study treatment, is also an AE. The percentage of all participants who discontinued study treatment due to an AE is presented. Per protocol, these results are based on a data cutoff date of 09-May-2018.

ORR was defined as the percentage of the participants who had complete response (CR) or partial response (PR) as assessed by investigator review. Participants in the AML cohort were assessed using bone marrow aspiration and hematologic criteria and response was evaluated based on European LeukemiaNet (Döhner et al, Blood, 2010). The criteria for complete response included: bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; absolute neutrophil count >1.0 × 10^9/Liter; platelet count >100 × 10^9/Liter; and independence of red cell transfusions. The criteria for partial response included: decrease of bone marrow blast percentage to 5% to 25%; decrease of pretreatment bone marrow blast percentage by at least 50%; and all hematologic criteria associated with CR. The percentage of participants who achieved CR or PR is presented.

ORR was defined as the percentage of the participants who had complete response (CR) or partial response (PR) as assessed by investigator review. Participants in the DLBCL cohort were assessed using computed tomography (CT) and positron emission tomography (PET)-CT and response was evaluated based on the Lugano Classification (Cheson et al, Journal of Clinical Oncology, 2014). The criteria for CR included complete metabolic (no/minimal fluorodeoxyglucose [FDG] uptake) and radiologic response (target lesions regress to ≤5 cm in longest transverse diameter of a lesion) and no new lesions. The criteria for PR included: partial metabolic (moderate/high FDG uptake) and radiologic response (≥50% decrease in sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable nodes and extranodal sites, no increase in lesions, and spleen regressed by >50% in length beyond normal). The percentage of participants who achieved CR or PR is presented.

DOR was defined as the time from complete response (CR) or partial response (PR) to documented disease progression or death as assessed by investigator review. Participants in the AML cohort were assessed using bone marrow aspiration and hematologic criteria and response was evaluated based on European LeukemiaNet (Döhner et al, Blood, 2010). The criteria for complete response included: bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; absolute neutrophil count >1.0 × 10^9/Liter; platelet count >100 × 10^9/Liter; and independence of red cell transfusions. The criteria for partial response included: decrease of bone marrow blast percentage to 5% to 25%; decrease of pretreatment bone marrow blast percentage by at least 50%; and all hematologic criteria associated with CR.

DOR was defined as the time from complete response (CR) or partial response (PR) to documented disease progression or death as assessed by investigator review. Participants in the DLBCL cohort were assessed using computed tomography (CT) and positron emission tomography (PET)-CT and response was evaluated based on the Lugano Classification (Cheson et al, Journal of Clinical Oncology, 2014). The criteria for CR included complete metabolic (no/minimal fluorodeoxyglucose [FDG] uptake) and radiologic response (target lesions regress to ≤5 cm in longest transverse diameter of a lesion) and no new lesions. The criteria for PR included: partial metabolic (moderate/high FDG uptake) and radiologic response (≥50% decrease in sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable nodes and extranodal sites, no increase in lesions, and spleen regressed by >50% in length beyond normal).

DCR was defined as the percentage of the participants who had stable disease, complete response (CR) or partial response (PR) as assessed by investigator review. Participants in the AML cohort were assessed using bone marrow aspiration and hematologic criteria and response was evaluated based on European LeukemiaNet (Döhner et al, Blood, 2010). The criteria for complete response included: bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; absolute neutrophil count >1.0 × 10^9/Liter; platelet count >100 × 10^9/Liter; and independence of red cell transfusions. The criteria for partial response included: decrease of bone marrow blast percentage to 5% to 25%; decrease of pretreatment bone marrow blast percentage by at least 50%; and all hematologic criteria associated with CR.

DCR was defined as the percentage of the participants in the DLBCL cohort who had stable disease, complete response (CR) or partial response (PR) as assessed by investigator review. Participants in the DLBCL cohort were assessed using computed tomography (CT) and positron emission tomography (PET)-CT and response was evaluated based on the Lugano Classification (Cheson et al, Journal of Clinical Oncology, 2014). The criteria for CR included complete metabolic (no/minimal fluorodeoxyglucose [FDG] uptake) and radiologic response (target lesions regress to ≤5 cm in longest transverse diameter of a lesion) and no new lesions. The criteria for PR included: partial metabolic (moderate/high FDG uptake) and radiologic response (≥50% decrease in sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable nodes and extranodal sites, no increase in lesions, and spleen regressed by >50% in length beyond normal).

Blood samples were collected to determine Cmax at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, Cmax for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The Cmax of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

Blood samples were collected to determine Tmax at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, Tmax for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The Tmax of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

Blood samples were collected to determine Cmin at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, Cmin for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The Cmin of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

Blood samples were collected to determine AUC 0-∞ at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, AUC 0-∞ for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The AUC 0-∞ of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

Blood samples were collected to determine t1/2 at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, t1/2 for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The t1/2 of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

Blood samples were collected to determine CL/F at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, CL/F for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The CL/F of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

Blood samples were collected to determine Vz/F at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, Vz/F for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The Vz/F of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

Fold change from baseline (predose on Day 1 of Cycle 1 [21-day cycle]) in normalized gene expression ratios (nGER) for 49 target genes was measured to assess target engagement of BET proteins predose and 3 hours postdose using quantitative polymerase chain reaction (qPCR). Data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Fold change from baseline was calculated as nGER at 3 hours postdose Day 1/baseline in logarithmic scale with a base of 2 (Log2 scale). Per protocol, target genes were assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The fold change in nGER for each target gene is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose. A two-fold increase in gene expression indicated a +1 Log2 fold change. Conversely, a two-fold decrease in gene expression indicated a -1 Log2 fold change.

Fold change from baseline (predose on Day 1 of Cycle 1 [21-day cycle]) in normalized gene expression ratios (nGER) for 49 target genes was measured to assess target engagement of BET proteins predose and 8 hours postdose using quantitative polymerase chain reaction (qPCR). Data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Fold change from baseline was calculated as nGER at 8 hours postdose Day 1/baseline in logarithmic scale with a base of 2 (Log2 scale). Per protocol, target genes were assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The fold change in nGER for each target gene is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose. A two-fold increase in gene expression indicated a +1 Log2 fold change. Conversely, a two-fold decrease in gene expression indicated a -1 Log2 fold change.

Fold change from baseline (predose on Day 1 of Cycle 1 [21-day cycle]) in normalized gene expression ratios (nGER) for 49 target genes was measured to assess target engagement of BET proteins predose and 12 hours postdose using quantitative polymerase chain reaction (qPCR). Data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Fold change from baseline was calculated as nGER at 12 hours postdose Day 1/baseline in logarithmic scale with a base of 2 (Log2 scale). Per protocol, target genes were assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The fold change in nGER for each target gene is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose. A two-fold increase in gene expression indicated a +1 Log2 fold change. Conversely, a two-fold decrease in gene expression indicated a -1 Log2 fold change.

Fold change from baseline (predose on Day 1 of Cycle 1 [21-day cycle]) in normalized gene expression ratios (nGER) for 49 target genes was measured to assess target engagement of BET proteins predose on Day 1 and predose on Day 8 of Cycle 1 (21-day cycle) using quantitative polymerase chain reaction (qPCR). Data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Fold change from baseline was calculated as nGER at predose Day 8/baseline in logarithmic scale with a base of 2 (Log2 scale). Per protocol, target genes were assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The fold change in nGER for each target gene is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose. A two-fold increase in gene expression indicated a +1 Log2 fold change. Conversely, a two-fold decrease in gene expression indicated a -1 Log2 fold change.

Total of all reporting groups

GERs for 49 Bromodomain and Extra-Terminal (BET) target genes were measured using messenger Ribonucleic Acid (mRNA) predose on Day 1 of Cycle 1 (21-day cycle). The expression level of target genes was quantitated by quantitative polymerase chain reaction and the data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Baseline normalized GERs were expressed in logarithmic scale with a base of 2 (Log2 scale). Positive values=greater expression and negative values=reduced expression of any gene relative to housekeeping genes.

An AE was defined as any untoward medical occurrence in a participant administered a study treatment and which does not necessarily have to have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the study treatment or protocol-specified procedure. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a pre-existing condition that is temporally associated with the use of study treatment, is also an AE. The percentage of all participants who experienced at least one AE is presented. Per protocol, these results are based on a data cutoff date of 09-May-2018.

The analysis population consisted of all participants who received at least one dose of study treatment.

An AE was defined as any untoward medical occurrence in a participant administered a study treatment and which does not necessarily have to have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the study treatment or protocol-specified procedure. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a pre-existing condition that is temporally associated with the use of study treatment, is also an AE. The percentage of all participants who discontinued study treatment due to an AE is presented. Per protocol, these results are based on a data cutoff date of 09-May-2018.

The analysis population consisted of all participants who received at least one dose of study treatment.

ORR was defined as the percentage of the participants who had complete response (CR) or partial response (PR) as assessed by investigator review. Participants in the AML cohort were assessed using bone marrow aspiration and hematologic criteria and response was evaluated based on European LeukemiaNet (Döhner et al, Blood, 2010). The criteria for complete response included: bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; absolute neutrophil count >1.0 × 10^9/Liter; platelet count >100 × 10^9/Liter; and independence of red cell transfusions. The criteria for partial response included: decrease of bone marrow blast percentage to 5% to 25%; decrease of pretreatment bone marrow blast percentage by at least 50%; and all hematologic criteria associated with CR. The percentage of participants who achieved CR or PR is presented.

The analysis population consisted of all participants in the AML cohort who received at least one dose of study treatment and had data evaluable for ORR analysis.

ORR was defined as the percentage of the participants who had complete response (CR) or partial response (PR) as assessed by investigator review. Participants in the DLBCL cohort were assessed using computed tomography (CT) and positron emission tomography (PET)-CT and response was evaluated based on the Lugano Classification (Cheson et al, Journal of Clinical Oncology, 2014). The criteria for CR included complete metabolic (no/minimal fluorodeoxyglucose [FDG] uptake) and radiologic response (target lesions regress to ≤5 cm in longest transverse diameter of a lesion) and no new lesions. The criteria for PR included: partial metabolic (moderate/high FDG uptake) and radiologic response (≥50% decrease in sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable nodes and extranodal sites, no increase in lesions, and spleen regressed by >50% in length beyond normal). The percentage of participants who achieved CR or PR is presented.

The analysis population consisted of all participants in the DLBCL cohort who received at least one dose of study treatment and had data evaluable for ORR analysis.

DOR was defined as the time from complete response (CR) or partial response (PR) to documented disease progression or death as assessed by investigator review. Participants in the AML cohort were assessed using bone marrow aspiration and hematologic criteria and response was evaluated based on European LeukemiaNet (Döhner et al, Blood, 2010). The criteria for complete response included: bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; absolute neutrophil count >1.0 × 10^9/Liter; platelet count >100 × 10^9/Liter; and independence of red cell transfusions. The criteria for partial response included: decrease of bone marrow blast percentage to 5% to 25%; decrease of pretreatment bone marrow blast percentage by at least 50%; and all hematologic criteria associated with CR.

The analysis population consisted of all participants in the AML cohort who received at least one dose of study treatment and had data evaluable for DOR analysis. DOR could not be calculated because no participants met criteria for analysis: CR or PR and documented disease progression or death.

DOR was defined as the time from complete response (CR) or partial response (PR) to documented disease progression or death as assessed by investigator review. Participants in the DLBCL cohort were assessed using computed tomography (CT) and positron emission tomography (PET)-CT and response was evaluated based on the Lugano Classification (Cheson et al, Journal of Clinical Oncology, 2014). The criteria for CR included complete metabolic (no/minimal fluorodeoxyglucose [FDG] uptake) and radiologic response (target lesions regress to ≤5 cm in longest transverse diameter of a lesion) and no new lesions. The criteria for PR included: partial metabolic (moderate/high FDG uptake) and radiologic response (≥50% decrease in sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable nodes and extranodal sites, no increase in lesions, and spleen regressed by >50% in length beyond normal).

The analysis population consisted of all participants in the DLBCL cohort who received at least one dose of study treatment and had data evaluable for DOR analysis. DOR could not be calculated because no participants met criteria for analysis: CR or PR and documented disease progression or death.

DCR was defined as the percentage of the participants who had stable disease, complete response (CR) or partial response (PR) as assessed by investigator review. Participants in the AML cohort were assessed using bone marrow aspiration and hematologic criteria and response was evaluated based on European LeukemiaNet (Döhner et al, Blood, 2010). The criteria for complete response included: bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; absolute neutrophil count >1.0 × 10^9/Liter; platelet count >100 × 10^9/Liter; and independence of red cell transfusions. The criteria for partial response included: decrease of bone marrow blast percentage to 5% to 25%; decrease of pretreatment bone marrow blast percentage by at least 50%; and all hematologic criteria associated with CR.

The analysis population consisted of all participants in the AML cohort who received at least one dose of study treatment and had data evaluable for DCR analysis.

DCR was defined as the percentage of the participants in the DLBCL cohort who had stable disease, complete response (CR) or partial response (PR) as assessed by investigator review. Participants in the DLBCL cohort were assessed using computed tomography (CT) and positron emission tomography (PET)-CT and response was evaluated based on the Lugano Classification (Cheson et al, Journal of Clinical Oncology, 2014). The criteria for CR included complete metabolic (no/minimal fluorodeoxyglucose [FDG] uptake) and radiologic response (target lesions regress to ≤5 cm in longest transverse diameter of a lesion) and no new lesions. The criteria for PR included: partial metabolic (moderate/high FDG uptake) and radiologic response (≥50% decrease in sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable nodes and extranodal sites, no increase in lesions, and spleen regressed by >50% in length beyond normal).

The analysis population consisted of all participants in the DLBCL cohort who received at least one dose of study treatment and had data evaluable for DCR analysis.

Blood samples were collected to determine Cmax at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, Cmax for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The Cmax of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received at least one dose of MK-8628 20 mg and had data available for Cmax analysis.

Blood samples were collected to determine Tmax at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, Tmax for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The Tmax of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received at least one dose of MK-8628 20 mg and had data available for the Tmax analysis.

Blood samples were collected to determine Cmin at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, Cmin for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The Cmin of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received at least one dose of MK-8628 20 mg and had data available for the Cmin analysis.

Blood samples were collected to determine AUC 0-∞ at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, AUC 0-∞ for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The AUC 0-∞ of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received at least one dose of MK-8628 20 mg and had data available for the AUC 0-∞ analysis.

Blood samples were collected to determine t1/2 at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, t1/2 for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The t1/2 of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received at least one dose of MK-8628 20 mg and had data available for the t1/2 analysis.

Blood samples were collected to determine CL/F at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, CL/F for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The CL/F of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received at least one dose of MK-8628 20 mg and had data available for CL/F analysis.

Blood samples were collected to determine Vz/F at the following time points: Cycle 1 (21-day cycle) Day 1 at predose and 20 minutes, 1 hour, 2.25 hours, 3.25 hours, 8 hours and 12 hours postdose; Cycle 1 (21-day cycle) at predose on Days 8 and 15; and Cycle 2 (21-day cycle) at predose on Day 1. Per protocol, Vz/F for MK-8628 was assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The Vz/F of MK-8628 after oral administration is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received at least one dose of MK-8628 20 mg and had data available for Vz/F analysis.

Fold change from baseline (predose on Day 1 of Cycle 1 [21-day cycle]) in normalized gene expression ratios (nGER) for 49 target genes was measured to assess target engagement of BET proteins predose and 3 hours postdose using quantitative polymerase chain reaction (qPCR). Data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Fold change from baseline was calculated as nGER at 3 hours postdose Day 1/baseline in logarithmic scale with a base of 2 (Log2 scale). Per protocol, target genes were assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The fold change in nGER for each target gene is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose. A two-fold increase in gene expression indicated a +1 Log2 fold change. Conversely, a two-fold decrease in gene expression indicated a -1 Log2 fold change.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received one dose of MK-8628 20 mg on Day 1 of Cycle 1 (21-day cycle) and had data available for the gene expression analysis.

Fold change from baseline (predose on Day 1 of Cycle 1 [21-day cycle]) in normalized gene expression ratios (nGER) for 49 target genes was measured to assess target engagement of BET proteins predose and 8 hours postdose using quantitative polymerase chain reaction (qPCR). Data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Fold change from baseline was calculated as nGER at 8 hours postdose Day 1/baseline in logarithmic scale with a base of 2 (Log2 scale). Per protocol, target genes were assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The fold change in nGER for each target gene is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose. A two-fold increase in gene expression indicated a +1 Log2 fold change. Conversely, a two-fold decrease in gene expression indicated a -1 Log2 fold change.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received one dose of MK-8628 20 mg on Day 1 of Cycle 1 (21-day cycle) and had data available for the gene expression analysis.

Fold change from baseline (predose on Day 1 of Cycle 1 [21-day cycle]) in normalized gene expression ratios (nGER) for 49 target genes was measured to assess target engagement of BET proteins predose and 12 hours postdose using quantitative polymerase chain reaction (qPCR). Data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Fold change from baseline was calculated as nGER at 12 hours postdose Day 1/baseline in logarithmic scale with a base of 2 (Log2 scale). Per protocol, target genes were assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The fold change in nGER for each target gene is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose. A two-fold increase in gene expression indicated a +1 Log2 fold change. Conversely, a two-fold decrease in gene expression indicated a -1 Log2 fold change.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received two doses of MK-8628 20 mg on Day 1 of Cycle 1 (21-day cycle) and had data available for the gene expression analysis.

Fold change from baseline (predose on Day 1 of Cycle 1 [21-day cycle]) in normalized gene expression ratios (nGER) for 49 target genes was measured to assess target engagement of BET proteins predose on Day 1 and predose on Day 8 of Cycle 1 (21-day cycle) using quantitative polymerase chain reaction (qPCR). Data were normalized by the delta-delta cycle threshold (Ct) method using housekeeping genes. Fold change from baseline was calculated as nGER at predose Day 8/baseline in logarithmic scale with a base of 2 (Log2 scale). Per protocol, target genes were assessed across all study participants by dose and this assessment was not related to any specific disease cohort. The fold change in nGER for each target gene is presented for participants pooled from the AML and DLBCL cohorts since both cohorts received the same dose. A two-fold increase in gene expression indicated a +1 Log2 fold change. Conversely, a two-fold decrease in gene expression indicated a -1 Log2 fold change.

The analysis population consisted of the total number of participants pooled from both cohorts (AML and DLBCL) who received 14 doses of MK-8628 20 mg by Day 8 of Cycle 1 (21-day cycle) and had data available for the gene expression analysis.

Participants in the DLBCL cohort received 20 mg of MK-8628 as an oral capsule twice a day for 21 consecutive days per cycle (21-day cycle).