CORPORATE OVERVIEW NASDAQ: VSTM January 7, 2016 Page

FORWARD-LOOKING STATEMENTS This presentation, and other matters discussed today, or answers that may be given to questions asked, includes forward-looking statements about the Company's strategy, future plans and prospects, including statements regarding the development and activity of the Company's product candidates, including VS-6063, VS-4718 and VS-5584, and the Company's FAK, PI3K/mTOR and diagnostics programs generally, the timeline for clinical development and regulatory approval of the Company’s product candidates, the expected timing for the enrollment and the reporting of data from on-going trials, the structure of the Company’s planned or pending clinical trials, additional planned studies, the Company’s rights to develop or commercialize its product candidates and the ability of the Company to finance contemplated development activities and fund operations for a specified period. The words "anticipate," "appear," "believe," "estimate," "expect," "intend," "may," "plan," "predict," "project," "target," "potential," "will," "would," "could," "should," "continue," and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Each forward-looking statement is subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied in such statement. Applicable risks and uncertainties include the risks that the preclinical testing of the Company's product candidates and preliminary or interim data from clinical trials may not be predictive of the results or success of ongoing or later clinical trials, that data may not be available when we expect it to be, that enrollment of clinical trials may take longer than expected, that the Company’s product candidates will cause unexpected safety events, that the Company will be unable to successfully initiate or complete the clinical development of the Company’s product candidates, that the development of the Company's product candidates will take longer or cost more than planned, and that the Company's product candidates will not receive regulatory approval or become commercially successful products. Other risks and uncertainties include those identified under the heading "Risk Factors" in the Company's Annual Report on Form 10-K for the year ended December 31, 2014, the Company’s Quarterly Report on form 10-Q for the quarter ended September 30, 2015 and in any subsequent SEC filings. The forward-looking statements contained in this presentation reflect the Company's current views with respect to future events, and the Company does not undertake and specifically disclaims any obligation to update any forward-looking statements. Page 2 Verastem, Inc.

THE VERASTEM OPPORTUNITY   Multi-faceted approach to improving outcomes for patients with cancer • • • Reduce cancer stem cells Boost immune attack Reduce stromal density   Two programs with clinical-stage multiple tumor types oral kinase inhibitors targeting FAK – VS-6063 and VS-4718 PI3K/mTOR – VS-5584 • •   Well capitalized • • $120.1M in cash and cash equivalents Sufficient operating capital into 2018 as of Sept. 30, 2015   Strong IP (Composition of Matter) • • • VS-6063: 2028 VS-4718: 2028 VS-5584: 2029   3 Experienced management and Board Verastem, Inc. Page

CHALLENGES IN IMPROVING OUTCOMES FOR PATIENTS WITH CANCER Resident cancer stem cells, limited immune response, and dense stroma contribute to the ineffectiveness of current treatments. Page Verastem, Inc.

MULTI-FACETED APPROACH PATIENT OUTCOMES TO IMPROVING CANCER BOOST IMMUNE ATTACK to increase proportion of responders and duration of response3 REDUCE CANCER STEM CELLS to prevent recurrence and metastasis1,2 REDUCE STROMAL DENSITY to increase drug and immune system penetration into tumors4 1. 2. 3. 4. Kolev VN et al. FAK inhibition targets cancer stem cells. EORTC 2015 Kolev VN et al. PI3K/mTOR dual inhibitor VS-5584 preferentially targets cancer stem cells. Cancer Res. 2015 Serrels et al. Nuclear FAK controls chemokine transcription, Tregs, and evasion of anti-tumor immunity. Cell. 2015 Stokes JB et al. Inhibition of Focal adhesion Kinase by PF-562,271 inhibits the growth and metastasis of pancreatic cancer concomitant with altering the tumor microenvironment. Mol Cancer Ther. 2011 Page 5 Verastem, Inc.

REDUCING CANCER STEM CELLS (CSC) AND BULK TUMOR TO IMPROVE DURATION OF RESPONSE Recurring tumor Tumor reduction, but CSCs survive Current therapies Initial tumor Addition of CSC-targeting agent (FAK or PI3K/mTOR) Durable response Page 6 Verastem, Inc.

FAK INHIBITORS SHOWN STEM CELLS TO REDUCE CANCER Ovarian mouse model (ID8) Ovarian patients, paired biopsies SOX2 RNA (CSC marker) In vivo tumor cells in ascites 2 0 1.8 1.6 1.4 1.2 1 0.8 0.6 0.4 0.2 0 1 5 1 0 5 0 02-306 01-316 03-302 03-301 03-315 Patient number C o n t r o l V S - 4 7 1 8 FAK Activity In vivo limiting dilutions 150 5000 * 03-315 4000 100 3000 2000 50 1000 0 0 Control VS-4718 Pre-treatment Post-treatment PageSource: Verastem data from preclinical and clinical studies 7 Verastem, Inc. Tumor-Initiating Capability per 106 cells 6 # o f C e l ls x 1 0 RNA Fold Change Pre-and Post-VS-6063 treatment pFAK (Y397; H-Score) 87-fold decrease in tumor formation

MULTI-FACETED APPROACH PATIENT OUTCOMES TO IMPROVING CANCER BOOST IMMUNE ATTACK to increase proportion of responders and duration of response3 REDUCE CANCER STEM CELLS to prevent recurrence and metastasis1,2 REDUCE STROMAL DENSITY to increase drug and immune system penetration into tumors4 1. 2. 3. 4. Kolev VN et al. FAK inhibition targets cancer stem cells. EORTC 2015 Kolev VN et al. PI3K/mTOR dual inhibitor VS-5584 preferentially targets cancer stem cells. Cancer Res. 2015 Serrels et al. Nuclear FAK controls chemokine transcription, Tregs, and evasion of anti-tumor immunity. Cell. 2015 Stokes JB et al. Inhibition of Focal adhesion Kinase by PF-562,271 inhibits the growth and metastasis of pancreatic cancer concomitant with altering the tumor microenvironment. Mol Cancer Ther. 2011 Page 8 Verastem, Inc.

BOOSTING IMMUNE ATTACK BY COMBINING FAK INHIBITION WITH IMMUNOTHERAPIES Immuno-Suppressive Cells Myeloid-derived suppressor cells, T-regs, M2 tumor-associated macrophages Cytotoxic CD8+ T cells Tumor infiltration & tumor cell killing Checkpoint inhibitor target presentation PD-L1 Treatment with FAK inhibitor + anti-PD-1/PD-L1 Increase responders and/or duration of response in responsive tumor types (e.g. NSCLC, ovarian) Opens up potential for targeting refractory or “cold” (e.g. tumor types pancreatic) Page 9 Verastem, Inc. INCREASE DECREASE

FAK INHIBITORS PRODUCE FAVORABLE CHANGES TO IMMUNE SYSTEM TO DECREASE TUMOR BURDEN Immunosuppressive T-regs Cytotoxic CD8+ T cells Tumor burden FAK wt Placebo Control FAK -/-Placebo Control FAK wt VS-4718 Treated FAK-wt FAK-/-FAK-wt FAK-/-Small-molecule inhibition or genetic knockout of FAK eliminates tumors via T cell attack Serrels et al. Cell 163: 160, 2015 VS-4718 treatment vs. FAK knock out, SCC 7.1 model T-regs: CD4+ FOXP3+ CD25+; CD8+ T cells: CD45+ CD3+ CD4-CD8+ p-values: ** = p < 0.01; *** = p < 0.001; **** = p < 0.0001 Page 10 Verastem, Inc.

MULTI-FACETED APPROACH PATIENT OUTCOMES TO IMPROVING CANCER BOOST IMMUNE ATTACK to increase proportion of responders and duration of response3 REDUCE CANCER STEM CELLS to prevent recurrence and metastasis1,2 REDUCE STROMAL DENSITY to increase drug and immune system penetration into tumors4 1. 2. 3. 4. Kolev VN et al. FAK inhibition targets cancer stem cells. EORTC 2015 Kolev VN et al. PI3K/mTOR dual inhibitor VS-5584 preferentially targets cancer stem cells. Cancer Res. 2015 Serrels et al. Nuclear FAK controls chemokine transcription, Tregs, and evasion of anti-tumor immunity. Cell. 2015 Stokes JB et al. Inhibition of Focal adhesion Kinase by PF-562,271 inhibits the growth and metastasis of pancreatic cancer concomitant with altering the tumor microenvironment. Mol Cancer Ther. 2011 Page 11 Verastem, Inc.

FAK INHIBITION REDUCES STROMAL DENSITY ENABLING THERAPIES & IMMUNE CELLS TO PENETRATE TUMORS STROMA CYTOTOXIC CD8+ T CELLS TUMOR FAK Inhibitors CANCER THERAPIES Stromal density = Tumor-associated fibroblasts + extracellular matrix proteins Verastem, Inc. Page 12

FAK INHIBITION REDUCES STROMAL DENSITY AND BOOSTS T CELL ENTRY INTO THE TUMOR Fibroblasts Fibroblast Proliferation Extracellular Matrix Cytotoxic CD8+ T cells D. Denardo, Wash U; Jiang H et al. Focal adhesion kinase inhibition enables efficacy of checkpoint immunotherapy in pancreatic cancer EORTC 2015 ECM, FAP+ Fibroblasts, Fibroblast proliferation: PDAC transgenic pancreatic model, VS-4718 treatment CD8+ T cells: Kras/p53 pancreatic tumors, Gem +/-anti-PD-1 +/-VS-4718 treatment Page 13 Verastem, Inc.

PROOF OF CONCEPT: MULTI-FACETED APPROACH IMPROVE SURVIVAL IN PANCREATIC CANCER TO 1. 2. 3. TARGET CSCs BOOST IMMUNE CELL RESPONSE REDUCE STROMAL DENSITY FAK Inhibitors Combined with Immuno-Oncology Therapies Improves Long term Survival in Aggressive Pancreatic Cancer VS-4718+Immuno (n=15) VS-4718 (n=10) Immuno (n=11) Vehicle (n=12) Transgenic Kras/p53 pancreatic model “Immuno” = anti-PD-1 + anti-CTLA-4 + GEM (25 mg/kg) D. Denardo, Wash U; Jiang H et al. Focal adhesion kinase inhibition enables efficacy of checkpoint immunotherapy in pancreatic cancer EORTC 2015 Page 14 Verastem, Inc.

FAK PROGRAM: NEWLY INITIATED COMBINATION STUDIES IN PANCREATIC CANCER DOSE ESCALATION (Ongoing) EXPANSION, 1ST LINE PANCREATIC (Planned) 1st line ancreatic RANDOMIZATION DOSE ESCALATION (Ongoing) EXPANSION, ADVANCED PANCREATIC (Planned) Page 15 Verastem, Inc. P2D RP2D Arm 2: VS-6063 + Pembrolizumab + Gem 1 – 2 prior lines of therapy (n = 10) Safety ORR PFS OS •Advanced solid tumors •21-day cycles of VS-6063 (oral BID) + pembrolizumab (IV on Day 1) + gemcitabine (IV on Days 1 and 8) •3+3 escalation R Arm 1: VS-6063 + Pembrolizumab + Gem Stable on front-line Gem/Abraxane (n = 10) Phase 1/1b, VS-6063 + Pembrolizumab (Merck anti-PD-1) + Gemcitabine Arm 2: Gem/Abraxane (n = 10) Safety ORR PFS •Advanced solid tumors •28-day cycles of VS-4718 (oral BID) + Gem/Abraxane •3+3 escalation p Arm 1: VS-4718 + Gem/Abraxane (n = 10) Phase 1/1b, VS-4718 + Gemcitabine + Abraxane

VERASTEM PORTFOLIO OF CANCER PROGRAMS PHASE 1 PHASE 2 PHASE 3 g term follow up up Page 16 Verastem, Inc. FOCAL ADHESION KINASE (FAK) PROGRAM VS-6063 - NSCLC; KRAS Mutant Ovarian; Paclitaxel combo Mesothelioma; Window of Opportunity Pancreatic; Pembrolizumab+Gemcitabine VS-4718 - Solid tumors Pancreatic; Gemcitabine+Abraxane   Lon   Long term follow PI3K/mTOR PROGRAM VS-5584 - Solid tumors & lymphomas

VS-6063 MONOTHERAPY IN KRAS-MUTANT NSCLC SHOWED ENCOURAGING PROGRESSION-FREE SURVIVAL RATES       16/44 (36%) evaluable patients alive and progression free at 12 weeks Best overall response (RECIST): PR = 1; SD = 26; PD = 15; NE = 2 Median PFS 11.7 weeks, with 6 patients on study for > 6 months and 1 patient continuing on study > 15 months 06021 06016 06028 06014 05004 05019 04016 06011 08001 05021 06012 08002 06025 05008 01009 06040 k PFS: months ths 07001 36% 06017 01014 06005 01016 04007 06033 04009 06030 01001 06001 04024 0 28 56 84 112 140 168 196 224 252 Days on study 280 308 336 364 392 420 448 476 504 Source: Unlocked, in-progress data as of 12/21/2015 Page 17 Verastem, Inc. Patient number 6 12 wee 9 months 12 months15 mon Reached 12 wk PFS, Ongoing Reached 12 wk PFS, Off study Off study Not evaluable

VS-6063 AS SINGLE AGENT IS COMPARABLE TO TARGETED AGENTS AND DOCETAXEL 12 week PFS rate of experimental agents for KRAS mt NSCLC 50% 36% 40% 33% 30% 20% 10% 0% VVSS-6-600663 PPllaacebo11 GGeeffitiniibb11 SSoorraaffeenniib2 Docettaaxxeel1l1,3,3,,4 TTrraammetiniibb33 “VS-6063 was generally well tolerated and suitable for long-term dosing. In this cohort of heavily pretreated patients, there were signs of single-agent activity comparable to other targeted agents and docetaxel. Future directions include possible combination studies with existing standard and emerging therapies, including checkpoint inhibitors.” Dr. David Gerber, IASLC 2015 1. Phase 3 INTEREST, Douillard et al., JCO 2010 2. Phase 3 MISSION, Mok et al., ESMO 2012 3. Phase 2, Blumenschein et al., Ann Oncol 2015 4. Phase 2, Janne et al., Lancet 2013 Page 18 Verastem, Inc. 30 - 45%45% 40% 1 median prior line 2 median prior lines 3 median prior lines 1 median prior line 1 median prior line 10%

VS-6063 PLUS PACLITAXEL SHOWED PROMISING DURATION OF RESPONSES IN OVARIAN CANCER     VS-6063 can be safely combined with paclitaxel 41% (9/22) disease control (objective response or SD > 6 months; 2 CR; 3 PR; 4 SD > 6 months) CR 03-202 SD 01-310 SD 02-314 PR 03-315 PR 03-301 SD 01-308 CR 03-102 SD 01-305 SD 03-311 SD 01-316 SD 02-307 SD 03-312 PR 02-309 02-304 24 months 12 months 18 months 30 months 01-201 02-203 02-306 03-313 01-101 01-103 03-302 02-303 Days on Study Unlocked, in-progress data as of 12/21/2015 Page 19 Verastem, Inc. SD On study Off study

DURABLE COMPLETE RESPONSE SHOWS POTENTIAL FOR FAK INHIBITION TO “FINISH THE JOB” Patient 03-202: Stage IV platinum-resistant serous ovarian cancer with 5 prior lines of therapy Stable disease (SD) with combination treatment 1 VS-6063 2 Complete response (CR) 3 Continues to tolerate VS-6063 well monotherapy at 4.5 months at 11.8 months carbo/cytoxan/taxol 160 Potential next steps: Combine VS-6063 with checkpoint inhibitors Page 20 Verastem, Inc. CA-125 (U/mL) MONTHS ON THERAPY0246810121416182022242628303234 carbo/taxol (adjuv) cisplatin/gem measles vaccine alimta VS-6063 + Paclitaxel 200123 120 80 40 0 CRUnlocked, in progress data as of 12/21/2015 SD PD PD PD

VS-5584, A PAN-PI3K/MTOR INHIBITOR, WILL BE MOVING SHORTLY INTO OVARIAN AND HEME EXPANSION COHORTS • VS-5584 is equipotent against mTORC1, mTORC2 and all four PI3K class I isoforms 50 • Combined inhibition of PI3K and mTOR is critical to CSC targeting1 Planned expansion cohorts at RP2D in ovarian & NHL/CLL Phase 1: Ongoing dose escalation of oral, intermittent dosing in advanced non-hematologic malignancies or lymphoma  Continues to be safe and well tolerated  5-75mg dose range. MTD reached Potential for PARPi combination in ovarian & endometrial Ongoing RP2D confirmation cohort at 55 mg dose o 1Kolev VN et al. PI3K/mTOR dual inhibitor VS-5584 preferentially targets cancer stem cells. Cancer Res. 2015 Page 21 Verastem, Inc. mTOR IC50 (nM) PI3K isoform IC(nM) Alpha Beta Delta Gamma 3.4 2.6 21 3.0 2.7

2016 MILESTONES Planned initiation in 2016 PHASE 1 / 1B PHASE 2 PHASE 3 g term follow up nsion in NSCLC cer ose escalation markers nsion in advanced ed biopsies nsion in 1st line nsion in Data Readouts in 2016 and 2017 Page 22 Verastem, Inc. FOCAL ADHESION KINASE (FAK) PROGRAM VS-6063 - NSCLC; KRAS Mutant Ovarian, Paclitaxel I-O comboD Mesothelioma; Window of Opportunity Pancreatic; Pembrolizumab+Gemcitabine VS-4718 - Solid tumors Pancreatic; Gemcitabine+Abraxane  Lon   Lo RP2D with expa and ovarian can 3rd cohort for IO RP2D with expa pancreatic RP2D with pair RP2D with expa pancreatic ng term follow up PI3K/mTOR PROGRAM VS-5584 - Solid tumors & lymphomas RP2D with expa NHL/CLL and ov arian

EXECUTIVE MANAGEMENT Robert Forrester Daniel Paterson President/CEO, BOD CEO/CFO, CombinatoRx/COLY MeesPierson, Barclays, UBS Chief Operating Officer CEO: The DNA Repair Co. (now On-Q-ity) PharMetrics (now IMS), Axion Steven Bloom VP, Corporate Development VP, Commercial Strategy and Business Development Ziopharm, PharMetrics (now IMS) , Eli Lilly and Company Jonathan Pachter, Ph.D. VP, Head of Research Head of Cancer Biology, OSI (now Astellas) Schering-Plough (now Merck) Jack Green Chief Financial Officer CFO, Genzyme Transgenics Corporation (GTC) Lou Vaickus, M.D., FACP Interim Chief Medical Officer VP, Head of Clinical Development Vertex Tolerx, Sunovion, EMD Serono BOARD OF DIRECTORS Timothy Barberich Former CEO/Chair Sepracor (SEPR) Henri Termeer Lead Director Former CEO/Chair Genzyme Alison Lawton Former Genzyme (now Sanofi) Paul Friedman, M.D. Former President/CEO Incyte (INCY) Louise Phanstiel BOD: Cedars Sinai, MYGN Christoph Westphal, M.D., Ph.D. Cofounder/CEO: MNTA, ALNY, XLRN, SIRT, VSTM Cofounder: Alnara (now Lilly), OvaScience (OVAS) Michael Kauffman, M.D., Ph.D. CEO Karyopharm (KPTI), former CMO Onyx Stephen Sherwin, M.D. BOD: BIIB; NBIX, RIGL Page 23 Verastem, Inc. Confidential

THE VERASTEM OPPORTUNITY Multi-faceted approach to improving outcomes Clinical programs targeting multiple cancers Experienced team Well capitalized with strong IP Page 24 Verastem, Inc. $120.1M IN CASH AND CASH EQUIVALENTS AS OF SEPT. 30, 2015 Sufficient operating capital into 2018 Intellectual Property (Composition of Matter) VS-6063:2028 VS-4718:2028 VS-5584:2029 EXECUTIVE MANAGEMENT Robert Forrester Daniel Paterson President/CEO, BOD Chief Operating Officer CEO/CFO, CombinatoRx/COLY CEO: The DNA Repair Co. (now On-Q-ity) MeesPierson, Barclays, UBS PharMetrics (now IMS), Axion Steven Bloom Jonathan Pachter, Ph.D. VP, Corporate Development VP, Head of Research VP, Commercial Strategy and Business Head of Cancer Biology, OSI (now Astellas) Development Schering-Plough (now Merck) Ziopharm, PharMetrics (now IMS) , Eli Lilly and Company Jack Green Lou Vaickus, M.D., FACP Chief Financial OfficerInterim Chief Medical Officer CFO, Genzyme Transgenics Corporation (GTC)VP, Head of Clinical Development Vertex Tolerx, Sunovion, EMD Serono BOARD OF DIRECTORS Timothy Barberich Henri Termeer Alison Lawton Former CEO/Chair Sepracor (SEPR) Lead Director Former Genzyme (now Sanofi) Former CEO/Chair Genzyme Paul Friedman, M.D. Christoph Westphal, M.D., Ph.D. Louise Phanstiel Former President/CEO Incyte (INCY)Cofounder/CEO: MNTA, ALNY, XLRN, SIRT, VSTMBOD: Cedars Sinai, MYGN Cofounder: Alnara (now Lilly), OvaScience (OVAS) Michael Kauffman, M.D., Ph.D. Stephen Sherwin, M.D. CEO Karyopharm (KPTI), former CMO Onyx BOD: BIIB; NBIX, RIGL