Exhibit 99.1 Developing Next-Generation Epigenetic Treatments for Cancer Patients Corporate Overview September 24, 2019 Stellar Science, Breakthrough MedicineExhibit 99.1 Developing Next-Generation Epigenetic Treatments for Cancer Patients Corporate Overview September 24, 2019 Stellar Science, Breakthrough Medicine

Forward-Looking Statements This presentation contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties, including statements regarding the implications of preclinical data and the development status of, and development plans and timelines for, the Company’s product candidates. All statements, other than statements of historical facts, contained in this press release, including statements regarding the Company’s strategy, future operations, future financial position, prospects, plans and objectives of management, are forward-looking statements. The words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” “would” and similar expressions are intended to identify forward- looking statements, although not all forward-looking statements contain these identifying words. Any forward-looking statements are based on management’s current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in, or implied by, such forward-looking statements. These risks and uncertainties include, but are not limited to, risks associated with Constellation’s ability to: obtain and maintain necessary approvals from the FDA and other regulatory authorities; continue to advance its product candidates in clinical trials; whether preliminary or interim results from preclinical studies or a clinical trial will be predictive of the final results of a clinical trial; advance the development of its product candidates under the timelines it anticipates, or at all, in current and future clinical trials; obtain, maintain or protect intellectual property rights related to its product candidates; manage expenses; and raise the substantial additional capital needed to achieve its business objectives. For a discussion of other risks and uncertainties, any of which could cause the Company’s actual results to differ from those contained in the forward-looking statements, see the “Risk Factors” section, as well as discussions of potential risks, uncertainties, and other important factors, in the Company’s most recent filings with the Securities and Exchange Commission. In addition, the forward- looking statements included in this press release represent the Company’s views as of the date hereof and should not be relied upon as representing the Company’s views as of any date subsequent to the date hereof. The Company anticipates that subsequent events and developments will cause the Company’s views to change. However, while the Company may elect to update these forward-looking statements at some point in the future, the Company specifically disclaims any obligation to do so. CPI-1205, CPI-0610, CPI-0209, and other product candidates are investigational in nature and have not yet been approved by the FDA or other regulatory authorities. 2Forward-Looking Statements This presentation contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties, including statements regarding the implications of preclinical data and the development status of, and development plans and timelines for, the Company’s product candidates. All statements, other than statements of historical facts, contained in this press release, including statements regarding the Company’s strategy, future operations, future financial position, prospects, plans and objectives of management, are forward-looking statements. The words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” “would” and similar expressions are intended to identify forward- looking statements, although not all forward-looking statements contain these identifying words. Any forward-looking statements are based on management’s current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in, or implied by, such forward-looking statements. These risks and uncertainties include, but are not limited to, risks associated with Constellation’s ability to: obtain and maintain necessary approvals from the FDA and other regulatory authorities; continue to advance its product candidates in clinical trials; whether preliminary or interim results from preclinical studies or a clinical trial will be predictive of the final results of a clinical trial; advance the development of its product candidates under the timelines it anticipates, or at all, in current and future clinical trials; obtain, maintain or protect intellectual property rights related to its product candidates; manage expenses; and raise the substantial additional capital needed to achieve its business objectives. For a discussion of other risks and uncertainties, any of which could cause the Company’s actual results to differ from those contained in the forward-looking statements, see the “Risk Factors” section, as well as discussions of potential risks, uncertainties, and other important factors, in the Company’s most recent filings with the Securities and Exchange Commission. In addition, the forward- looking statements included in this press release represent the Company’s views as of the date hereof and should not be relied upon as representing the Company’s views as of any date subsequent to the date hereof. The Company anticipates that subsequent events and developments will cause the Company’s views to change. However, while the Company may elect to update these forward-looking statements at some point in the future, the Company specifically disclaims any obligation to do so. CPI-1205, CPI-0610, CPI-0209, and other product candidates are investigational in nature and have not yet been approved by the FDA or other regulatory authorities. 2

Constellation Highlights Three wholly owned clinical programs: CPI-0610 (BET) and CPI-1205 and CPI-0209 (EZH2) CPI-0610 has possible disease-modifying effects in myelofibrosis CPI-1205 has been well tolerated and active in clinical studies in combination with ARS inhibitors in prostate cancer CPI-0209 expands the potential of our EZH2 franchise Program updates in 2H 2019 Robust discovery platform fuels the pipeline 3Constellation Highlights Three wholly owned clinical programs: CPI-0610 (BET) and CPI-1205 and CPI-0209 (EZH2) CPI-0610 has possible disease-modifying effects in myelofibrosis CPI-1205 has been well tolerated and active in clinical studies in combination with ARS inhibitors in prostate cancer CPI-0209 expands the potential of our EZH2 franchise Program updates in 2H 2019 Robust discovery platform fuels the pipeline 3

Multiple Near-Term Opportunities for Success Product Candidates Indications Preclinical Phase 1 Phase 2 Phase 3 Milestones BET Inhibitor 2L Myelofibrosis✓ Interim Ph 2 data at ASCO/EHA CPI-0610 MANIFEST Trial 1L Myelofibrosis❑ Additional data update in 4Q19 EZH2 Franchise ✓ Phase 1b data at AACR CPI-1205 2L mCRPC* ProSTAR Trial ❑ Program update in 4Q19 ✓ File IND in mid-2019 CPI-0209 Solid Tumors (2nd Generation) ✓ First patient dosed in Phase 1 Preclinical Tumor Targeted Solid Tumors / (Undisclosed) Heme Malignancies Tumor Microenvironment Solid Tumors Targeted (Undisclosed) 4 * Metastatic castration-resistant prostate cancerMultiple Near-Term Opportunities for Success Product Candidates Indications Preclinical Phase 1 Phase 2 Phase 3 Milestones BET Inhibitor 2L Myelofibrosis✓ Interim Ph 2 data at ASCO/EHA CPI-0610 MANIFEST Trial 1L Myelofibrosis❑ Additional data update in 4Q19 EZH2 Franchise ✓ Phase 1b data at AACR CPI-1205 2L mCRPC* ProSTAR Trial ❑ Program update in 4Q19 ✓ File IND in mid-2019 CPI-0209 Solid Tumors (2nd Generation) ✓ First patient dosed in Phase 1 Preclinical Tumor Targeted Solid Tumors / (Undisclosed) Heme Malignancies Tumor Microenvironment Solid Tumors Targeted (Undisclosed) 4 * Metastatic castration-resistant prostate cancer

Vision for 2019: A Year of Data Transition into a Late-Stage Oncology Development Company with an Exciting Pipeline of Development and Discovery Programs ● Generate positive POC and begin planning for pivotal registration studies with CPI-0610 and CPI-1205 ● Expand our EZH2 franchise by advancing CPI-0209 into clinical trials targeting solid tumors 2019 ● Deliver novel candidates into discovery and development portfolio 5Vision for 2019: A Year of Data Transition into a Late-Stage Oncology Development Company with an Exciting Pipeline of Development and Discovery Programs ● Generate positive POC and begin planning for pivotal registration studies with CPI-0610 and CPI-1205 ● Expand our EZH2 franchise by advancing CPI-0209 into clinical trials targeting solid tumors 2019 ● Deliver novel candidates into discovery and development portfolio 5

Epigenetics: Instructions for Genetic Code Focused on Three Distinct Classes That Tumor Microenvironment Chemically Modify Chromatin Writers Erasers Readers Tumor Cells T Cell NK Cell MDSC Target Re-program Immune Transcriptional Cells to Overcome Transcriptional Control to Turn Genes On or Off Networks That Resistance to Cancer Result in Cell Death Immunotherapies 6Epigenetics: Instructions for Genetic Code Focused on Three Distinct Classes That Tumor Microenvironment Chemically Modify Chromatin Writers Erasers Readers Tumor Cells T Cell NK Cell MDSC Target Re-program Immune Transcriptional Cells to Overcome Transcriptional Control to Turn Genes On or Off Networks That Resistance to Cancer Result in Cell Death Immunotherapies 6

CPI-0610CPI-0610

BET Family of Proteins Control of Key Immune, Fibrotic, and Oncogenic Pathways Leads to Opportunity in Myelofibrosis (MF) Immune Signaling ● NF-κB target genes Fibrosis ● TGF-β target genes Transcription Factor Enhancer Cancer Genetics BRD4 ● MYC, BCL2 … TSS 8BET Family of Proteins Control of Key Immune, Fibrotic, and Oncogenic Pathways Leads to Opportunity in Myelofibrosis (MF) Immune Signaling ● NF-κB target genes Fibrosis ● TGF-β target genes Transcription Factor Enhancer Cancer Genetics BRD4 ● MYC, BCL2 … TSS 8

In Vivo Support for BET Inhibition Enhancing JAK Inhibition in MF BET Inhibitor + Ruxolitinib Led to Synergistic Improved Bone Marrow Fibrosis Score Reduction in Spleen * Vehicle JQ1 (BETi) 1–2+ 1+ * 900 800 700 600 500 * 400 300 200 100 Ruxolitinib Combo 0 1+ 0 Vehicle JQ1 (BETi) Ruxolitinib Combo * Bar graph showing spleen weights (mg) of animals treated for 21 days (vehicle and JQ1) or 28 days (ruxolitinib and combo). n=4–5.*p value <0.05. Data is representative of three independent experiments. 9 Kleppe et al., 2018 Cancer Cell Spleen Weight (mg)In Vivo Support for BET Inhibition Enhancing JAK Inhibition in MF BET Inhibitor + Ruxolitinib Led to Synergistic Improved Bone Marrow Fibrosis Score Reduction in Spleen * Vehicle JQ1 (BETi) 1–2+ 1+ * 900 800 700 600 500 * 400 300 200 100 Ruxolitinib Combo 0 1+ 0 Vehicle JQ1 (BETi) Ruxolitinib Combo * Bar graph showing spleen weights (mg) of animals treated for 21 days (vehicle and JQ1) or 28 days (ruxolitinib and combo). n=4–5.*p value <0.05. Data is representative of three independent experiments. 9 Kleppe et al., 2018 Cancer Cell Spleen Weight (mg)

Myelofibrosis Patient Journey Multiple Positioning Options for CPI-0610 1L: Treatment 2L: Continue on Symptomatic MF with ruxolitinib ruxolitinib CPI-0610 CPI-0610 + Rux Combo Add-On Vision for CPI-0610 Provide Differentiated Diseased Treatment for 2L Bone Marrow Ruxolitinib-Resistant Patients 2L: Discontinue ruxolitinib Transform CPI-0610 Standard of Care in Monotherapy Diseased Diseased 1L JAK-Inhibitor-Naïve Bone Marrow Bone Marrow Patients Diseased Bone Marrow Disease Progression 10Myelofibrosis Patient Journey Multiple Positioning Options for CPI-0610 1L: Treatment 2L: Continue on Symptomatic MF with ruxolitinib ruxolitinib CPI-0610 CPI-0610 + Rux Combo Add-On Vision for CPI-0610 Provide Differentiated Diseased Treatment for 2L Bone Marrow Ruxolitinib-Resistant Patients 2L: Discontinue ruxolitinib Transform CPI-0610 Standard of Care in Monotherapy Diseased Diseased 1L JAK-Inhibitor-Naïve Bone Marrow Bone Marrow Patients Diseased Bone Marrow Disease Progression 10

Mechanism of Potential Disease Modification in Myelofibrosis Reduce Inflammation and Suppress Cells in the Bone Marrow that Drive MF (Megakaryocytes) Cytoplasm JAK/STAT Nucleus Signaling BET Signaling STAT STAT NF-kB Target Genes BETs P P CPI-0610 Pro-Inflammatory Cytokines Differentiation of Myeloid (e.g., IL-8) Cells into Megakaryocytes = Pathway Blocked by CPI-0610 11Mechanism of Potential Disease Modification in Myelofibrosis Reduce Inflammation and Suppress Cells in the Bone Marrow that Drive MF (Megakaryocytes) Cytoplasm JAK/STAT Nucleus Signaling BET Signaling STAT STAT NF-kB Target Genes BETs P P CPI-0610 Pro-Inflammatory Cytokines Differentiation of Myeloid (e.g., IL-8) Cells into Megakaryocytes = Pathway Blocked by CPI-0610 11

CPI-0610 is a Potential Best-in-Class BET Inhibitor ● Potent and selective inhibitor of BET proteins Selected BET Inhibitors with Published Phase 1 Lymphoma Data ● Treated 138 patients in Phase 1 trials of various hematologic malignancies 300 ● Preliminary clinical activity observed: 200 – Potentially disease modifying in MF (Phase 2) – Lymphoma – e.g., ABC-DLBCL (Phase 1) Active Lymphoma Dose/MF Ph2 Dose** 100 ● Signals of potentially differentiated safety Lowest Active profile Dose* – Phase 1 data suggest that thrombocytopenia 0 (DLT) is dose dependent, reversible and non-cumulative # ^ CPI-0610 INCB057643 OTX-015 ^ MK-8628 – Activity seen at range of doses below the MTD Active Doses Maximum Tolerated Dose *CR also achieved at lower dose of 48mg QD capsule **Ability to titrate up to 225 mg #Source – Forero-Torres et al. (2017) – Poster at American Society for Hematology 2017 Annual Meeting 12 ^Sources – Amorin et al. (2016) Lancet Haematology, Volume 3, Issue 4 196-204 Dose – mg (once daily)CPI-0610 is a Potential Best-in-Class BET Inhibitor ● Potent and selective inhibitor of BET proteins Selected BET Inhibitors with Published Phase 1 Lymphoma Data ● Treated 138 patients in Phase 1 trials of various hematologic malignancies 300 ● Preliminary clinical activity observed: 200 – Potentially disease modifying in MF (Phase 2) – Lymphoma – e.g., ABC-DLBCL (Phase 1) Active Lymphoma Dose/MF Ph2 Dose** 100 ● Signals of potentially differentiated safety Lowest Active profile Dose* – Phase 1 data suggest that thrombocytopenia 0 (DLT) is dose dependent, reversible and non-cumulative # ^ CPI-0610 INCB057643 OTX-015 ^ MK-8628 – Activity seen at range of doses below the MTD Active Doses Maximum Tolerated Dose *CR also achieved at lower dose of 48mg QD capsule **Ability to titrate up to 225 mg #Source – Forero-Torres et al. (2017) – Poster at American Society for Hematology 2017 Annual Meeting 12 ^Sources – Amorin et al. (2016) Lancet Haematology, Volume 3, Issue 4 196-204 Dose – mg (once daily)

Working to Meet Unmet Need for a Disease-Modifying Therapy that Impacts All Four Hallmarks of MF Hallmarks of Myelofibrosis Spleen Constitutional Anemia & Transfusion Bone Marrow Volume Symptoms Dependence Fibrosis 2018 Rux WW Sales: ~$2.4B** JAKi’s 2018 Rux WW MF Sales: ~$1.4B*** CPI-0610* * Based on preliminary data ** Full-year 2018 earnings releases of Incyte and Novartis 13 *** Constellation estimateWorking to Meet Unmet Need for a Disease-Modifying Therapy that Impacts All Four Hallmarks of MF Hallmarks of Myelofibrosis Spleen Constitutional Anemia & Transfusion Bone Marrow Volume Symptoms Dependence Fibrosis 2018 Rux WW Sales: ~$2.4B** JAKi’s 2018 Rux WW MF Sales: ~$1.4B*** CPI-0610* * Based on preliminary data ** Full-year 2018 earnings releases of Incyte and Novartis 13 *** Constellation estimate

MANIFEST Study Design Overview Treatment Study Population Arm / Cohort Cohort 1A: TD ▪No longer on ruxolitinib n = up to 16 CPI-0610 ▪Refractory or intolerant Mono Cohort 1B: Non-TD or ineligible Data Cut as of April 17, 2019 n = up to 25 • 44 patients enrolled Cohort 2A: TD • No patient experienced ▪“Add on” to ruxolitinib n = up to 16 CPI-0610 + disease progression ▪Sub-optimal response or Ruxolitinib Cohort 2B: Non-TD MF progression • Poor prognostic factors n = up to 25 • 16 patients for at least 12 weeks ▪No prior JAK inhibitor CPI-0610 + Cohort 3: JAKi Naive Ruxolitinib n = up to 43 use Data cutoff April 17, 2019 TD = Transfusion dependent, defined as receiving an average of ≥ 2 RBC transfusions per month during the 12 weeks prior to enrollment Non-TD = Non-transfusion-dependent, defined as receiving an average of < 2 RBC transfusions per month during the 12 weeks prior to enrollment 14 Cohorts 1A/1B and Cohorts 2A/2B will apply a Simon 2 stage designMANIFEST Study Design Overview Treatment Study Population Arm / Cohort Cohort 1A: TD ▪No longer on ruxolitinib n = up to 16 CPI-0610 ▪Refractory or intolerant Mono Cohort 1B: Non-TD or ineligible Data Cut as of April 17, 2019 n = up to 25 • 44 patients enrolled Cohort 2A: TD • No patient experienced ▪“Add on” to ruxolitinib n = up to 16 CPI-0610 + disease progression ▪Sub-optimal response or Ruxolitinib Cohort 2B: Non-TD MF progression • Poor prognostic factors n = up to 25 • 16 patients for at least 12 weeks ▪No prior JAK inhibitor CPI-0610 + Cohort 3: JAKi Naive Ruxolitinib n = up to 43 use Data cutoff April 17, 2019 TD = Transfusion dependent, defined as receiving an average of ≥ 2 RBC transfusions per month during the 12 weeks prior to enrollment Non-TD = Non-transfusion-dependent, defined as receiving an average of < 2 RBC transfusions per month during the 12 weeks prior to enrollment 14 Cohorts 1A/1B and Cohorts 2A/2B will apply a Simon 2 stage design

Baseline Demographics and Disease Characteristics Cohort 1A Cohort 1B Cohort 2A Cohort 2B Cohort 3 TOTAL Parameter 0610 Mono 0610 Mono 0610 + Rux 0610 + Rux 0610 + Rux (n=44) TD (n=2) Non-TD (n=8) TD (n=16) Non-TD (n=15) JAKi Naïve (n=3) Age Median (range) 68 (67, 69) 70 (46, 80) 72.5 (41, 83) 66 (49, 75) 71 (67, 76) 69 (41, 83) Female (n, %) 1 (50.0) 5 (62.5) 6 (37.5) 6 (40.0) 0 (0.0) 18 (40.9) Sex Male (n, %) 1 (50.0) 3 (37.5) 10 (62.5) 9 (60.0) 3 (100.0) 26 (59.1) ≤1 (n, %) 2 (100.0) 7 (87.5) 14 (87.5) 14 (93.3) 2 (66.7) 39 (88.6) 2 (n, %) 0 (0.0) 1 (12.5) 1 (6.3) 1 (6.7) 1 (33.3) 4 (9.1) ECOG Unknown (n, %) 0 (0.0) 0 (0.0) 1 (6.3) 0 (0.0) 0 (0.0) 1 (2.3) Intermediate 1-2 2 (100.0) 5 (62.5) 13 (81.2) 12 (80.0) 3 (100.0) 35 (79.6) DIPSS High 0 (0.0) 3 (37.5) 3 (18.8) 3 (20.0) 0 (0.0) 9 (20.4) Primary MF (n, %) 1 (50.0) 6 (75.0) 10 (62.5) 9 (60.0) 3 (100.0) 29 (65.9) Post PV MF (n, %) 0 (0.0) 1 (12.5) 3 (18,8) 3 (20.0) 0 (0.0) 7 (15.9) MF Subtype Post ET MF (n, %) 1 (50.0) 0 (0.0) 2 (12.5) 3 (20.0) 0 (0.0) 6 (13.6) Unknown (n, %) 0 (0.0) 1 (12.5) 1 (6.3) 0 (0.0) 0 (0.0) 2 (4.5) n 2 7 16 15 2 42 Mutation Status ≥3 mutations (n, %) 1 (50.0) 3 (42.9) 9 (56.3 ) 10 (66.7) 1 (50.0) 24 (57.1) ASXL1 (n, %) 1 (50.0) 4 (57.1) 8 (50.0) 12 (80.0) 1 (50.0) 26 (61.9) <6 months 0 (0.0) 1 (12.5) 3 (18.8) 2 (13.3) 0 (0.0) 6 (13.6) ≥6 months 0 (0.0) 6 (75.0) 12 (75.0) 13 (86.7) 0 (0.0) 31 (70.5) Prior Ruxolitinib Tx Duration Unknown 1 (50.0) 1 (12.5) 1 (6.3) 0 (0.0) 0 (0.0) 3 (6.8) Not Applicable 1 (50.0) 0 (0.0) 0 (0.0) 0 (0.0) 3 (100.0) 4 (9.1) Median (range) 292.5 (157, 428) 548.0 (89, 895) 188.5 (77, 631) 224.0 (108, 673) 165 (112, 174) 211.5 (89, 895) 9 Platelets <450 x 10 /L 2 (100.0) 3 (37.5) 14 (87.5) 14 (93.3) 3 (100.0) 36 (81.8) 9 ≥450 x 10 /L 0 (0.0) 5 (62.5) 2 (12.5) 1 (6.7) 0 (0.0) 8 (18.2) Median (range) 7.55 (7.0, 8.1) 9.25 (7.9, 11.8) 8.35 (6.4, 9.4) 10.3 (8.1, 13.0) 8.7 (7.9, 8.9) 8.9 (6.4, 13.0) Hemoglobin <10g/dL 2 (100.0) 6 (75.0) 16 (100.0) 6 (40.0) 3 (100.0) 33 (75.0) ≥10g/dL 0 (0.0) 2 (25.0) 0 (0.0) 9 (60.0) 0 (0.0) 11 (25.0) n 2 8 11 13 3 37 Spleen Volume Median (range) 1514.5 (452, 2577) 2114.5 (635, 3997) 1179.0 (167.9, 4007) 2409.0 (123, 4941) 1810.0 (1379, 2409) 2164.0 (123, 4941) n 0 6 13 13 3 35 Total Symptoms Score (TSS) Median (range) NA 22.2 (9.2, 42.6) 13.0 (1.4, 37.3) 28.0 (5.0, 56.0) 14.6 (9.1, 16.7) 17.0 (1.4, 56.0) 15 Data cutoff April 17, 2019Baseline Demographics and Disease Characteristics Cohort 1A Cohort 1B Cohort 2A Cohort 2B Cohort 3 TOTAL Parameter 0610 Mono 0610 Mono 0610 + Rux 0610 + Rux 0610 + Rux (n=44) TD (n=2) Non-TD (n=8) TD (n=16) Non-TD (n=15) JAKi Naïve (n=3) Age Median (range) 68 (67, 69) 70 (46, 80) 72.5 (41, 83) 66 (49, 75) 71 (67, 76) 69 (41, 83) Female (n, %) 1 (50.0) 5 (62.5) 6 (37.5) 6 (40.0) 0 (0.0) 18 (40.9) Sex Male (n, %) 1 (50.0) 3 (37.5) 10 (62.5) 9 (60.0) 3 (100.0) 26 (59.1) ≤1 (n, %) 2 (100.0) 7 (87.5) 14 (87.5) 14 (93.3) 2 (66.7) 39 (88.6) 2 (n, %) 0 (0.0) 1 (12.5) 1 (6.3) 1 (6.7) 1 (33.3) 4 (9.1) ECOG Unknown (n, %) 0 (0.0) 0 (0.0) 1 (6.3) 0 (0.0) 0 (0.0) 1 (2.3) Intermediate 1-2 2 (100.0) 5 (62.5) 13 (81.2) 12 (80.0) 3 (100.0) 35 (79.6) DIPSS High 0 (0.0) 3 (37.5) 3 (18.8) 3 (20.0) 0 (0.0) 9 (20.4) Primary MF (n, %) 1 (50.0) 6 (75.0) 10 (62.5) 9 (60.0) 3 (100.0) 29 (65.9) Post PV MF (n, %) 0 (0.0) 1 (12.5) 3 (18,8) 3 (20.0) 0 (0.0) 7 (15.9) MF Subtype Post ET MF (n, %) 1 (50.0) 0 (0.0) 2 (12.5) 3 (20.0) 0 (0.0) 6 (13.6) Unknown (n, %) 0 (0.0) 1 (12.5) 1 (6.3) 0 (0.0) 0 (0.0) 2 (4.5) n 2 7 16 15 2 42 Mutation Status ≥3 mutations (n, %) 1 (50.0) 3 (42.9) 9 (56.3 ) 10 (66.7) 1 (50.0) 24 (57.1) ASXL1 (n, %) 1 (50.0) 4 (57.1) 8 (50.0) 12 (80.0) 1 (50.0) 26 (61.9) <6 months 0 (0.0) 1 (12.5) 3 (18.8) 2 (13.3) 0 (0.0) 6 (13.6) ≥6 months 0 (0.0) 6 (75.0) 12 (75.0) 13 (86.7) 0 (0.0) 31 (70.5) Prior Ruxolitinib Tx Duration Unknown 1 (50.0) 1 (12.5) 1 (6.3) 0 (0.0) 0 (0.0) 3 (6.8) Not Applicable 1 (50.0) 0 (0.0) 0 (0.0) 0 (0.0) 3 (100.0) 4 (9.1) Median (range) 292.5 (157, 428) 548.0 (89, 895) 188.5 (77, 631) 224.0 (108, 673) 165 (112, 174) 211.5 (89, 895) 9 Platelets <450 x 10 /L 2 (100.0) 3 (37.5) 14 (87.5) 14 (93.3) 3 (100.0) 36 (81.8) 9 ≥450 x 10 /L 0 (0.0) 5 (62.5) 2 (12.5) 1 (6.7) 0 (0.0) 8 (18.2) Median (range) 7.55 (7.0, 8.1) 9.25 (7.9, 11.8) 8.35 (6.4, 9.4) 10.3 (8.1, 13.0) 8.7 (7.9, 8.9) 8.9 (6.4, 13.0) Hemoglobin <10g/dL 2 (100.0) 6 (75.0) 16 (100.0) 6 (40.0) 3 (100.0) 33 (75.0) ≥10g/dL 0 (0.0) 2 (25.0) 0 (0.0) 9 (60.0) 0 (0.0) 11 (25.0) n 2 8 11 13 3 37 Spleen Volume Median (range) 1514.5 (452, 2577) 2114.5 (635, 3997) 1179.0 (167.9, 4007) 2409.0 (123, 4941) 1810.0 (1379, 2409) 2164.0 (123, 4941) n 0 6 13 13 3 35 Total Symptoms Score (TSS) Median (range) NA 22.2 (9.2, 42.6) 13.0 (1.4, 37.3) 28.0 (5.0, 56.0) 14.6 (9.1, 16.7) 17.0 (1.4, 56.0) 15 Data cutoff April 17, 2019

Treatment Duration 11-245 ● Total 44 patients enrolled 11-246 11-247 ▪ 39 patients active on treatment; 5 patients 11-248 discontinued 11-252 14-251 14-258 ● Evaluable patients population 11-261 11-264 ▪ Safety: Received C1D1 treatment – n=44 11-265 14-263 14-267 ▪ SVR: Baseline and one post-baseline data 41-259 available – n=16 @ 12 weeks; n=12 @ 24 weeks 40-271 19-277 11-276 ▪ TSS: Baseline TSS data available – n=11 @ 12 40-270 weeks 40-280 12-293 14-262 ▪ Bone marrow morphology: Baseline and one post- 14-281 baseline data available – n=10 @ 24 weeks 11-283 40-285 31-286 ● Reasons for treatment discontinuation 44-287 44-288 ▪ 11-250 – Depression Grade 4 and alcohol 12-289 11-290 intoxication Grade 2 12-294 12-295 ▪ 14-262 – Squamous cell carcinoma Grade 3 (due 31-296 11-303 Cohort 1A (TD - CPI-0610 Mono) to prior ruxolitinib therapy) 12-304 11-250 Cohort 1B (Non-TD - CPI-0610 Mono) ▪ 40-270 – Acute renal failure Grade 5 (unlikely 39-282 43-291 related) Cohort 2A (TD - CPI-0610 + Ruxo) 43-292 19-298 Cohort 2B (Non-TD - CPI-0610 + Ruxo) ▪ 39-282 – Diarrhea Grade 2 (withdrew consent) 14-300 24-wk, C9D1 12-wk, C5D1 43-302 Cohort 3 (JAKi Naive - CPI-0610 + Ruxo) ▪ 43-291 – Diarrhea Grade 2 (pre-existent condition 40-305 CT/MRI, TSS, BM Bx CT/MRI, TSS 11-309 IBD, withdrew consent) 11-306 Discontinued treatment 11-308 0 4 8 12 16 20 24 28 32 16 Data cutoff April 17, 2019 Treatment CycleTreatment Duration 11-245 ● Total 44 patients enrolled 11-246 11-247 ▪ 39 patients active on treatment; 5 patients 11-248 discontinued 11-252 14-251 14-258 ● Evaluable patients population 11-261 11-264 ▪ Safety: Received C1D1 treatment – n=44 11-265 14-263 14-267 ▪ SVR: Baseline and one post-baseline data 41-259 available – n=16 @ 12 weeks; n=12 @ 24 weeks 40-271 19-277 11-276 ▪ TSS: Baseline TSS data available – n=11 @ 12 40-270 weeks 40-280 12-293 14-262 ▪ Bone marrow morphology: Baseline and one post- 14-281 baseline data available – n=10 @ 24 weeks 11-283 40-285 31-286 ● Reasons for treatment discontinuation 44-287 44-288 ▪ 11-250 – Depression Grade 4 and alcohol 12-289 11-290 intoxication Grade 2 12-294 12-295 ▪ 14-262 – Squamous cell carcinoma Grade 3 (due 31-296 11-303 Cohort 1A (TD - CPI-0610 Mono) to prior ruxolitinib therapy) 12-304 11-250 Cohort 1B (Non-TD - CPI-0610 Mono) ▪ 40-270 – Acute renal failure Grade 5 (unlikely 39-282 43-291 related) Cohort 2A (TD - CPI-0610 + Ruxo) 43-292 19-298 Cohort 2B (Non-TD - CPI-0610 + Ruxo) ▪ 39-282 – Diarrhea Grade 2 (withdrew consent) 14-300 24-wk, C9D1 12-wk, C5D1 43-302 Cohort 3 (JAKi Naive - CPI-0610 + Ruxo) ▪ 43-291 – Diarrhea Grade 2 (pre-existent condition 40-305 CT/MRI, TSS, BM Bx CT/MRI, TSS 11-309 IBD, withdrew consent) 11-306 Discontinued treatment 11-308 0 4 8 12 16 20 24 28 32 16 Data cutoff April 17, 2019 Treatment Cycle

Summary of CPI-0610 Data Update from ASCO/EHA 2019 Hallmarks of Myelofibrosis Spleen Constitutional Anemia & Transfusion Bone Marrow Volume Symptoms Dependence Fibrosis ● 14 of 16 (88%) ● 6 of 11 (55%) of ● Trend of rising HgB ● 6 of 10 (60%) patients achieve patients achieve due to CPI-0610 patients achieved spleen reduction >50% improvement in treatment improvement in TSS bone marrow ● 2 of 3 combo morphology ● 15 of 16 (94%) patients converted achieve improvement from TD to TI in Patient Global Impression of Change (PGIC) Data cutoff April 17, 2019 TD = Transfusion dependent, defined as receiving an average of ≥ 2 RBC transfusions per month during the 12 weeks prior to enrollment TI = Transfusion independent, defined as absence of RBC transfusions over any consecutive 12-week period 17 *Please see poster A Phase 2 Study of CPI-0610…, which was presented at ASCO on June 3, 2019, in the Investors & Media/Presentations section of http://www.constellationpharma.comSummary of CPI-0610 Data Update from ASCO/EHA 2019 Hallmarks of Myelofibrosis Spleen Constitutional Anemia & Transfusion Bone Marrow Volume Symptoms Dependence Fibrosis ● 14 of 16 (88%) ● 6 of 11 (55%) of ● Trend of rising HgB ● 6 of 10 (60%) patients achieve patients achieve due to CPI-0610 patients achieved spleen reduction >50% improvement in treatment improvement in TSS bone marrow ● 2 of 3 combo morphology ● 15 of 16 (94%) patients converted achieve improvement from TD to TI in Patient Global Impression of Change (PGIC) Data cutoff April 17, 2019 TD = Transfusion dependent, defined as receiving an average of ≥ 2 RBC transfusions per month during the 12 weeks prior to enrollment TI = Transfusion independent, defined as absence of RBC transfusions over any consecutive 12-week period 17 *Please see poster A Phase 2 Study of CPI-0610…, which was presented at ASCO on June 3, 2019, in the Investors & Media/Presentations section of http://www.constellationpharma.com

Best Spleen Volume Reduction (n=16) 20 * Cohort 1A (TD - CPI-0610 Mono) ● 14 of 16 evaluable patients had spleen * Cohort 1B (Non-TD - CPI-0610 Mono) volume reductions 10 Cohort 2A (TD - CPI-0610 + Ruxo) Cohort 2B (Non-TD - CPI-0610 + Ruxo) 0 ● Median change of -19.2% -10 ● Spleen volume reduction observed in 4 of 4 evaluable non-TD monotherapy MF patients -20 (depicted in blue) -30 -40 -50 -60 Data cutoff April 17, 2019 18 *Patient ineligible for ruxolitinib due to very low hemoglobin 11-264 11-248 11-247 11-276 14-258 19-277 14-251 11-252 40-271 11-246 41-259 14-263 11-261 11-245 11-265 14-267 % Change from BaselineBest Spleen Volume Reduction (n=16) 20 * Cohort 1A (TD - CPI-0610 Mono) ● 14 of 16 evaluable patients had spleen * Cohort 1B (Non-TD - CPI-0610 Mono) volume reductions 10 Cohort 2A (TD - CPI-0610 + Ruxo) Cohort 2B (Non-TD - CPI-0610 + Ruxo) 0 ● Median change of -19.2% -10 ● Spleen volume reduction observed in 4 of 4 evaluable non-TD monotherapy MF patients -20 (depicted in blue) -30 -40 -50 -60 Data cutoff April 17, 2019 18 *Patient ineligible for ruxolitinib due to very low hemoglobin 11-264 11-248 11-247 11-276 14-258 19-277 14-251 11-252 40-271 11-246 41-259 14-263 11-261 11-245 11-265 14-267 % Change from Baseline

Improvements in Symptoms Best % Total Symptom Score (TSS) Improvement Best Patient Global Impression of Change (PGIC) (n=11) Observed (n=16) 4 20 Cohort 1B (Non-TD - CPI-0610 Mono) Cohort 2A (TD - CPI-0610 + Ruxo) 10 Very much worse 7 Cohort 2B (Non-TD - CPI-0610 + Ruxo) Cohort 1A (TD - CPI-0610 Mono) 0 Cohort 1B (Non-TD - CPI-0610 Mono) Much worse 6 Cohort 2A (TD - CPI-0610 + Ruxo) -10 Cohort 2B (Non-TD - CPI-0610 + Ruxo) -20 Minimally worse 5 -30 No Change 4 -40 -50 Minimally improved 3 -60 -70 Much improved 2 -80 Very much improved 1 -90 -100 -4 ● Improvement in TSS observed in 100% of patients ● Improvement in PGIC observed in 15 of 16 (94%) patients ● 6 of 11 (55%) patients achieve > 50% improvement in TSS ● No patient worsened 19 Data cutoff April 17, 2019 11-276 14-258 11-252 40-271 19-277 14-251 14-263 41-259 11-261 11-265 14-267 11-264 11-248 11-276 14-258 11-247 19-277 40-271 11-252 11-246 14-251 41-259 14-263 11-261 11-245 14-267 11-265 % Change from BaselineImprovements in Symptoms Best % Total Symptom Score (TSS) Improvement Best Patient Global Impression of Change (PGIC) (n=11) Observed (n=16) 4 20 Cohort 1B (Non-TD - CPI-0610 Mono) Cohort 2A (TD - CPI-0610 + Ruxo) 10 Very much worse 7 Cohort 2B (Non-TD - CPI-0610 + Ruxo) Cohort 1A (TD - CPI-0610 Mono) 0 Cohort 1B (Non-TD - CPI-0610 Mono) Much worse 6 Cohort 2A (TD - CPI-0610 + Ruxo) -10 Cohort 2B (Non-TD - CPI-0610 + Ruxo) -20 Minimally worse 5 -30 No Change 4 -40 -50 Minimally improved 3 -60 -70 Much improved 2 -80 Very much improved 1 -90 -100 -4 ● Improvement in TSS observed in 100% of patients ● Improvement in PGIC observed in 15 of 16 (94%) patients ● 6 of 11 (55%) patients achieve > 50% improvement in TSS ● No patient worsened 19 Data cutoff April 17, 2019 11-276 14-258 11-252 40-271 19-277 14-251 14-263 41-259 11-261 11-265 14-267 11-264 11-248 11-276 14-258 11-247 19-277 40-271 11-252 11-246 14-251 41-259 14-263 11-261 11-245 14-267 11-265 % Change from Baseline

Improvement in Bone Marrow Morphology Fibrosis Score Improvements Observed in Monotherapy and Combination Contexts Patient 11-248 Mutation Marrow Fibrosis Grading Reticulin Staining Grading Best % Best Tx Arm / Subject Heavily Pre-Treated, TSS % Cohort ID ≥3 ASXL1 HMR Baseline 24 Wk 48 Wk 72 Wk Baseline 24 Wk 48 Wk 72 Wk ASXL1 and JAK2 Mutation Improve SVR CPI-0610 11-247 Y Y N/E -25.4 3 3 2 3 3 2 Mono 11-248 Y Y Y NE -10.9 2 1 1 3 1 1 Baseline Cycle 17 Non-TD 14-258 -72.3 -33.1 2 2 ND ND 1B CPI-0610 11-246 NE -50.7 3 ND 2 2 3 ND 2 2 + Rux 11-252 Y Y -45.5 -19.9 2 2 2 1 MF Grade 2 MF Grade 1 TD 14-251 Y Y Y -86.2 -12.2 3 1 ND 2A 11-261 Y Y Y -45.0 -14.7 3 3 ND 3 CPI-0610 11-265 Y Y Y -44.8 -21.9 3 2 ND 2 + Rux Non-TD 14-263 Y Y Y -6.4 -13.8 3 3 ND ND 2B 14-267 Y Y -85.5 -26.5 3 3 ND ND Evidence of 4 of 6 patients improved within first 6 months of treatment Reduced Fibrosis Data cutoff April 17, 2019 HMR = High Molecular Risk; Patients with one of these mutations: ASXL1, EZH2, IDH1/2, SRSF2, and U2AF1 20 Bone marrow evaluable population: Baseline reading available and at least one reading at or after 24 weeks – 10 of 44 patientsImprovement in Bone Marrow Morphology Fibrosis Score Improvements Observed in Monotherapy and Combination Contexts Patient 11-248 Mutation Marrow Fibrosis Grading Reticulin Staining Grading Best % Best Tx Arm / Subject Heavily Pre-Treated, TSS % Cohort ID ≥3 ASXL1 HMR Baseline 24 Wk 48 Wk 72 Wk Baseline 24 Wk 48 Wk 72 Wk ASXL1 and JAK2 Mutation Improve SVR CPI-0610 11-247 Y Y N/E -25.4 3 3 2 3 3 2 Mono 11-248 Y Y Y NE -10.9 2 1 1 3 1 1 Baseline Cycle 17 Non-TD 14-258 -72.3 -33.1 2 2 ND ND 1B CPI-0610 11-246 NE -50.7 3 ND 2 2 3 ND 2 2 + Rux 11-252 Y Y -45.5 -19.9 2 2 2 1 MF Grade 2 MF Grade 1 TD 14-251 Y Y Y -86.2 -12.2 3 1 ND 2A 11-261 Y Y Y -45.0 -14.7 3 3 ND 3 CPI-0610 11-265 Y Y Y -44.8 -21.9 3 2 ND 2 + Rux Non-TD 14-263 Y Y Y -6.4 -13.8 3 3 ND ND 2B 14-267 Y Y -85.5 -26.5 3 3 ND ND Evidence of 4 of 6 patients improved within first 6 months of treatment Reduced Fibrosis Data cutoff April 17, 2019 HMR = High Molecular Risk; Patients with one of these mutations: ASXL1, EZH2, IDH1/2, SRSF2, and U2AF1 20 Bone marrow evaluable population: Baseline reading available and at least one reading at or after 24 weeks – 10 of 44 patients

Hemoglobin (g/dL) Hemoglobin (g/dL) Two Transfusion-Dependent Patients Converted to Transfusion Independence Patient 11-246: CPI-0610 + Ruxolitinib, Patient 11-252: CPI-0610 + Ruxolitinib, CALR Mutation JAK2, TET2, SRSF2 and U2AF1 Mutations 12 11 400 250 350 10 200 300 10 250 9 150 200 8 100 150 8 100 7 50 50 2U 2U 1U 2U 1U 1U 2U No transfusions for >24 weeks No transfusions for >69 weeks 6 6 0 0 1 5 10 15 20 25 30 1 5 10 30 45 60 75 90 15 30 3 15 3 Weeks on study Treatment Cycles Treatment Cycles Weeks on study • Patients no longer anemic • Hemoglobin increase sustained for >69 weeks and >24 weeks Data cutoff April 17, 2019 TD = Transfusion dependent, defined as receiving an average of ≥ 2 RBC transfusions per month during the 12 weeks prior to enrollment 21 TI = Transfusion independent, defined as absence of RBC transfusions over any consecutive 12-week period 9 Platelet count (x10 /L) 9 Platelet count (x10 /L)Hemoglobin (g/dL) Hemoglobin (g/dL) Two Transfusion-Dependent Patients Converted to Transfusion Independence Patient 11-246: CPI-0610 + Ruxolitinib, Patient 11-252: CPI-0610 + Ruxolitinib, CALR Mutation JAK2, TET2, SRSF2 and U2AF1 Mutations 12 11 400 250 350 10 200 300 10 250 9 150 200 8 100 150 8 100 7 50 50 2U 2U 1U 2U 1U 1U 2U No transfusions for >24 weeks No transfusions for >69 weeks 6 6 0 0 1 5 10 15 20 25 30 1 5 10 30 45 60 75 90 15 30 3 15 3 Weeks on study Treatment Cycles Treatment Cycles Weeks on study • Patients no longer anemic • Hemoglobin increase sustained for >69 weeks and >24 weeks Data cutoff April 17, 2019 TD = Transfusion dependent, defined as receiving an average of ≥ 2 RBC transfusions per month during the 12 weeks prior to enrollment 21 TI = Transfusion independent, defined as absence of RBC transfusions over any consecutive 12-week period 9 Platelet count (x10 /L) 9 Platelet count (x10 /L)

Improvement in Hemoglobin Mean Hemoglobin Levels by Treatment Regimen ● Substantial increase in hemoglobin is 3.0 observed in CPI-0610 monotherapy 2.5 patients 2.0 ● With CPI-0610 + ruxolitinib combination, observed improvement 1.5 in hemoglobin is delayed 1.0 ● Patients potentially need to overcome 0.5 effect of ruxolitinib in JAK-2 signaling, a critical component of EPO pathway 0.0 12 24 36 48 60 72 84 96 4 8 12 16 20 24 28 32 Weeks on study Treatment Cycle -0.5 2 2 4 4 2 2 CPI-0610 Mono; n= 5 7 3 2 2 2 2 CPI-0610 + Rux; n=11 11 22 Data cutoff April 17, 2019 Mean Change in Hemoglobin (g/dL)Improvement in Hemoglobin Mean Hemoglobin Levels by Treatment Regimen ● Substantial increase in hemoglobin is 3.0 observed in CPI-0610 monotherapy 2.5 patients 2.0 ● With CPI-0610 + ruxolitinib combination, observed improvement 1.5 in hemoglobin is delayed 1.0 ● Patients potentially need to overcome 0.5 effect of ruxolitinib in JAK-2 signaling, a critical component of EPO pathway 0.0 12 24 36 48 60 72 84 96 4 8 12 16 20 24 28 32 Weeks on study Treatment Cycle -0.5 2 2 4 4 2 2 CPI-0610 Mono; n= 5 7 3 2 2 2 2 CPI-0610 + Rux; n=11 11 22 Data cutoff April 17, 2019 Mean Change in Hemoglobin (g/dL)

Hemoglobin (g/dL) Hematologic Improvements with CPI-0610 Monotherapy Patient 11-247, Non-TD, CPI-0610 Monotherapy, ASXL1 and CALR mutations History CPI-0610 Therapy Observations Patient Global Impression Change (PGIC) ● Resistant to Ruxolitinib; ● Monotherapy (225 mg) Very much worse 7 increase in spleen and 6 ● Spleen volume reduction by MRI (Best: 25.4%) worsening symptoms 5 ● Normalization of platelet levels over 1 year while on Rux No Change 4 ● >1.5 g/dl Hgb increase over >12 weeks 3 ● Prior treatment: 2 Imetelstat, HU, ● Improvement in PGIC Very much improved 1 Pembrolizumab ● Resolution of headache, less frequent night sweats 0 6 12 18 24 30 36 42 48 54 60 66 72 78 ● Bone marrow improvement Weeks on study Platelets Normalization, Hb Improvement Bone Marrow Effects 1100 14 Baseline: MF Gr 3 C17: MF Gr 2 950 12 800 650 10 500 350 8 200 50 6 -49 1 2 2 4 4 6 7 8 10 13 16 20 23 26 28 31 35 38 41 44 46 50 53 55 59 62 65 68 Weeks on study 23 Data cutoff April 17, 2019 9 Platelet count (x10 /L) Reticulin H&EHemoglobin (g/dL) Hematologic Improvements with CPI-0610 Monotherapy Patient 11-247, Non-TD, CPI-0610 Monotherapy, ASXL1 and CALR mutations History CPI-0610 Therapy Observations Patient Global Impression Change (PGIC) ● Resistant to Ruxolitinib; ● Monotherapy (225 mg) Very much worse 7 increase in spleen and 6 ● Spleen volume reduction by MRI (Best: 25.4%) worsening symptoms 5 ● Normalization of platelet levels over 1 year while on Rux No Change 4 ● >1.5 g/dl Hgb increase over >12 weeks 3 ● Prior treatment: 2 Imetelstat, HU, ● Improvement in PGIC Very much improved 1 Pembrolizumab ● Resolution of headache, less frequent night sweats 0 6 12 18 24 30 36 42 48 54 60 66 72 78 ● Bone marrow improvement Weeks on study Platelets Normalization, Hb Improvement Bone Marrow Effects 1100 14 Baseline: MF Gr 3 C17: MF Gr 2 950 12 800 650 10 500 350 8 200 50 6 -49 1 2 2 4 4 6 7 8 10 13 16 20 23 26 28 31 35 38 41 44 46 50 53 55 59 62 65 68 Weeks on study 23 Data cutoff April 17, 2019 9 Platelet count (x10 /L) Reticulin H&E

Reduction in Pro-inflammatory Cytokine Levels ▪ Cytokine reductions observed in MF patients with CPI-0610 monotherapy or combo with ruxolitinib Cohort 1B (Non-TD - CPI-0610 Mono) Cohort 2A (TD - CPI-0610 + Ruxo) Cohort 2B (Non-TD - CPI-0610 + Ruxo) 24 Data cutoff April 17, 2019Reduction in Pro-inflammatory Cytokine Levels ▪ Cytokine reductions observed in MF patients with CPI-0610 monotherapy or combo with ruxolitinib Cohort 1B (Non-TD - CPI-0610 Mono) Cohort 2A (TD - CPI-0610 + Ruxo) Cohort 2B (Non-TD - CPI-0610 + Ruxo) 24 Data cutoff April 17, 2019

Treatment Emergent Adverse Events (TEAE) Summary of TEAE by ≥10% Frequency and AESI Treatment Emergent Adverse Event All Grade n=44 (n, %) ≥3 Grade* n=44 (n, %) Blood and Lymphatic System Disorders ● All ≥3 grade TEAE were Anemia 2 (4.5) 2 (4.5) Thrombocytopenia 3 (6.8) 2 (4.5) observed in patients treated Neutropenia 1 (2.3) 1 (2.3) Investigations with CPI-0610 + ruxolitinib Platelet Count Decreased 3 (6.8) 2 (4.5) Blood Creatinine Increased 1 (2.3) 1 ( 2.3) therapy; no ≥3 grade TEAE Gastrointestinal Disorders was observed with CPI-0610 Diarrhea 10 (22.7) 1 (2.3) Vomiting 6 (13.6) 1 (2.3) monotherapy Nausea 4 (9.1) 1 (2.3) Metabolism and Nutrition Disorders Decreased appetite 3 (6.8) 0 (0.0) Dehydration 1 (2.3) 1 (2.3) Hyponatremia 1 (2.3) 1 (2.3) Renal and Urinary Disorders Acute Kidney Injury 1 (2.3) 1 (2.3) Proteinuria 1 (2.3) 1 (2.3) General Disorders and Administration Site Conditions Fatigue 5 (11.4) 1 (2.3) Infections and Infestations Upper respiratory tract infection 6 (13.6) 0 (0.0) Pneumonia 1 (2.3) 1 (2.3) Respiratory, Thoracic and Mediastinal Disorders Epistaxis 6 (13.6) 0 (0.0) Cough 5 (11.4) 0 (0.0) Skin and Subcutaneous Tissue Disorder Pruritis 5 (11.4) 0 (0.0) Rash 3 (6.8) 0 (0.0) Psychiatric Disorder Depression 0 (0.0) 1 ( 2.3) Alcohol With 1 ( 2.3) 0 (0.0) Nervous System Disorders 25 Headache 6 (13.6) 0 (0.0) Data cutoff April 17, 2019 Dysgeusia 5 (11.4) 0 (0.0)Treatment Emergent Adverse Events (TEAE) Summary of TEAE by ≥10% Frequency and AESI Treatment Emergent Adverse Event All Grade n=44 (n, %) ≥3 Grade* n=44 (n, %) Blood and Lymphatic System Disorders ● All ≥3 grade TEAE were Anemia 2 (4.5) 2 (4.5) Thrombocytopenia 3 (6.8) 2 (4.5) observed in patients treated Neutropenia 1 (2.3) 1 (2.3) Investigations with CPI-0610 + ruxolitinib Platelet Count Decreased 3 (6.8) 2 (4.5) Blood Creatinine Increased 1 (2.3) 1 ( 2.3) therapy; no ≥3 grade TEAE Gastrointestinal Disorders was observed with CPI-0610 Diarrhea 10 (22.7) 1 (2.3) Vomiting 6 (13.6) 1 (2.3) monotherapy Nausea 4 (9.1) 1 (2.3) Metabolism and Nutrition Disorders Decreased appetite 3 (6.8) 0 (0.0) Dehydration 1 (2.3) 1 (2.3) Hyponatremia 1 (2.3) 1 (2.3) Renal and Urinary Disorders Acute Kidney Injury 1 (2.3) 1 (2.3) Proteinuria 1 (2.3) 1 (2.3) General Disorders and Administration Site Conditions Fatigue 5 (11.4) 1 (2.3) Infections and Infestations Upper respiratory tract infection 6 (13.6) 0 (0.0) Pneumonia 1 (2.3) 1 (2.3) Respiratory, Thoracic and Mediastinal Disorders Epistaxis 6 (13.6) 0 (0.0) Cough 5 (11.4) 0 (0.0) Skin and Subcutaneous Tissue Disorder Pruritis 5 (11.4) 0 (0.0) Rash 3 (6.8) 0 (0.0) Psychiatric Disorder Depression 0 (0.0) 1 ( 2.3) Alcohol With 1 ( 2.3) 0 (0.0) Nervous System Disorders 25 Headache 6 (13.6) 0 (0.0) Data cutoff April 17, 2019 Dysgeusia 5 (11.4) 0 (0.0)

Effects on Platelet Levels CPI-0610 Monotherapy (n=10) CPI-0610 + Ruxolitinib (n=34) No Patients with Grade 3 Thrombocytopenia 4 of 34 Patients with Grade 3 Thrombocytopenia 1050 1050 900 900 TD TD Non-TD Non-TD 750 750 JAKi Naive 600 600 450 450 300 300 150 150 Gr 3 50 Gr 3 50 25 25 0 0 0 6 12 18 24 30 36 48 60 72 84 96 0 6 12 18 24 30 36 48 60 72 84 96 Weeks on study Weeks on study ● CPI-0610 monotherapy demonstrated minimal, non-cumulative, and manageable thrombocytopenia ● Combination therapy of CPI-0610 and ruxolitinib showed non-cumulative, manageable, and generally reversible asymptomatic Grade 3 thrombocytopenia 26 Data cutoff April 17, 2019 9 Platelet count (x10 /L) 9 Platelet count (x10 /L)Effects on Platelet Levels CPI-0610 Monotherapy (n=10) CPI-0610 + Ruxolitinib (n=34) No Patients with Grade 3 Thrombocytopenia 4 of 34 Patients with Grade 3 Thrombocytopenia 1050 1050 900 900 TD TD Non-TD Non-TD 750 750 JAKi Naive 600 600 450 450 300 300 150 150 Gr 3 50 Gr 3 50 25 25 0 0 0 6 12 18 24 30 36 48 60 72 84 96 0 6 12 18 24 30 36 48 60 72 84 96 Weeks on study Weeks on study ● CPI-0610 monotherapy demonstrated minimal, non-cumulative, and manageable thrombocytopenia ● Combination therapy of CPI-0610 and ruxolitinib showed non-cumulative, manageable, and generally reversible asymptomatic Grade 3 thrombocytopenia 26 Data cutoff April 17, 2019 9 Platelet count (x10 /L) 9 Platelet count (x10 /L)

Key Takeaways from ASCO/EHA 2019 Update Activity across all four hallmarks of myelofibrosis: spleen, symptoms, hematologic function, and bone marrow fibrosis CPI-0610-driven activity in ruxolitinib-resistant patients as monotherapy and as an add-on to ruxolitinib Evidence of early effects on bone marrow fibrosis and trend of increasing hemoglobin over time suggest potential disease-modifying effects Substantial symptom and spleen improvement observed CPI-0610 generally well-tolerated as a monotherapy and in combination with ruxolitinib 27Key Takeaways from ASCO/EHA 2019 Update Activity across all four hallmarks of myelofibrosis: spleen, symptoms, hematologic function, and bone marrow fibrosis CPI-0610-driven activity in ruxolitinib-resistant patients as monotherapy and as an add-on to ruxolitinib Evidence of early effects on bone marrow fibrosis and trend of increasing hemoglobin over time suggest potential disease-modifying effects Substantial symptom and spleen improvement observed CPI-0610 generally well-tolerated as a monotherapy and in combination with ruxolitinib 27

Potential Paths to Registration for CPI-0610 † 1L JAKi-Naïve Patients*^ 2L Transfusion-Dependent Patients Anticipated Data By End of 2019 100% 100% Ruxolitinib Spleen Volume Response (SVR%) Momelotinib BAT (89% Rux) 80% 80% • Results from approximately 40 COMFORT-1 SIMPLIFY-1 64.0% 60% 56.0% ruxolitinib-resistant patients 60% 52.0% 40% 50.0% 41.9% 29% SVR35 SVR35 20% 40% • Transfusion dependence to 0% independence conversion results -20% 20% from approx. 16 patients treated w/ -40% CPI-0610 + ruxolitinib 41.9% 0% -60% SVR35 Baseline Week 24 Goal: áSVR35 due to CPI-0610/rux • Spleen Volume Reduction and synergy and improved tolerability of rux Total Symptom Score results from 10-15 JAK-inhibitor-naïve patients • Planning has begun for potential pivotal trials Convert to Transfusion Independence Increase Rate of SVR35 Response *SIMPLIFY-1: A Phase III Randomized Trial of Momelotinib Versus Ruxolitinib in Janus Kinase Inhibitor-Naïve Patients With Myelofibrosis. Mesa, R., et al. J Clin Oncol 2017: 35(34):3844-3850. ^COMFORT-1: A Double-Blind, Placebo-Controlled Trial of Ruxolitinib for Myelofibrosis Verstovsek, S., et al; N Engl J Med 2012;366:799-807. † Momelotinib Versus Best Available Therapy in Patients with Myelofibrosis Previously Treated with Ruxolitinib (Simplify 2): A Randomised, Open-Label, Phase 3 Trial. Harrison, C., et al. Lancet 28 Haematol. 2018 Feb;5(2):e73-e81. Spleen Volume Change from Baseline (%) Rate of Transfusion Dependence (%)Potential Paths to Registration for CPI-0610 † 1L JAKi-Naïve Patients*^ 2L Transfusion-Dependent Patients Anticipated Data By End of 2019 100% 100% Ruxolitinib Spleen Volume Response (SVR%) Momelotinib BAT (89% Rux) 80% 80% • Results from approximately 40 COMFORT-1 SIMPLIFY-1 64.0% 60% 56.0% ruxolitinib-resistant patients 60% 52.0% 40% 50.0% 41.9% 29% SVR35 SVR35 20% 40% • Transfusion dependence to 0% independence conversion results -20% 20% from approx. 16 patients treated w/ -40% CPI-0610 + ruxolitinib 41.9% 0% -60% SVR35 Baseline Week 24 Goal: áSVR35 due to CPI-0610/rux • Spleen Volume Reduction and synergy and improved tolerability of rux Total Symptom Score results from 10-15 JAK-inhibitor-naïve patients • Planning has begun for potential pivotal trials Convert to Transfusion Independence Increase Rate of SVR35 Response *SIMPLIFY-1: A Phase III Randomized Trial of Momelotinib Versus Ruxolitinib in Janus Kinase Inhibitor-Naïve Patients With Myelofibrosis. Mesa, R., et al. J Clin Oncol 2017: 35(34):3844-3850. ^COMFORT-1: A Double-Blind, Placebo-Controlled Trial of Ruxolitinib for Myelofibrosis Verstovsek, S., et al; N Engl J Med 2012;366:799-807. † Momelotinib Versus Best Available Therapy in Patients with Myelofibrosis Previously Treated with Ruxolitinib (Simplify 2): A Randomised, Open-Label, Phase 3 Trial. Harrison, C., et al. Lancet 28 Haematol. 2018 Feb;5(2):e73-e81. Spleen Volume Change from Baseline (%) Rate of Transfusion Dependence (%)

EZH2 Franchise CPI-1205 and CPI-0209EZH2 Franchise CPI-1205 and CPI-0209

Franchise Approach to Address the Breadth of EZH2 Biology Polycomb Repressive Complex 2 First Generation CPI-1205 EZH2 Synergy w/ Oncogenic • Potent Drivers • Typical enzyme inhibitor kinetics • Partial target coverage over time • Best for hypersensitive contexts Activating Mutations Tumor Immunity Second Generation CPI-0209 • Even more potent Drug Resistance • Durable inhibition of EZH2 • Comprehensive target coverage over time … Methylates Histone H3 at Lysine 27 st • Expands beyond 1 gen contexts Synthetic Lethality SUPPRESSED TRANSCRIPTION 30Franchise Approach to Address the Breadth of EZH2 Biology Polycomb Repressive Complex 2 First Generation CPI-1205 EZH2 Synergy w/ Oncogenic • Potent Drivers • Typical enzyme inhibitor kinetics • Partial target coverage over time • Best for hypersensitive contexts Activating Mutations Tumor Immunity Second Generation CPI-0209 • Even more potent Drug Resistance • Durable inhibition of EZH2 • Comprehensive target coverage over time … Methylates Histone H3 at Lysine 27 st • Expands beyond 1 gen contexts Synthetic Lethality SUPPRESSED TRANSCRIPTION 30

EZH2 Inhibition Offers Broad Therapeutic Potential EZH2 “Writer” Activity Suppresses Gene Transcription Polycomb Repressive Complex 2 CPI-1205 CPI-0209 EZH2 Synergy w/ Oncogenic Prostate Potential Drivers Cancer Add’l st Oppt’y 1 nd for 2 Gen Activating Mutations Lymphoma Gen EZH2i EZH2i Tumor Immunity Solid Tumors Initial Solid Tumors Drug Resistance Focus nd for 2 … Methylates Histone H3 at Lysine 27 Gen Genetically-defined EZH2i Synthetic Lethality Solid Tumors SUPPRESSED TRANSCRIPTION 31EZH2 Inhibition Offers Broad Therapeutic Potential EZH2 “Writer” Activity Suppresses Gene Transcription Polycomb Repressive Complex 2 CPI-1205 CPI-0209 EZH2 Synergy w/ Oncogenic Prostate Potential Drivers Cancer Add’l st Oppt’y 1 nd for 2 Gen Activating Mutations Lymphoma Gen EZH2i EZH2i Tumor Immunity Solid Tumors Initial Solid Tumors Drug Resistance Focus nd for 2 … Methylates Histone H3 at Lysine 27 Gen Genetically-defined EZH2i Synthetic Lethality Solid Tumors SUPPRESSED TRANSCRIPTION 31

Model for EZH2 Role in Prostate Cancer EZH2 Gene Signature* Predicts Outcomes in Prostate Cancer Coregulators AR AR 1.0 0.9 Synergistically Pro-Tumor EZH2 Enhances AR 0.8 Signaling Signaling 0.7 0.6 0.5 Prostate 0.4 Tumor Growth 0.3 0.2 0 2 4 6 8 10 Time to relapse (years) Yu et al., Cancer Research 2007 32 *Signature of H3K27me3-occupied EZH2 target genes repressed in metastatic relative to clinically localized prostate cancer and benign prostate tissue Probability of survivalModel for EZH2 Role in Prostate Cancer EZH2 Gene Signature* Predicts Outcomes in Prostate Cancer Coregulators AR AR 1.0 0.9 Synergistically Pro-Tumor EZH2 Enhances AR 0.8 Signaling Signaling 0.7 0.6 0.5 Prostate 0.4 Tumor Growth 0.3 0.2 0 2 4 6 8 10 Time to relapse (years) Yu et al., Cancer Research 2007 32 *Signature of H3K27me3-occupied EZH2 target genes repressed in metastatic relative to clinically localized prostate cancer and benign prostate tissue Probability of survival

EZH2 Synergy with Androgen Receptor Signaling (ARS) CPI-1205 Intensifies Gene Expression Effects CPI-1205 is Active as Monotherapy and Synergistic of Enzalutamide in Prostate Cancer Cells* with Enzalutamide in Killing Prostate Cancer Cells Enzalu- CPI- 1.80 Combo tamide 1205 Theoretical concentration of each agent required to kill 90% of cancer 1.60 cells if no synergistic activity 1.40 Actual concentration of each agent required to kill 90% of cancer cells when combined 1.20 1.00 0.80 0.60 0.40 0.20 0.00 0.00 2.00 4.00 6.00 8.00 CPI-1205 (µM) 33 *Bradley, WD, et al., ”EZH2 Inhibition as an Effective Treatment for Metastatic Castration-Resistant Prostate Cancer,” presentation at 2018 EORTC/NCI/AACR meeting Enzalutamide (µM)EZH2 Synergy with Androgen Receptor Signaling (ARS) CPI-1205 Intensifies Gene Expression Effects CPI-1205 is Active as Monotherapy and Synergistic of Enzalutamide in Prostate Cancer Cells* with Enzalutamide in Killing Prostate Cancer Cells Enzalu- CPI- 1.80 Combo tamide 1205 Theoretical concentration of each agent required to kill 90% of cancer 1.60 cells if no synergistic activity 1.40 Actual concentration of each agent required to kill 90% of cancer cells when combined 1.20 1.00 0.80 0.60 0.40 0.20 0.00 0.00 2.00 4.00 6.00 8.00 CPI-1205 (µM) 33 *Bradley, WD, et al., ”EZH2 Inhibition as an Effective Treatment for Metastatic Castration-Resistant Prostate Cancer,” presentation at 2018 EORTC/NCI/AACR meeting Enzalutamide (µM)

Current Treatment Paradigm in mCRPC Pre-Metastatic mCRPC Prostate Cancer nd 2 Line rd st 3 Line 1 Line Enzalutamide or Chemotherapy or Abiraterone or Abiraterone Palliative Care Enzalutamide (Poor Activity) CPI-1205 may enhance the activity of ARS inhibitors and reduce need for chemotherapy 34Current Treatment Paradigm in mCRPC Pre-Metastatic mCRPC Prostate Cancer nd 2 Line rd st 3 Line 1 Line Enzalutamide or Chemotherapy or Abiraterone or Abiraterone Palliative Care Enzalutamide (Poor Activity) CPI-1205 may enhance the activity of ARS inhibitors and reduce need for chemotherapy 34

2L mCRPC Patients Treated with Abiraterone or Enzalutamide Suffer Poor Response Rate and Short Time to Progression* Abiraterone + prednisone Enzalutamide *ASCO 2018 Poster Khalaf, et al. (Kim Chi lab) > PSA30 = 6% > PSA30 = 43% > PSA50 = 4% > PSA50 = 31% > PSA80 = 0% > PSA80 = 10% TTP = 1.6 months TTP = 2.7 months GOAL Treat with CPI-1205 combination therapy to achieve deeper and more durable responses 352L mCRPC Patients Treated with Abiraterone or Enzalutamide Suffer Poor Response Rate and Short Time to Progression* Abiraterone + prednisone Enzalutamide *ASCO 2018 Poster Khalaf, et al. (Kim Chi lab) > PSA30 = 6% > PSA30 = 43% > PSA50 = 4% > PSA50 = 31% > PSA80 = 0% > PSA80 = 10% TTP = 1.6 months TTP = 2.7 months GOAL Treat with CPI-1205 combination therapy to achieve deeper and more durable responses 35

ProSTAR Trial Design Phase 2 Initiated Phase 1b – Advanced mCRPC Phase 2 – 2L mCRPC Patients Only C CP PII- -1 12 20 05 5 + + A Abi bira rat te erone rone CPI-1205 + Abiraterone** C AP bi I- ra 12 te 0ron 5 + e A bi + ra CP te I-rone* 1205 ( ( (P P Progre rogre rogres s ss s se e ed d d on on on E E Enz nz nza a alllut ut uta a am m miiide) de) de) (Prior Enzalutamide Progression) (Prior Enzalutamide Progression) n n n ~ 30 ~ ~ 30 30 ✓Initiated E Enz nza allut uta am miide de + + C CP PII- -1205 1205 CPI-1205 + Enzalutamide** ( ( (P P Progre rogre rogres s ss s se e ed d d on on on A A Abi bi bira ra rat t te e erone rone rone) ) ) n n n ~ ~ ~ 3 3 35 5 5 ✓Initiated CPI-1205 + Enzalutamide* (Prior Abiraterone Progression) vs. E E E nz nz nz aa a lut llut ut aa a m m m ide iide de A A A lone llone one ** ( (P Progre rogres ss se ed d on on A Abi bira rat te erone) rone) (Progressed on Abiraterone) n n ~ 35 ~ 35 n ~ 35 ✓Initiated Enzalutamide + CPI-1205*** (Progressed on Abiraterone, Enzalutamide, * Primary endpoint: maximum tolerated dose, recommended Phase 2 dose and Chemotherapy) ** Primary endpoint: Response rate: PSA reduction, CTC reduction, objective response rate (ORR) *** Primary endpoint: ORR ✓Initiated Testing Biomarkers for Patient Enrichment 36 Note: In ProSTAR, abiraterone is dosed in combination with prednisoneProSTAR Trial Design Phase 2 Initiated Phase 1b – Advanced mCRPC Phase 2 – 2L mCRPC Patients Only C CP PII- -1 12 20 05 5 + + A Abi bira rat te erone rone CPI-1205 + Abiraterone** C AP bi I- ra 12 te 0ron 5 + e A bi + ra CP te I-rone* 1205 ( ( (P P Progre rogre rogres s ss s se e ed d d on on on E E Enz nz nza a alllut ut uta a am m miiide) de) de) (Prior Enzalutamide Progression) (Prior Enzalutamide Progression) n n n ~ 30 ~ ~ 30 30 ✓Initiated E Enz nza allut uta am miide de + + C CP PII- -1205 1205 CPI-1205 + Enzalutamide** ( ( (P P Progre rogre rogres s ss s se e ed d d on on on A A Abi bi bira ra rat t te e erone rone rone) ) ) n n n ~ ~ ~ 3 3 35 5 5 ✓Initiated CPI-1205 + Enzalutamide* (Prior Abiraterone Progression) vs. E E E nz nz nz aa a lut llut ut aa a m m m ide iide de A A A lone llone one ** ( (P Progre rogres ss se ed d on on A Abi bira rat te erone) rone) (Progressed on Abiraterone) n n ~ 35 ~ 35 n ~ 35 ✓Initiated Enzalutamide + CPI-1205*** (Progressed on Abiraterone, Enzalutamide, * Primary endpoint: maximum tolerated dose, recommended Phase 2 dose and Chemotherapy) ** Primary endpoint: Response rate: PSA reduction, CTC reduction, objective response rate (ORR) *** Primary endpoint: ORR ✓Initiated Testing Biomarkers for Patient Enrichment 36 Note: In ProSTAR, abiraterone is dosed in combination with prednisone

ProSTAR Phase 1b Conclusions* ● CPI-1205 observed to be well-tolerated and clinically active Cycle 1 Cycle 4 ● Recommended Phase 2 dose of 800 mg three times daily Day 1 Day 1 ● Patients’ PSA responses tended to be deeper (e.g., PSA80) and more durable than expected with ARSi alone ● Activity observed in combo with abiraterone, which has poor 2L responses, or enzalutamide and in AR-V7-negative patients ● CPI-1205 + abiraterone: – PSA80: 2/18 (11%) of all patients – PSA80: 2/10 (20%) of AR-V7-negative patients Resolution of bone metastases in patient on CPI- 1205 + enzalutamide for one month followed by – ORR: **DCR = 6/8 (75%) or **DCR ≥ 3 months = 4/8 (50%) CPI-1205 monotherapy for two months ● CPI-1205 + enzalutamide: – PSA80: 3/16 (19%) of all patients – PSA80: 3/11 (27%) of AR-V7 negative patients – ORR: PR = 1/5 (20%) **DCR = 3/5 (60%) or **DCR ≥ 3 months = 3/5 (60%) *Please see poster CT094/18, which was presented at AACR on April 1, 2019, in the Investors & Media/Presentations section of http://www.constellationpharma.com 37 **Disease Control Rate (DCR): Complete Response (CR) + Partial Response (PR) + Stable Disease (SD)ProSTAR Phase 1b Conclusions* ● CPI-1205 observed to be well-tolerated and clinically active Cycle 1 Cycle 4 ● Recommended Phase 2 dose of 800 mg three times daily Day 1 Day 1 ● Patients’ PSA responses tended to be deeper (e.g., PSA80) and more durable than expected with ARSi alone ● Activity observed in combo with abiraterone, which has poor 2L responses, or enzalutamide and in AR-V7-negative patients ● CPI-1205 + abiraterone: – PSA80: 2/18 (11%) of all patients – PSA80: 2/10 (20%) of AR-V7-negative patients Resolution of bone metastases in patient on CPI- 1205 + enzalutamide for one month followed by – ORR: **DCR = 6/8 (75%) or **DCR ≥ 3 months = 4/8 (50%) CPI-1205 monotherapy for two months ● CPI-1205 + enzalutamide: – PSA80: 3/16 (19%) of all patients – PSA80: 3/11 (27%) of AR-V7 negative patients – ORR: PR = 1/5 (20%) **DCR = 3/5 (60%) or **DCR ≥ 3 months = 3/5 (60%) *Please see poster CT094/18, which was presented at AACR on April 1, 2019, in the Investors & Media/Presentations section of http://www.constellationpharma.com 37 **Disease Control Rate (DCR): Complete Response (CR) + Partial Response (PR) + Stable Disease (SD)

Objective Response by CT Scan Example Patient 2 CPI-1205 + Enzalutamide Baseline: December 2017 February 2018 38Objective Response by CT Scan Example Patient 2 CPI-1205 + Enzalutamide Baseline: December 2017 February 2018 38

Experience with a Compassionate-Use Patient Significant PSA Reduction in Heavily Pre-Treated and Refractory Patient Start CPI-1205 + Enzalutamide 3,000 (PSA ~ 2900) 2,500 2,000 1,500 1,000 12 agents prior to CPI-1205, including second-generation 500 androgen inhibitors, chemotherapy, PARP inhibitors, tyrosine kinase inhibitors, checkpoint inhibitors, radium 223, and 50 radiotherapy ● 80% reduction in PSA levels 40 30 ● Evidence of tumor size 20 reduction in the neck 10 0 6/1/2016 9/1/2016 12/1/2016 3/1/2017 6/1/2017 9/1/2017 12/1/2017 3/1/2018 ● PSA levels escalated significantly in final year of treatment prior to CPI-1205 + enzalutamide. ● Treatment interrupted due to non-treatment-related pneumonia. ● Subsequent progression in liver led to discontinuation. Patient later died. ● Expansion cohort of CPI-1205 + enzalutamide initiated in heavily pre-treated patients who have progressed after treatment with each of enzalutamide, abiraterone, and chemotherapy. 39 PSA Score (ng/mL)Experience with a Compassionate-Use Patient Significant PSA Reduction in Heavily Pre-Treated and Refractory Patient Start CPI-1205 + Enzalutamide 3,000 (PSA ~ 2900) 2,500 2,000 1,500 1,000 12 agents prior to CPI-1205, including second-generation 500 androgen inhibitors, chemotherapy, PARP inhibitors, tyrosine kinase inhibitors, checkpoint inhibitors, radium 223, and 50 radiotherapy ● 80% reduction in PSA levels 40 30 ● Evidence of tumor size 20 reduction in the neck 10 0 6/1/2016 9/1/2016 12/1/2016 3/1/2017 6/1/2017 9/1/2017 12/1/2017 3/1/2018 ● PSA levels escalated significantly in final year of treatment prior to CPI-1205 + enzalutamide. ● Treatment interrupted due to non-treatment-related pneumonia. ● Subsequent progression in liver led to discontinuation. Patient later died. ● Expansion cohort of CPI-1205 + enzalutamide initiated in heavily pre-treated patients who have progressed after treatment with each of enzalutamide, abiraterone, and chemotherapy. 39 PSA Score (ng/mL)

CPI-0209: Second-Generation EZH2 Inhibitor Once-Daily Treatment Resulted in Rapid and Durable Tumor Regression Bladder Cancer (EZH2 Wild-Type, ARID1A Mutant) – Lymphoma Xenograft – Mutated EZH2 Model More Effective than Cisplatin 2,500 Group 1 Vehicle PO, QD*29 days Group 2 CPI-701532 25 mg/kg PO, QD*29 days Vehicle CPI-0209, 25 mg/kg oral, once daily PO QD 2,000 iv iv 1,500 1,000 500 Cessation of treatment 0 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 Days Post Grouping Days Post Grouping CPI-0209 May Provide More Comprehensive EZH2 Coverage, Expanding Addressable Populations 40 3 Tumor volume (mm 3 ) Tumor Volume (mm ) 3 Tumor Volume (mm )CPI-0209: Second-Generation EZH2 Inhibitor Once-Daily Treatment Resulted in Rapid and Durable Tumor Regression Bladder Cancer (EZH2 Wild-Type, ARID1A Mutant) – Lymphoma Xenograft – Mutated EZH2 Model More Effective than Cisplatin 2,500 Group 1 Vehicle PO, QD*29 days Group 2 CPI-701532 25 mg/kg PO, QD*29 days Vehicle CPI-0209, 25 mg/kg oral, once daily PO QD 2,000 iv iv 1,500 1,000 500 Cessation of treatment 0 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 Days Post Grouping Days Post Grouping CPI-0209 May Provide More Comprehensive EZH2 Coverage, Expanding Addressable Populations 40 3 Tumor volume (mm 3 ) Tumor Volume (mm ) 3 Tumor Volume (mm )

Design of Phase 1/2 Clinical Trial of CPI-0209 Phase 1 Dose Escalation: Phase 2 Expansion at RP2D*: CPI-0209 Monotherapy CPI-0209 Monotherapy Biomarker-Defined Solid Tumor Populations Advanced, Relapsed Solid Tumors Including Patients w/ ARID1A Mutations ✓Initiated Clear-Cell Ovarian Carcinoma Primary endpoints: Safety, Recommended Phase Primary endpoint: Objective Response Rate 2 Dose (RP2D) ✓Initiated Phase 1 Dose Escalation*: Phase 2 Expansion at RP2D: CPI-0209 Combo with Standard of Care CPI-0209 Combo with Standard of Care ✓Initiated Biomarker-Defined Solid Tumor Populations Advanced, Relapsed Solid Tumors Resistant to Standard of Care ✓Initiated Primary endpoints: Safety, RP2D Primary endpoint: Objective Response Rate * Expected to be conducted simultaneously 41Design of Phase 1/2 Clinical Trial of CPI-0209 Phase 1 Dose Escalation: Phase 2 Expansion at RP2D*: CPI-0209 Monotherapy CPI-0209 Monotherapy Biomarker-Defined Solid Tumor Populations Advanced, Relapsed Solid Tumors Including Patients w/ ARID1A Mutations ✓Initiated Clear-Cell Ovarian Carcinoma Primary endpoints: Safety, Recommended Phase Primary endpoint: Objective Response Rate 2 Dose (RP2D) ✓Initiated Phase 1 Dose Escalation*: Phase 2 Expansion at RP2D: CPI-0209 Combo with Standard of Care CPI-0209 Combo with Standard of Care ✓Initiated Biomarker-Defined Solid Tumor Populations Advanced, Relapsed Solid Tumors Resistant to Standard of Care ✓Initiated Primary endpoints: Safety, RP2D Primary endpoint: Objective Response Rate * Expected to be conducted simultaneously 41

Discovery Platform Fueling the Pipeline Discovery Programs Targeting Epigenetic Regulators in the Tumor and Immune Microenvironment Tumor Cells Immune Cells Adaptive Innate ● Alter aberrant gene expression within ● Re-program immune cells to overcome cancer cells resistance to cancer immunotherapies ● Increase tumor immunogenicity 42Discovery Platform Fueling the Pipeline Discovery Programs Targeting Epigenetic Regulators in the Tumor and Immune Microenvironment Tumor Cells Immune Cells Adaptive Innate ● Alter aberrant gene expression within ● Re-program immune cells to overcome cancer cells resistance to cancer immunotherapies ● Increase tumor immunogenicity 42

Potential Value Creation Catalysts 2018 –Year of Execution 2019 –Year of Data 1H 2018 1H 2019 2H 2019 ✓ Complete crossover financing✓ CPI-1205 – Determine ORIOn-E ✓ CPI-0209 – First patient dosed in safety and recommended Phase 2 Phase 1 ✓ Expand enrollment in ProSTAR dose (RP2D) ❑ CPI-1205 – Provide program ✓ Initiate ORIOn-E ✓ CPI-1205 – Provide update from update from ProSTAR trial nd ✓ Select 2 generation EZH2 Phase 1b portion of ProSTAR trial at ❑ CPI-0610 – Provide additional data inhibitor candidate (CPI-0209) AACR on April 1 update from MANIFEST trial ✓ CPI-0610 – Provide interim update 2H 2018 from MANIFEST Phase 2 trial ✓ Complete IPO ✓ CPI-0209 – File IND for CPI-0209 ✓ Activate additional sites in US, Canada / EU for CPI-0610 in myelofibrosis ✓ Initiate Phase 2 portion of ProSTAR trial 43Potential Value Creation Catalysts 2018 –Year of Execution 2019 –Year of Data 1H 2018 1H 2019 2H 2019 ✓ Complete crossover financing✓ CPI-1205 – Determine ORIOn-E ✓ CPI-0209 – First patient dosed in safety and recommended Phase 2 Phase 1 ✓ Expand enrollment in ProSTAR dose (RP2D) ❑ CPI-1205 – Provide program ✓ Initiate ORIOn-E ✓ CPI-1205 – Provide update from update from ProSTAR trial nd ✓ Select 2 generation EZH2 Phase 1b portion of ProSTAR trial at ❑ CPI-0610 – Provide additional data inhibitor candidate (CPI-0209) AACR on April 1 update from MANIFEST trial ✓ CPI-0610 – Provide interim update 2H 2018 from MANIFEST Phase 2 trial ✓ Complete IPO ✓ CPI-0209 – File IND for CPI-0209 ✓ Activate additional sites in US, Canada / EU for CPI-0610 in myelofibrosis ✓ Initiate Phase 2 portion of ProSTAR trial 43

Strong Cash Position ● Cash, cash equivalents and marketable $ Millions, 2Q19 2Q18 Except Per-Share Amounts securities as of June 30, 2019, of $98.1 million ● Current cash, cash equivalents and marketable R&D Expenses $16.0 $9.5 securities expected to fund operations until late Q3 2020, including: G&A Expenses $4.9 $2.5 – Ongoing clinical trials to determine efficacy and safety of CPI-1205 and CPI-0610 necessary to begin pivotal trials Other Income, Net $0.1 $0.1 – Continued advancement of CPI-0209 Net Loss Attributable to – Support for robust discovery/preclinical pipeline ($20.8) ($11.9) Common Stockholders ● Crossover financing round in April 2018 and Net Loss Per Share Attributable ($0.80) ($9.96) IPO in July 2018 raised $160 million from high- to Common Stockholders quality investors ● Venture debt of $30 million has been added in 2019; $10 million more available, in part upon achievement of milestones 44Strong Cash Position ● Cash, cash equivalents and marketable $ Millions, 2Q19 2Q18 Except Per-Share Amounts securities as of June 30, 2019, of $98.1 million ● Current cash, cash equivalents and marketable R&D Expenses $16.0 $9.5 securities expected to fund operations until late Q3 2020, including: G&A Expenses $4.9 $2.5 – Ongoing clinical trials to determine efficacy and safety of CPI-1205 and CPI-0610 necessary to begin pivotal trials Other Income, Net $0.1 $0.1 – Continued advancement of CPI-0209 Net Loss Attributable to – Support for robust discovery/preclinical pipeline ($20.8) ($11.9) Common Stockholders ● Crossover financing round in April 2018 and Net Loss Per Share Attributable ($0.80) ($9.96) IPO in July 2018 raised $160 million from high- to Common Stockholders quality investors ● Venture debt of $30 million has been added in 2019; $10 million more available, in part upon achievement of milestones 44

Experienced Management Team, Board, and Scientific Advisors Management Team Board of Directors Jigar Raythatha Mark Goldsmith, M.D., Tony Evnin, Ph.D., President and CEO Ph.D. (Chairman), Venrock Revolution Medicines Steven Hoerter, Emma Reeve Jigar Raythatha Deciphera SVP & Chief Financial Officer Pharmaceuticals Jim Audia, Ph.D., Chicago Biomedical Bob Tepper, M.D., Adrian Senderowicz, M.D. Consortium Third Rock Ventures SVP & Chief Medical Officer Scott Braunstein, M.D., Elizabeth Tréhu, M.D., Marinus Pharmaceuticals Jounce Therapeutics Patrick Trojer, PhD SVP & Chief Scientific Officer Karen Valentine Founders & Scientific Advisory Board SVP, Chief Legal Officer & General Counsel Danny Reinberg, Ph.D., David Livingston, M.D., NYU, HHMI, NAS Dana Farber Cancer Jessica Christo Center SVP & Chief Product Development Officer David Allis, Ph.D., Rockefeller Univ., NAS Scott Lowe, Ph.D., Memorial Sloan-Kettering Brad Prosek Yang Shi, Ph.D., Harvard SVP, Corporate Development Medical School Robert Schreiber, Washington U. School Pam Sharma, M.D., of Medicine Brenda Sousa Ph.D., MD Anderson SVP, HR and Operations Cancer Center 45Experienced Management Team, Board, and Scientific Advisors Management Team Board of Directors Jigar Raythatha Mark Goldsmith, M.D., Tony Evnin, Ph.D., President and CEO Ph.D. (Chairman), Venrock Revolution Medicines Steven Hoerter, Emma Reeve Jigar Raythatha Deciphera SVP & Chief Financial Officer Pharmaceuticals Jim Audia, Ph.D., Chicago Biomedical Bob Tepper, M.D., Adrian Senderowicz, M.D. Consortium Third Rock Ventures SVP & Chief Medical Officer Scott Braunstein, M.D., Elizabeth Tréhu, M.D., Marinus Pharmaceuticals Jounce Therapeutics Patrick Trojer, PhD SVP & Chief Scientific Officer Karen Valentine Founders & Scientific Advisory Board SVP, Chief Legal Officer & General Counsel Danny Reinberg, Ph.D., David Livingston, M.D., NYU, HHMI, NAS Dana Farber Cancer Jessica Christo Center SVP & Chief Product Development Officer David Allis, Ph.D., Rockefeller Univ., NAS Scott Lowe, Ph.D., Memorial Sloan-Kettering Brad Prosek Yang Shi, Ph.D., Harvard SVP, Corporate Development Medical School Robert Schreiber, Washington U. School Pam Sharma, M.D., of Medicine Brenda Sousa Ph.D., MD Anderson SVP, HR and Operations Cancer Center 45