CORPORATE PRESENTATION

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1 CORPORATE PRESENTATION June 2017

2 FORWARD LOOKING SAFE HARBOR STATEMENT This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of These statements are often, but not always, made through the use of words or phrases such as anticipates, expects, plans, believes, intends, and similar words or phrases. Such statements involve risks and uncertainties that could cause Checkpoint Therapeutics actual results to differ materially from the anticipated results and expectations expressed in these forward-looking statements. These statements are only predictions based on current information and expectations and involve a number of risks and uncertainties. Actual events or results may differ materially from those projected in any such statements due to various factors, including the risks and uncertainties inherent in clinical trials, drug development, and commercialization. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. All forwardlooking statements are qualified in their entirety by this cautionary statement and Checkpoint Therapeutics undertakes no obligation to update these statements, except as required by law. 2

3 CHECKPOINT THERAPEUTICS CORPORATE HIGHLIGHTS Building portfolio of leading-edge immune-enhanced combination cancer therapies Technologies licensed from Dana Farber, Teva, others Primary focus on validated targets $58 million raised in private rounds in 4Q 2015 Went public in 4Q 2016 via Form 10 Quoted on OTCQX with ticker CKPT Application to up-list to Nasdaq under review Majority-controlled sub of Fortress Biotech (FBIO) 3

4 EVOLUTION OF CANCER THERAPY Chemotherapy Targeted therapy Immuno-oncology Immuno-oncology Combinations Not tumor specific Targets all rapidly dividing cells Highly toxic Targets specific genes/proteins found in cancer cells Rapid responses Better tolerated Stimulates immune system to activate against tumor Long-lasting responses in subsets of patients Wide variety of tumors Combination of I/O - targeted therapy or I/O - I/O provides one-two punch Higher response rates The goal of I/O therapy is to engage the immune system (particularly Killer T-Cells) to attack and kill cancer cells 4

5 WHAT WE DO AT CHECKPOINT Acquire, develop, commercialize immune-enhanced combination treatments for patients with solid tumor cancers Two immuno-oncology I/O monoclonal antibodies (mabs) Four targeted anti-cancer agents Collaborate with TG Therapeutics (Nasdaq:TGTX) to develop I/O antibodies in combination with TG s targeted therapies for liquid tumors (e.g. Non-Hodgkin s Lymphoma and CLL) 5

6 PIPELINE Pipeline Compound & Indication Preclinical Phase I Phase II Phase III Originator Immuno- Oncology Agents CK-301 Anti-PD-L1 (Multiple forms of Cancer) CK-302 Anti-GITR (Multiple forms of Cancer) Target Phase 1 3Q 2017 Target IND: 2018 Dana Farber Dana Farber CK-101 EGFR Inhibitor (Lung Cancer) Phase 1/2 ongoing NeuPharma Targeted Anti- Cancer Agents CK-102 PARP Inhibitor (Multiple forms of Cancer) CK-103 BET Inhibitor (Multiple forms of Cancer) Phase 1b planned Target IND: YE 2017 Teva / Cephalon Jubilant Anti-CAIX (Renal cell Carcinoma, CAIX+ solid tumors) Target IND: 2018 Dana Farber 6

7 LARGE POTENTIAL MARKETS Estimated Compound Indication Current Stage Market Size I/O CK-301 (PD-L1) Multiple solid tumors Pre-clinical >$30B CK-302 (GITR) Multiple solid tumors Pre-clinical >$1B Targeted CK-101 (EGFR) EGFR mutant lung cancer Phase 1 >$3B CK-102 (PARP) Multiple solid tumors Phase 1 >$3B CK-103 (BET) Multiple tumors Pre-clinical >$1B Anti-CAIX Renal cell carcinoma Pre-clinical >$500M 7

8 CHECKPOINT STRATEGY Develop first-in-class or best-in-class combination treatments in targeted solid tumor cancers and liquid tumors in collaboration with TGTX Cancer cells Targeted Anti-Cancer Agents Validated targets for anti-cancer therapy e.g., mutant EGFR lung cancer I/O Agents Anti-PD-L1 Additional I/O agents to augment immune system engagement Achieve pricing leverage by owning all component drugs of combination 8

9 I/O AGENTS: CURRENT PIPELINE CK-301 (Anti-PD-L1) mab Removes cancer cells ability to shield themselves from attack by the immune system s killer T-cells Proven technology, widely applicable among tumor types Unlike most other anti-pd-l1s, Checkpoint s retains native features for potentially greater killing power CK-302 (Anti-GITR) mab Up-regulates the activity of killer T-cells to attack cancer cells Designed to be synergistic with anti-pd-l1 9

10 PD-L1 AND EFFECT OF ANTI-PD-L1 ANTIBODIES Tumor cells up-regulate PD-L1, shielding cancer cells by de-activating T-cell responses Y Anti-PD-L1 monoclonal antibody PD-L1 ligand on tumor cells T-Cell T-Cell T-Cell T-Cell T-Cell T-Cell T-Cell T-Cell Anti-PD-L1 mabs block PD-L1 binding to PD-1 and B7.1, allowing the immune system s T-cells to attack the cancer Cancer cells 10

11 T Cell-Specific Transcription F o l d i n c r e a s e o v e r b c k g r d (Fold increase) CK-301: PRE-CLINICAL ACTIVITY CK-301 potency similar to competitor anti-pd-l1 antibodies in PD-1/PD-L1 blockade bioassay (reversing T-Cell inhibition) 8 6 a t e z o l i z u m a b * d u r v a l u m a b * l o w a f f i n i t y a n t i - P D - L 1 c o n t r o l a v e l u m a b * C K N o r m a l I g G 1 c o n t r o l A n t i b o d y, g / m l Poster: AACR Annual Meeting 2017 * surrogate 11

12 GITR AND EFFECT OF ANTI-GITR ANTIBODIES In addition to the tumor s defense, the immune system may also block T-Cells from attacking the cancer Anti-GITR antibodies are believed to be able to block T-reg function, permitting T-cells to attack the cancer Y Anti-GITR monoclonal antibody GITR ligand on T-reg cells T-REG T-REG T-REG T-REG T-Cell T-Cell T-Cell T-Cell T-Cell T-Cell T-Cell T-Cell Cancer cells 12

13 I/O AGENTS: CURRENT STATUS CK-301 (Anti-PD-L1) Phase 1 initiation targeted for 3Q 2017 CK-302 (Anti-GITR) IND-enabling program ongoing IND targeted for 2018 Other I/O targeted agents in exploratory stages 13

14 TARGETED ANTI-CANCER THERAPIES Goal of targeted anti-cancer therapy is to smart bomb specific cancer pathways or driver mutations Pipeline Compound & Indication Preclinical Phase I Phase II Phase III CK-101 EGFR Inhibitor (Lung Cancer) Phase 1/2 ongoing CK-102 PARP Inhibitor (Multiple forms of Cancer) CK-103 BET Inhibitor (Multiple forms of Cancer) Phase 1b planned Target IND: YE 2017 Four unique mechanisms for targeting cancer cells Anti-CAIX (Renal cell Carcinoma, CAIX+ solid tumors) Target IND:

15 CK-101: 3 RD GENERATION EGFR INHIBITOR RATIONALE EGFR Mutations Validated Target Success of 1 st generation EGFR s have led to acquired resistance through further mutations to EGFR (T790M) One 3 rd generation EGFR inhibitor (Tagrisso ) is approved for patients with lung cancer with T790M mutation Est. peak sales: $3 billion CK-101 has potential safety advantages Tagrisso has significant skin tox due to also inhibiting wild-type EGFR CK-101 has limited targeting of wild-type 15

16 CK-101: 3 RD GENERATION EGFR INHIBITOR PRE-CLINICAL EFFICACY In vitro, CK-101 showed: Strong efficacy for T790M and other EGFR mutations Good selectivity for mutant over wild-type EGFR A431/H1975 ratio ~ 100 fold Target profile: Strong efficacy and tolerability IC 50 (nm) Cell Line H1975 HCC827 A431 Mutation L858R/T790M Exon 19 del EGFR WT Afatinib Tagrisso CK Poster: AACR Annual Meeting

17 CK-101: 3 RD GENERATION EGFR INHIBITOR PRE-CLINICAL EFFICACY In mice, CK-101 showed strong activity against T790M mutant NSCLC with increasing dose. Vehicle Control T790M NSCLC xenograft model CK mg/kg Afatinib 20 mg/kg CK mg/kg CK mg/kg Poster: AACR Annual Meeting

18 CK-101: 3 RD GENERATION EGFR INHIBITOR PRE-CLINICAL EFFICACY In mice, CK-101 showed no activity against wild-type EGFR with increasing dose. Vehicle Control, 0 mg/kg CK-101, 50 mg/kg CK-101, 100 mg/kg CK-101, 200 mg/kg WT EGFR xenograft model Afatinib, 6 mg/kg Poster: AACR Annual Meeting

19 CK-101: PHASE 1/2 CLINICAL STUDY NSCLC T790M MUTATION-POSITIVE PATIENTS Phase 1 dose escalation ongoing to identify Phase 2 dose Phase 2 will confirm safety and efficacy profile Enrollment expected to begin by year-end 2017 ~60 NSCLC T790M mutation-positive patients Mutation confirmed by Roche diagnostic to rule out non-responders Primary endpoint: Objective response rate (ORR) Plan to develop as a monotherapy and in combination with synergistic I/O agents 19

20 CK-101 EXPECTED PHASE 3 STUDY DESIGN SIMILAR DESIGN AS USED BY TAGRISSO Open-label, randomized study of CK-101 vs platinum-based doublet chemotherapy in 2 nd line EGFR T790M mutation-positive NSCLC, following progression on a 1 st generation EGFR inhibitor Patients pre-screened for T790M mutation Primary endpoint: Progression-free survival Tagrisso : 419 patients, 2:1 ratio; PFS 10.1 months vs 4.4 months (chemo); patients crossed over after progression. Est. enrollment of 200 pts CK-101 vs 100 pts chemo and allow crossover post-progression Target initiation of Phase 3 by YE 2018; ~18-24 months to enroll and reach PFS endpoint 20

21 ANNUAL INCIDENCE OF NSCLC WITH T790M MUTATION MAJOR MARKETS Type U.S. E.U. Japan NSCLC Annual Incidence 190, ,000 80,000 EGFR Mutations L858R, del(19) 19,000 26,000 24,000 T790M Resistant 11,000 15,000 14,000 Est. Annual Incidence: ~40,000 patients Sources: American Cancer Society; GLOBOCAN, Jeffrey A Engelman, et al., Clinical Cancer Research,

22 ADDITIONAL TARGETED ANTI-CANCER AGENTS CK-102 (PARPi) Oral, small molecule inhibitor of PARP, an enzyme essential for DNA repair PARP inhibitors have activity in multiple tumors (breast, ovarian, prostate), particularly those with existing DNA repair defects: BRCA1 and BRCA2 Re-formulating for Phase 1b clinical study CK-103 (BETi) Oral, small molecule inhibitor of the BET protein, BRD4 BRD4 is often required for expression of c-myc oncogene, a growth promoting transcription factor Inhibition of BET can lead to selective killing of tumor cells Targeting IND filing YE 2017 Anti-CAIX mab For CAIX+ RCC and other CAIX+ solid tumors CAIX overexpressed in over 85% of RCC Glycoengineering to enhance ADCC activity; potential synergy with anti-pd-l1 22

23 COLLABORATION WITH TG THERAPEUTICS Joint development of anti-pd-l1, anti-gitr, and BET inhibitor programs Checkpoint to develop in solid tumor indications and TG to develop in liquid tumors Checkpoint is eligible for royalties and milestones 23

24 KEY TAKEAWAYS Building a platform to combine targeted agents with I/O agents to maximize anti-cancer effect On-going: CK-101 (EGFR) Phase 1/2 study 3Q17: CK-301 (anti-pd-l1) Phase 1 initiation Four additional agents in portfolio Large potential market opportunities based on reasonably sized registration studies Funded with cash to support development programs through

25 CORPORATE PRESENTATION June 2017

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