JPMorgan Healthcare Conference

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1 Pioneering a first-in-class, oral immuno-oncology therapy JPMorgan Healthcare Conference January 2018

2 Forward-Looking Statements This presentation contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of Such forward-looking statements include those regarding the company s expectations about: the therapeutic potential of PI3K-gamma selective inhibition and IPI-549, alone and in combination with immune checkpoint inhibitors, including Opdivo ; clinical trial plans regarding IPI-549, including enrollment projections and timing for trial expansion; the timing and type of plans to report clinical and translational data of IPI-549; patent protection for IPI-549; the market sizes and commercial opportunity for IPI-549; 2017 year-end cash and investments balance and 2018 financial guidance as of January 8, 2018; and the company s ability to execute on its strategic plans. Such statements are subject to numerous important factors, risks and uncertainties that may cause actual events or results to differ materially from the company s current expectations. For example, there can be no guarantee that IPI-549 will successfully complete necessary preclinical and clinical development phases or that any positive developments with IPI-549 will result in stock price appreciation. Management s expectations and, therefore, any forward-looking statements in this presentation could also be affected by risks and uncertainties relating to a number of other factors, including the following: Infinity s results of clinical trials and preclinical studies, including subsequent analysis of existing data and new data received from ongoing and future studies; Infinity s ability to obtain, maintain and enforce patent and other intellectual property protection for IPI-549; the content and timing of decisions made by the U.S. FDA and other regulatory authorities; Infinity s ability to obtain and maintain requisite regulatory approvals and to enroll patients in its clinical trials; unplanned cash requirements and expenditures; and development of agents by Infinity's competitors for diseases in which Infinity is currently developing or intends to develop IPI-549. These and other risks which may impact management s expectations are described in greater detail under the caption Risk Factors included in Infinity s quarterly report on Form 10-Q filed with the Securities and Exchange Commission (SEC) on November 7, 2017, and other filings filed by Infinity with the SEC. Any forwardlooking statements contained in this presentation speak only as of the date hereof, and Infinity expressly disclaims any obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise. Infinity s website is Infinity regularly uses its website to post information regarding its business, product development programs and governance. Infinity encourages investors to use particularly the information in the section entitled Investors/Media, as a source of information about Infinity. References to in this presentation are not intended to, nor shall they be deemed to, incorporate information on into this presentation by reference. 2

3 IPI-549: Potential First-in-Class, Transformative Approach Within Immuno-Oncology Only potent, oral, selective PI3K-γ inhibitor in clinical development 1 Targeting macrophages with IPI-549 is a compelling approach to reducing pro-tumor immune suppression and increasing anti-tumor immune activation 2 Discovered and developed by Infinity Composition of matter patents into 2034 Encouraging clinical and translational data from monotherapy dose-escalation 3 Favorable tolerability profile alone and in combination with Opdivo Clinically active with objective response in monotherapy Initial translational data demonstrate on-mechanism reduction in immune suppression and increase in immune activation Robust Phase 1/1b study in advanced solid tumors 4 with new results anticipated starting in Q2 18 Evaluating as monotherapy and in combination with Opdivo Plan to evaluate ~ 200 patients Clinical and translational (including biopsy data) monotherapy and combination therapy data anticipated throughout January 8, Kaneda et al. Nature, 2016 Nov;539: De Henau et al. Nature, 2016 Nov;539: Hong et al., SITC NCT

4 Checkpoint Inhibitors Can Generate an Effective Anti-Tumor Immune Response in Patients With a Broad Range of Cancers Cancer Type NSCLC Gastric Liver Head and neck Bladder Kidney Breast (TN) Ovarian Melanoma CRC MSI hi Breast HR+ CRC non-msi hi Prostate NSCLC (EGFR Mu, ALK+) Patients Responsive to PD-1/PD-L1 Inhibitors 0 200, , , ,000 1,000,000 1,200,000 1,400,000 Patients Diagnosed Globally Per Year Source: GLOBOCAN Estimated cancer incidence in

5 But an Effective Immune Response is Not Generated in the Majority of Patients Cancer Type NSCLC Gastric Liver Head and neck Bladder Kidney Breast (TN) Ovarian Melanoma CRC MSI hi Breast HR+ CRC non-msi hi Prostate NSCLC (EGFR Mu, ALK+) Patients Responsive to PD-1/PD-L1 Inhibitors Patients Unresponsive to PD-1/PD-L1 Inhibitors 0 200, , , ,000 1,000,000 1,200,000 1,400,000 Patients Diagnosed Globally Per Year Source: GLOBOCAN Estimated cancer incidence in

6 And In Some Indications No Clinically Meaningful Immune Response Is Generated Cancer Type NSCLC Gastric Liver Head and neck Bladder Kidney Breast (TN) Ovarian Melanoma CRC MSI hi Breast HR+ CRC non-msi hi Prostate NSCLC (EGFR Mu, ALK+) Patients Responsive to PD-1/PD-L1 Inhibitors Patients Unresponsive to PD-1/PD-L1 Inhibitors 0 200, , , ,000 1,000,000 1,200,000 1,400,000 Patients Diagnosed Globally Per Year Source: GLOBOCAN Estimated cancer incidence in

7 Significant Patient Need Remains Given Limitations of Checkpoint Inhibitors NSCLC Gastric Liver Head and neck Bladder Opportunity to improve outcomes for: Kidney Breast (TN) ~1.2M Ovarian patients who respond to immune Patients Responsive checkpoint to PD-1/PD-L1 inhibitors Inhibitors Melanoma Patients Unresponsive to PD-1/PD-L1 Inhibitors CRC MSI hi ~8.0M patients unresponsive to immune checkpoint inhibitors Cancer Type Breast HR+ CRC non-msi hi Prostate NSCLC (EGFR Mu, ALK+) 0 200, , , ,000 1,000,000 1,200,000 1,400,000 Patients Diagnosed Globally Per Year Source: GLOBOCAN Estimated cancer incidence in

8 Targeting the Myeloid/Macrophage Compartment Is Emerging As a Compelling Approach to Overcoming Limitations of Checkpoint Inhibitors Tumors evade immune attack through multiple mechanisms, with a key role played by the myeloid/macrophage compartment Pro-tumor macrophages dominate in the tumor microenvironment and prevent anti-tumor attack Targeting macrophages to enhance anti-tumor immune attack can be achieved in two ways Reduce pro-tumor macrophage function Increase anti-tumor macrophage function 8

9 There Are a Growing Number of Macrophage Targeted Approaches in Development to Address the Limitations of Checkpoint Inhibitors Immuno-Oncology Therapies in Development or Launched 200 ~180 Number of Molecules T cell Targeted IPI-549 ~30 Myeloid / Macrophage Targeted IPI-549 is only selective PI3Kgamma inhibitor in development 9

10 IPI-549 Is Differentiated Within Macrophage Targeted Approaches Immuno-Oncology Therapies in Development or Launched 200 ~180 Number of Molecules T cell Targeted IPI-549 ~30 Myeloid / Macrophage Targeted IPI-549 is only selective PI3Kgamma inhibitor in development 10

11 IPI-549 Is Differentiated Within Macrophage Targeted Approaches Distinct role in reducing pro-tumor macrophage function and increasing anti-tumor macrophage function Immuno-Oncology Therapies in Development or Launched 200 ~180 Targeting macrophages to enhance anti-tumor immune attack can be achieved in two ways Number of Molecules T cell Targeted IPI-549 ~30 Myeloid / Macrophage Targeted IPI-549 is only selective PI3Kgamma inhibitor in development Reduce pro-tumor macrophage function e.g. CSF1r + Increase anti-tumor macrophage function e.g. CD40 + IPI

12 IPI-549 Is Differentiated Within Macrophage Targeted Approaches Distinct role in reducing pro-tumor macrophage function and increasing anti-tumor macrophage function Immuno-Oncology Therapies in Development or Launched 200 ~180 Targeting macrophages to enhance anti-tumor immune attack can be achieved in two ways Number of Molecules T cell Targeted IPI-549 ~30 Myeloid / Macrophage Targeted IPI-549 is only selective PI3Kgamma inhibitor in development Reduce pro-tumor macrophage function e.g. CSF1r + Increase anti-tumor macrophage function e.g. CD40 + IPI

13 IPI-549 Is Differentiated Within Macrophage Targeted Approaches Distinct role in reducing pro-tumor macrophage function and increasing anti-tumor macrophage function Immuno-Oncology Therapies in Development or Launched 200 ~180 Targeting macrophages to enhance anti-tumor immune attack can be achieved in two ways Number of Molecules T cell Targeted IPI-549 ~30 Myeloid / Macrophage Targeted IPI-549 is only selective PI3Kgamma inhibitor in development Reduce pro-tumor macrophage function e.g. CSF1r + Increase anti-tumor macrophage function e.g. CD40 + IPI Enhanced anti-tumor attack with IPI

14 Reprogramming Tumor-Associated Macrophages by Targeting PI3K-γ with IPI

15 IPI-549: First in Class, Oral Selective Inhibitor of PI3K-γ Assay PI3K-γ PI3K-α PI3K-β PI3K-δ Binding Affinity Kd (nm) Biochemical IC 50 (nm) >8421 Cellular IC 50 (nm) DeHenau et al. AACR 2016 # X selectivity in cellular assay Chemical Structure of IPI-549 Composition of matter patents into 2034 Evans et al. ACS Med. Chem. Lett. (2016). 15

16 IPI-549 Reprograms Macrophages Resulting in Reduced Pro-Tumor Immune Suppression and Increased Anti-Tumor Immune Activation Pro-tumor (M2) macrophages Suppressed T cells Tumor cells Kaneda et al. Nature, 2016 Nov;539:

17 IPI-549 Reprograms Macrophages Resulting in Reduced Pro-Tumor Immune Suppression and Increased Anti-Tumor Immune Activation Anti-tumor (M1) macrophages Activated T cells Tumor cells IPI-549 Kaneda et al. Nature, 2016 Nov;539:

18 IPI-549 Reprograms Macrophages Resulting in Reduced Pro-Tumor Immune Suppression and Increased Anti-Tumor Immune Activation Kaneda et al. Nature, 2016 Nov;539:

19 IPI-549 Monotherapy Demonstrates Tumor Growth Delay in the Lewis Lung Carcinoma Model 2,500 Tumor volume (mm 3 ) 2,000 1,500 1, * Vehicle n=13 15 mg/kg QD n=15 p < Treatment start Day post-implant IPI-549 effects are both macrophage-dependent and T cell-dependent Kutok et al., Immune Microenvironment: Transforming the Future of Cancer Therapies Meeting,

20 IPI-549 Monotherapy Demonstrates Tumor Growth Delay in Multiple Syngeneic Solid Tumor Models Cancer Type Cell Line % Tumor Growth Inhibition Range [n experiments] Lung LLC-luc brei 28-52% [10] Colon MC % [3] Colon CT % [12] Breast 4T1-luc 19-38% [6] Melanoma B16-GMCSF 24-56% [6] De Henau et al. Nature, 2016 Nov;539:

21 Preclinical Data Demonstrate Targeting PI3K-γ in Macrophages Overcomes Resistance to Checkpoint Blockade De Henau et al. Nature, 2016 Nov;539:

22 Pro-Tumor Macrophages Drive Checkpoint Inhibitor Resistance and Can Be Overcome by IPI-549 Treatment, Providing Survival Benefit 2000 Macrophage-Rich Breast Cancer (4T1) Model Reduced Tumor Growth Enhanced Survival Tumor Size (mm 3 ) PD-1 Vehicle IPI-549 (15 mg/kg) PD-1 + IPI-549 * * ** Percent Survival IPI anti-ctla4 + anti-pd-1 Anti-CTLA4 + anti PD-1 Vehicle **** * **** **** Days post-implant Days post-implant IPI-549 in combination with anti-pd-1 and anti-ctla4 therapies significantly extends survival with 30% complete regression * P <0.05, ** P <0.01, ****P < De Henau et al. Nature, 2016 Nov;539:

23 Key Preclinical Takeaways Reprograms macrophages from pro-tumor (M2) function to the anti-tumor (M1) function Demonstrated monotherapy activity Greater tumor growth inhibition and survival in combination with checkpoint inhibitors Reverses resistance to checkpoint inhibitors 23

24 Initial Clinical and Translational Data 24

25 IPI Sites/Investigators Investigator(s) Jedd Wolchok, MD PhD (PI) Michael Postow, MD David Hong, MD Anthony W. Tolcher MD FRCP FACP Amita Patnaik, MD Geoff Shapiro, MD PhD Steve Hodi, MD PhD Keith Flaherty MD Ryan Sullivan, MD James Miers, MD Toni Ribas, MD PhD Bartosz Chmielowski, MD Ezra Cohen, MD Institution MSKCC MDACC South Texas Accelerated Research Therapeutics (START) DFCI MGH BIDMC UCLA UCSD 25

26 IPI-549 Phase 1/1b Study Monotherapy Dose Escalation in Solid Tumors 40 mg QD 60 mg QD Completed No DLTs - MTD was not identified Expansion initiated based on PK/PD 30 mg QD 10 mg QD 15 mg QD 20 mg QD Endpoints PK/PD Safety Activity Peripheral blood samples for translational analysis 3+3 design N=19 total, 18 evaluable Hong et al., SITC

27 Safety Summary (N=19) Data as of October 18, 2017 IPI-549 monotherapy has been well tolerated (doses up to 60 mg QD) No DLTs - MTD was not identified Majority of reported AEs have been Grade 1-2 No treatment-related SAEs or treatment-related deaths 2 patients discontinued study drug due to treatment-related AEs Grade 2 rash and Grade 2 ALT/AST increase Grade 3 ALT/AST increase Hong et al., SITC

28 IPI-549 Phase 1/1b Trial in ~200 Patients in Advanced Solid Tumors Dose Escalation Peripheral Blood Samples Monotherapy* 10 mg to 60 mg QD 3+3 design RP2D: 60 mg QD Expansion Peripheral Blood Samples and Mandatory Pre-Treatment and On-Treatment Biopsies All Solid Tumors NSCLC Melanoma Checkpoint inhibitor-resistant**** Combination IPI-549* + Nivolumab** 6+6 design Completed Enrolled Enrolling RP2D: 40 mg QD + Nivolumab** SCCHN TNBC Mesothelioma Adrenocortical Carcinoma Checkpoint inhibitor-naïve Checkpoint inhibitor-independent * 28 day cycles, continuous QD dosing ** Flat-dose 240 mg Q2W *** Enrollment expected to initiate in Q **** Must have de novo or acquired resistance to immediately prior anti-pd-1/anti-pd-l1 therapy MDSC High*** Prospectively identified 28

29 New Cohort of Patients Selected Based on High Myeloid Derived Suppressor Cell (MDSC) Baseline Status Is Being Initiated MDSCs limit the response to immune therapies and IPI-549 can overcome their suppressive effect 1 Poor response to checkpoint inhibitor therapy is correlated with the presence of high pre-treatment levels of MDSCs 2 Responses to IPI-549 were seen in patients with high basal levels of MDSCs, alone and in combination with nivolumab New cohort of MDSC high patients to be treated with IPI-549 in combination with nivolumab 1. De Henau et al. Nature, 2016 Nov;539:443. Talmadge and Gabrilovich Nat Rev Canc 2013, 13: Kitano et al ASCO annual meeting #2518, 2013; Postow et al NEJM 2012, 366;10; Kitano et al. Cancer Immunol Res. 2014, 2(8):

30 IPI-549 Monotherapy Dose Escalation Time on Study (N=19) Dose (mg) Tumor Type 15 Adenoid 20 Mesothelioma MSS 20 Colorectal 15 Ovarian 10 Endometrial 20 Endometrial 40 Head & Neck 60 Breast 30 Neuroendocrine MSS 30 Colorectal 30 Adenoid 10 Ovarian 60 Endometrial 60 Esophageal 40 Merkel Cell 10 Pancreatic 15 Pancreatic 40 Ovarian 40 Head & Neck Weeks On Study Partial Response Disease Progression Discontinued Drug Related Discontinued Week Partial Response Occurred Data as of October 18, 2017 Hong et al., SITC

31 IPI-549 Monotherapy Dose Escalation Time on Study (N=19) Dose (mg) Tumor Type 15 Adenoid 20 Mesothelioma MSS 20 Colorectal 15 Ovarian 10 Endometrial 20 Endometrial 40 Head & Neck 60 Breast 30 Neuroendocrine MSS 30 Colorectal 30 Adenoid 10 Ovarian 60 Endometrial 60 Esophageal 40 Merkel Cell 10 Pancreatic 15 Pancreatic 40 Ovarian 40 Head & Neck Weeks Partial Response Disease Progression Discontinued Drug Related Discontinued Week Partial Response Occurred Weeks Clinical benefit defined as patients who have not progressed at 16 weeks (8/18 evaluable patients) On Study Data as of October 18, 2017 Hong et al., SITC

32 Partial Response in a Patient with Advanced Peritoneal Mesothelioma 50 yo Male with Peritoneal Mesothelioma (epithelioid type) Original Dx October prior regimens, last regimen pemetrexed/carboplatin (duration of last prior therapy 2.5 months) Started on 20 mg IPI-549 August 2016 % Change 10% 0% -10% -20% -30% 0% % Change in Lesion Size (RECIST) 3% -6% -12% -23% -25% -36% PR Patient remains on study as of January 8, % -50% -42% BL C3 C5 C7 C9 C11 C13 C15 Hong et al., SITC Cycle Number (1 Cycle = 4 Weeks) 32

33 Partial Response in a Patient with Advanced Peritoneal Mesothelioma Radiologic Evidence of Tumor Reduction in Abdominal Cavity Baseline End of Cycle 15 Hong et al., SITC

34 Improvement of Malignant Pleural Effusions and Ascites in Heavily Pre-Treated Patient with KRAS+ MSS Colorectal Cancer Stage IV diagnosed July 2012 with 8 prior regimens (duration of last prior therapy~2 months) Extensive peritoneal carcinoma with ascites; bilateral pleural effusion, as well as liver and lung lesions Remained on monotherapy for 36 weeks Baseline End of Cycle 2 Hong et al., SITC

35 Partial Response in Patient With Adrenocortical Carcinoma Treated With IPI mg QD and Nivolumab 57 year old male diagnosed with adrenocortical carcinoma July 2013 underwent surgery 10% 0% % Change in Lesion Size (RECIST) 0% April 2014, six cycles chemotherapy (Adriamycin, Platinum, Etoposide and Mitotane) with maintenance Mitotane until February 2017 % Change -10% -20% -30% -40% -37% PR No prior anti-pd1/pd-l1 therapy Patient remains on study as of January 8, 2018 Hong, Infinity Investor Presentation SITC % -60% -70% -55% -60% BL C3 C5 C7 Cycle Number (1 Cycle = 4 Weeks) 35

36 Partial Response in Patient With Adrenocortical Carcinoma Treated With IPI mg QD and Nivolumab Radiologic Evidence of Tumor Reduction in Liver Metastases Extensive metastatic disease including liver (typically poor prognosis), lung, retroperitoneum, spleen, lymph nodes Baseline Cycle 3 Day 1 Courtesy of Dr. Ryan Sullivan/Dr. Dejan Juric Hong, Infinity Investor Presentation SITC

37 Initial Translational Data in Peripheral Blood Following Monotherapy Treatment with IPI-549 Support the Dual Mechanism of Action of IPI-549 Targeting macrophages to enhance anti-tumor immune attack can be achieved in two ways Reduce pro-tumor macrophage function IPI IPI-549 reduces immune suppression Reinvigoration (proliferation) of exhausted CD8+ T-cells Increase anti-tumor macrophage function + IPI-549 increases immune activation Up-regulation of interferon-gamma responsive factors Increased myeloid cell activation markers, which are associated with clinical benefit (>16 weeks on study) Hong et al., SITC

38 Encouraging Early Phase 1/1b Data for IPI-549 from Dose Escalations Monotherapy* Combination Therapy PK/PD Maximal and sustained inhibition of PI3K-γ signaling IPI-549 PK/PD unaffected in the presence of nivolumab Safety Favorable safety profile in patients treated up to 60 mg QD Combination well tolerated 40 mg selected as recommended Phase 2 dose Activity Objective partial response in patient with mesothelioma, with 44% of patients on IPI-549 for over four months Objective partial response in patient with adrenocortical cancer Expansion cohorts initiated based on signals of clinical activity Hong et al., SITC New Results Anticipated Starting in Q

39 2018 Milestones and Financial Guidance 39

40 2018: Multiple Clinical Data Readouts Anticipated Starting in 2Q 2Q2018 Report data from the monotherapy expansion cohort, including clinical and translational data from paired tumor biopsies Report data from the combination dose-escalation Report initial data from combination expansion cohorts 2H2018 Report additional combination expansion data with more mature clinical and translational data including insights from paired tumor biopsies 40

41 2018 Financial Guidance Cash and investments at 12/31/17 (unaudited): $57.6 million Net loss: $40 million to $50 million Year-end cash: $10 million and $20 million Cash runway: Into Q The company s 2018 financial guidance is provided as of January 8, 2018, excludes additional funding or business development activities and does not include the potential $22 million milestone from Verastem upon the first regulatory approval of duvelisib. Verastem has provided its expectation that it plans to submit a New Drug Application to the U.S. Food and Drug Administration for duvelisib in the first quarter of

42 IPI-549: Potential First-in-Class, Transformative Approach Within Immuno-Oncology Only potent, oral, selective PI3K-γ inhibitor in clinical development 1 Encouraging clinical and translational data from monotherapy dose-escalation 2 Robust Phase 1/1b study in advanced solid tumors 3 with new results anticipated starting in Q January 8, Hong et al., SITC NCT

43 Pioneering a first-in-class, oral immuno-oncology therapy JPMorgan Healthcare Conference January 2018

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