Heat Biologics  Corporate PresentationFebruary 28, 2019 

 Forward Looking Statements  This presentation includes statements that are, or may be deemed, ‘‘forward-looking statements’’ within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. In some cases, these forward-looking statements can be identified by the use of forward-looking terminology, including the terms “believes,” “estimates,” “anticipates,” “expects,” “plans,” “intends,” “may,” “could,” “might,” “will,” “should,” “approximately” or, in each case, their negative or other variations thereon or comparable terminology, although not all forward-looking statements contain these words. They appear in a number of places throughout this presentation and include statements regarding our intentions, beliefs, projections, outlook, analyses or current expectations concerning, among other things, our ongoing and planned discovery and development of drugs targeting cancer, the strength and breadth of our intellectual property, our ongoing and planned preclinical studies and clinical trials, the timing of and our ability to complete clinical trials and make regulatory filings and obtain and maintain regulatory approvals for our product candidates, our ability to partner our product development, the degree of clinical utility of our products, particularly in specific patient populations, expectations regarding clinical trial data, our results of operations, financial condition, liquidity, prospects, growth and strategies, the length of time that we will be able to continue to fund our operating expenses and capital expenditures, our expected financing needs and sources of financing, the industry in which we operate and the trends that may affect the industry or us.  By their nature, forward-looking statements involve risks and uncertainties because they relate to events, competitive dynamics, and healthcare, regulatory and scientific developments and depend on the economic circumstances that may or may not occur in the future or may occur on longer or shorter timelines than anticipated. Although we believe that we have a reasonable basis for each forward-looking statement contained in this presentation, we caution you that forward-looking statements are not guarantees of future performance and that our actual results of operations, financial condition and liquidity, and the development of the industry in which we operate may differ materially from the forward-looking statements contained in this presentation as a result of, among other factors, the factors referenced in the “Risk Factors” section of our Annual Report on Form 10-K for the year ended December 31, 2017 and our quarterly report on Form 10-Q for the subsequent quarters (collectively, our “SEC Filings”). In addition, even if our results of operations, financial condition and liquidity, and the development of the industry in which we operate are consistent with the forward-looking statements contained in this presentation, they may not be predictive of results or developments in future periods. Any forward-looking statements that we make in this presentation speak only as of the date of such statement, and we undertake no obligation to update such statements to reflect events or circumstances after the date of this presentation, except as required by law.You should read carefully the factors described in the “Risk Factors” sections of our SEC Filings to better understand the risks and uncertainties inherent in our business.   2 

 Our Mission  To improve patient outcomes by developing more effective immunotherapies designed to   Turn “COLD” tumors “HOT   3 

             T-cell Activation  Co-stimulation  Heat’s Core Focus  Checkpoint Inhibition  Effective Immuno-Oncology TherapyThe three legs of an Immuno-Oncology Stool  4 

   Combination TherapiesUnlocking the Body’s Natural Defenses with a Broad Range of Combination Therapies  Checkpoint Inhibitors  PD1/PDL1CTLA-4Lag-3TIM-3Plus others  Combined with    Co-Stimulation      T-cell Activation  Pelican PTX-35Monoclonal AntibodyPelican PTX-45Fusion Protein  ImPACT® TherapyCell-based Delivery of Multiple Antigens Activation of Patients’CD8+ “Killer” T-cells  ComPACT™ TherapyCell-based Delivery ofMultiple Antigens Activation of Patients’CD8+ “Killer” T-cells  Co-Stimulation to Enhance T-cell Activation and Expansion    Heat Technologies  5 

 Product Pipeline   Combination Therapies Designed to Activate CD8+ T-cells Against Cancer  Combination Therapies  Indication    Comments  ImPACT® HS-110  NSCLC    ImPACT™ activation technology in combination with nivolumab and pembrolizumab  ComPACT® HS-130  Multiple Solid Tumors    ComPACT™ activation technology in combination with checkpoint inhibitors  Co-stimulators        PTX-35  Multiple Solid Tumors    Humanized monoclonal antibody, functional agonist of human TNFRSF25 ($15.2M CPRIT grant)  PTX-45  TBA    TL1A-Ig fusion protein, functional agonist of human TNFRSF25  Pre-clinical  Phase 1  Phase 2  Phase 3                                  6 

 ImPACT® “Off-the-shelf” ManufacturingDesigned for Robust, Pan-antigen T-cell Activation  Frozen, fully-diluted single-dose vialFinal drug product: 10 million cellsEasily scaled manufacturing  Low COG, off-the-shelf alternative to autologous therapies   7  Sample  Screen  Select  Scale  Collect Cancer Cell Line & Patient Tissue Samples  Compare Using Our Proprietary Technology  ID Cell Line with Most Antigen Overlap  Scale-up for Manufacturing by CMO  Transfect with Activation Technology 

   Introducing gp96 – Its dual roleThe Immune System’s “Swiss Army Knife”*  *Schild, H. & Rammensee, H. Gp-96 – The Immune System’s Swiss Army Knife. Nature Immunology 2, 100-101 (2000)  “Molecular Warning System”  A natural biological process to deliver proteins (antigens) & gp96 to our immune systemGp96 “chaperones” newly-created proteins to the cell membrane where they are released and embeddedGp96 chaperoned proteins are only naturally released via necrosisGp96, when present outside the cell, alerts the immune system and then becomes one of the most powerful adjuvants that show exclusive specificity to CD8+ (“killer”) T-cells  Tethered to our cells with a “KDEL” leash          gp96  antigen  Leash  Endoplasmic Reticulum  Cell Membrane    Antigen    Antigen  8 

 ImPACT® technology genetically modifies tumor cells by “severing the leash” that binds the gp96 to the endoplasmic reticulum, and replacing it with a secretory sequence that pumps gp96 out of the cellMimics necrotic cell death by enabling fully-allogeneic “off-the-shelf” living cancer cells to “pump-out” their own antigens along with their gp96 chaperone  Heat Biologics ImPACT® technology reprograms cancer cells to continuously secrete their own antigens  ImPACT technology removes the leash that binds gp96 to the cell  ImPACT Platform“Severing the Leash”        gp96  antigen  Leash  Endoplasmic Reticulum  Cell Membrane    Antigen                                Designed to activate a powerful pan-antigen cytotoxic T-cell immune response  9 

     ImPACT®: Immune Pan-antigen Cytotoxic Therapy                    ImPACT Cell      Cancer-killing T-cell    ImPACT cells secrete antigens designed to specifically activate patient’s killer T-cells  T-cells circulate to destroy patient’s tumor  Cluster of five 0.1 mL intradermal injections  Activated cells EXPRESS chaperoned antigens  Activation Cell   CD8+ T Cell  Dendritic Cell  Chaperoned antigens activate dendritic cells, which thenACTIVATE & PROLIFERATE CD8+ T-cells  Dendritic Cell  ChaperonedAntigen   CD8+ T-cells locate and ELIMINATE cancer cells  Tumor Cells  CD8+ T Cells  Heat’s unique cell-secreted gp96 firstly activates dendritic cells via TLR signaling and subsequently CD8+ T cells via antigen cross presentation  10 

 ImPact Generates an Adaptive Immune Response  Secretion of gp96-Ig carrying tumor specific proteins represented on the patients tumorActivation of APCs (TLR2/4) and cross- presentation of antigens (CD91)Specific T-cell receptor engagementClonal Expansion of Tumor Antigen Specific T cells.  2 signals Delivered to APCs: Antigen cross presentation to MHC class I via CD91Up regulation of co-stimulatory signals via TLR2/4        11 

 ImPACT + Opdivo Combination TherapyPotential to improve clinical responses and survival, without additional toxicity   Source: BMS images  12 

 HS-110 Trial DesignA Phase 1b/2 study of HS-110 in combination with multiple treatment regimens for patients with non-small cell lung cancer (The “DURGA” Trial)  Primary EndpointsPhase 1b: SafetyPhase 2: Cohort A&B: ORRCohort C&D: PFSSecondary EndpointsOS, PFS, DCR, DOR  Exploratory EndpointsCorrelation of clinical outcomes to the following factorsBaseline CD8+ TILs (Low defined as ≤ 10% stromal CD8+ TILs)PD-L1 expression (Negative defined as < 1% on tumor cells)Peripheral blood tumor mutation burden count (Low defined as < 10 mutation count)ELISPOT cytokine analysis   Patient Treatment Setting  Treatment Arm    Enroll  2nd Line or GreaterN=100  1st Line MaintenanceN=20  Cohort      HS110 + Nivolumab  Cohort A: CPI naïve (N=40, including Phase 1b)    Cohort B: CPI progressor (N=60)  HS110 + Pembrolizumab +/- Pemetrexed  Cohort C: Maintenance pembrolizumab    Cohort D: Maintenance pembrolizumab + pemetrexed  13 

                 Baseline(Cold)  Week 10(Hot)  CD8+ TIL Infiltration Associated with Clinical Response                  Patient 1:Partial Response at Week 18  High CD8+ TIL (>10%)                  Patient 2:Partial Response at Week 9  High CD8+ TIL (>10%)      Patient 3:Partial Response at Week 18  Low CD8+ TIL (<10%)  High CD8+ TIL (>10%)              Combination treatment drives “killer” CD8+ T-cells deep into tumors  Low CD8+ TIL (<10%)  Low CD8+ TIL (<10%)  Clinical Support for HS-110 + Nivolumab Mechanism of Action “Turning COLD Tumors HOT”    14 

   Combination Treatment Substantially Increased Killing Activity in Patient Tumor Microenvironment  RECIST 1.1 Stable Disease for 19+ months  Pathology analysis performed by Yale School of Medicine  CD3+ TILsCD3+ Ki67 TILsPD-1+ Cells  CD3+ Granzyme B + TILsPD-L1+ Tumor CellsCD4+ Foxp3+ Cells (Tregs)CD4+ T cells  Baseline Week 10  60000  40000  20000  AQUA Pixels #  InForm cell %  Substantial increase of CD3+ TILs and CD3+ Granzyme B+ TILs for enhanced tumor killing activity  15 

 Progression-Free Survival (PFS)    Cohort A:CPI Naïve pts treated by HS-110 + Nivolumab at >2L  * Borghaei et al. 2015 Nivolumab versus Docetaxel in Advanced Nonsquamous Non–Small-Cell Lung Cancer. New England Journal of Medicine  Median PFS2.6 months(95% CI: 1.8 - 8 months)  Months  0  6  12  18  24  30  25  50  75  100  Median PFS of nivolumab alone 2.3 months *(95% CI: 2.2 – 3.3 months)   Progression Free Survival (%)  # at risk 42 14 8 5 1 0   N=42 (All patients enrolled)  16   

 Overall Survival (%)    Overall Survival (OS)  Cohort A:CPI Naïve pts treated by HS-110 + Nivolumab at >2L  Median OS of nivolumab alone 12.2 months*(95% CI: 9.7 – 15.0 months)  *Borghaei et al. 2015 NEJM  Median OS Not Reached (95% CI: 8.1 months - NR)60% of patients still alive with median follow-up time of 14.4 months   Months  25  50  75  100  0  6  12  18  24  30  36  42  # at risk 42 29 21 13 5 3 1 0   N=42 (All patients enrolled)  17   

 Best Target Lesion Response  PR  9 (21%)  SD  12 (29%)  Not evaluable  4 (10%)  DCR  21 (50%)  RECIST 1.1 Objective Response Rate = 21.4% (95% CI: 10.3 - 36.8%)  Change from Baseline (%)    Best Target Lesion Response  Best Overall Response   Cohort A:CPI Naïve pts treated by HS-110 + Nivolumab at >2L  Nivolumab alone in CPI naïve patients* ORR = 19% (95% CI: 15% - 24%)DCR = 44%*Borghaei et al 2015 NEJM    Waterfall plot of best target lesion response using percent change from baseline of the SLD (sum of longest diameters) for all patients who received at least 1 post-baseline scan (n=38)  18 

   Duration of Benefit  Cohort A:CPI Naïve pts treated by HS-110 + Nivolumab at >2L  19  Responses and disease stabilization are durable and long-lasting  25  50  75  100  0  -30    -50  -75  -100  Change from Baseline (%)  0  3  6  9  12  15  18  21  24  27  Months from the First Dose of HS-110 

   Improved Survival in “Cold” Tumor PatientsOverall Survival (OS) by Baseline CD8+ TIL  Cohort A:CPI Naïve pts treated by HS-110 + Nivolumab at >2L  *TIL NE = Tumor infiltrating lymphocyte not evaluable    Low CD8+ TIL(< 10%)  High CD8+ TIL (> 10%)  Median OS  NR  NR  HR 0.39(95% CI: 0.06 – 2.31)      CD8+ TIL (<10%), N = 12CD8+ TIL (>10%), N = 8CD8+ TIL NE*, N = 22  Months  0  6  12  18  24  30  36  42  25  50  75  Overall Survival (%)  100  20   

   Benefit Independent of PD-L1 StatusOverall Survival (OS) by Baseline PD-L1 Status  Cohort A:CPI Naïve pts treated by HS-110 + Nivolumab at >2L    Negative PD-L1(< 1%)  Positive PD-L1(> 1%)  Median OS  NR  NR  HR 0.85(95% CI: 0.26 – 2.79)      PD-L1 (<1%), N = 16PD-L1 (>1%), N = 13PD-L1 NE, N = 13  0  6  12  18  24  30  36  42  25  50  100  75  Overall Survival (%)  Months  21   

 OS by Injection Site Reaction (ISR)  Cohort A:CPI Naïve pts treated by HS-110 + Nivolumab at >2L  Overall Survival (%)    Typical Injection Site Reaction    Injection Site Reaction  Yes (n = 24)No (n=18)    mOS: NR vs. 7.2 monthsHR: 0.15 (95% CI: 0.05-0.45)p = 0.0001  Survival is significantly better in patients who experienced dermal injection site reaction, thus supporting the HS-110 mechanism of action  Months  0  6  12  18  24  30  36  42  25  50  100  75  # at risk  2418  229  194  132  60  40  20  00  22   

 Median OS (months)  17.3  23.5  Survival Benefit with Increased Immune Activity  Cohort A:CPI Naïve pts treated by HS-110 + Nivolumab at >2L  OS (Months)  0  12  24  36  High  Low  HS-110 Generated ELISPOTs  High = Patients with absolute ELISPOT increases above the group medianLow = Patients with absolute ELISPOT increases below the group median  Peripheral blood obtained before and during treatment to measure HS-110 derived immune reactivity. ELISPOTs represent INF-Ɣ secretion from T cells in culture after stimulation with HS-110 lysate.   A 6-month improvement of median survival in patients with high HS-110 stimulated immune activity  23 

 Objective Response Rate  Cohort B:CPI progressors treated by HS-110 + Nivolumab at >2L  RECIST 1.1 ORR = 15% (95% CI, 3.2 - 37.9%)  PR*  4 (20%)  SD  7 (35%)  Not evaluable  2 (10%)  DCR  11 (55%)  Best Target Lesion Response with # of Prior Lines of Therapy  25  50  100  75  0  -25  -50  -75  Change from Baseline (%)  Stabilization of disease in > 50% of patientsResponse rates suggest that addition of HS-110 can restore responsiveness to CPI therapyThe 3 RECIST partial responses were in patients who failed CPI immediately preceding study entry  * Per Investigator assessment  -100  24 

 Duration of Clinical Benefit  Cohort B:CPI progressors treated by HS-110 + Nivolumab at >2L  Median Progression-Free Survival (PFS)2.7 months(95% CI: 1.8 - 4.0 months)  4 out of 20 patients have not progressed on therapy      25 

 Safety Profile to Date1,000+ Doses - No Serious Adverse Reactions  Over 1,000 doses administered to ~200 patients  Only one patient ended treatment due to a non-serious adverse reaction*  No systemic use of steroids required to treat reactionsNo treatment-related serious adverse reactions  Favorable Safety Profile To Date  *Represents the only patient of ~200 patients dosed who discontinued treatment for a vaccine-related adverse event      Immune Reaction*≤ Grade 3 toxicity      Injection ReactionsWeek 1 Week 2          No additive toxicities to standard of care  26 

 Summary of HS-110 Phase 2 Interim Data  HS-110 in combination with nivolumab is well tolerated Preliminary results demonstrate the ability of HS-110 plus nivolumab to induce CD8+ T-cell tumor infiltration in previously “cold” tumorsIn Cohort A, the occurrence of injection site reactions and increased INF-γ ELISPOTs appears to be associated with improved overall survivalData in Cohort B suggests that the addition of HS-110 to nivolumab may restore responsiveness after tumor progression on prior checkpoint inhibitors  27 

 Heat acquired 80% controlling interest in Pelican in May 2017Pre-clinical synergy with Heat’s ImPACT® and checkpoint therapy$15.2M grant award from the Cancer Prevention Research Institute of Texas (CPRIT) propels PTX-35 through a 70-patient, first-in-human clinical programPTX-35 is a potential best-in-class, T-cell co-stimulator specific to “killer” CD8+ “memory” T-cells    TNFRSF25 represents an emerging target in immuno-oncology  Heat Biologics Acquires Pelican TherapeuticsUnlocking the Body’s Natural Defenses with a Broad Range of Combination Therapies  28 

 TNFRSF25 is preferentially expressed on CD8+ T-cells compared to other T-cell co-stimulatorsCo-stimulation occurs only in the context of TCR recognition of antigenDrives the development of antigen-specific CD8+ T-cells (mimics TL1A, the specific ligand of TNFRSF25)Compared to agonists OX40, GITR, 4-1BB:TNFRSF25 shows superior activity in stimulating memory CD8+ cells in miceTNFRSF25 agonism plus ImPACT results in improved survival in mouse melanoma models  Pre-clinical data of PTX-35 highlights CD8+ T-cell specificity           In mice, TNFRSF25 agonists increases  29 

 Corporate Milestones  ImPACT NSCLC Phase 2 interim data readout  File IND for HS-130 ComPACT trial  File IND for PTX-35 Phase 1 trial  ImPACT NSCLC Complete Phase 2 enrollment  ImPACT NSCLC Milestones  Pelican and ComPACT Milestones  Interim PTX-35 data readout  Interim ComPACT data readout      ImPACT NSCLC Phase 2 interim data readout  30 

 Corporate Highlights  NasdaqHTBX  Shares Outstanding32.5M  Cash & Equiv.$27.7M  Capitalization Table(as of 12/31/2018)  Shares  Common shares outstanding  32.5 M  Warrants  9.0 M  Outstanding stock options  3.1 M  Unvested restricted stock  1.6 M  Fully Diluted Shares Outstanding  46.2 M  Founded in2008  Grant Awarded$15.2 M  Employees30  31 

 Investment Highlights  Potential Best in Class Oncology Treatment - T-cell activating platform (TCAP)  produces allogeneic, off-the-shelf therapies designed to activate the immune system to turn immunologically “cold” tumors “hot”Combination Effect - Our therapies are designed to be administered with checkpoint inhibitors and other immuno-modulators to enhance immune responseOff-the-shelf Therapies - We can administer drug immediately without extracting patient material, simplifying treatment and substantially lowering cost of goodsClinical Data with Checkpoint Inhibitors (CPI) - Positive interim data from ongoing Phase 2 trial of HS-110 + CPI in non-small cell lung cancer (NSCLC) patients (both CPI naïve and CPI progressors)Diverse Technology Platforms - Multiple complementary platform technologiesStrong Management Team - Senior team with broad experience in biotech, pharma, clinical development and research   32 

   Appendix  33 

 Cohort A & B: Patient Characteristics      Cohort A (N = 42)  Cohort B (N = 20)  EGFR or ALK positive    9 (22%)  2 (10%)  Prior lines   12 or more Unavailable  27 (64%)13 (30%)2 (5%)  3 (15%)16 (80%)1 (5%)  PD-L1  < 1%≥ 1%Unevaluable  16 (38%)13 (31%)13 (31%)  7 (35%)8 (40%)5 (25%)  CD8+ TIL  ≤ 10%> 10%Unevaluable  12 (29%)8 (19%)22 (52%)  7 (35%)6 (30%)7 (35%)      Cohort A (N = 42)  Cohort B (N = 20)  Median age (range)    64 (37-87)  65 (56-84)  Female gender     22 (52%)  14 (70%)  Caucasian    38 (90%)  15 (75%)  ECOG PS 1     26 (62%)  10 (50%)  Histology  AdenoSquamous  39 (93%)3 (7%)  17 (85%)3 (15%)  Smoking Status   Current/pastNever  37 (88%)5 (12%)  17 (85%)3 (15%)  Stage III or IV advanced NSCLC  34 

         Preclinical Data of CD8+ T cell ActivationImPACT® alone and in combination with co-stimulator agonists: OX40, TNFRSF25, PD-1  Source: Fromm et al. Society for Immunotherapy of Cancer Annual Meeting, 2016  Higher T-cell responses observed in mice treated with ImPACT aloneImPACT® boosted CD8+ T-cells to even higher levels when combined with co-stimulator agonist antibodies: OX40, TNFRSF25, PD-1Findings suggest synergies when combining ImPACT with Pelican’s TNFRSF25 antibody  ImPACT  ImPACT  CD8+ T-cell Activation  ImPACT  ImPACT  ImPACT  ImPACT  ImPACT  ImPACT  ImPACT          35 

 ComPACT™ Platform Technology  gp96-Ig  OX40L-Fc  The first potential dual-acting immunotherapy designed to deliver T-cell activation andco-stimulation in a single product – combination therapy without additive costs  36 

       ComPACT™ Outperforms OX40 Monoclonal Antibodies in Pre-clinical Models   ComPACT generates ~50% complete tumor rejection compared to ~16% with OX40 agonist antibody combinations  Superior primary and memory T-cell response in mouse model    Translates into increased overall survival and tumor reduction in a mouse tumor model  37 

 TNFRSF25 - An Emerging Target for T-cell Co-stimulation  38  Target  Companies  Co-stimulator Combinations  4-1BB  Pfizer, ISA Pharma, Gilead, Bristol Myers, Inhibrx, Immatics, Pieris, NCI  Phase 1/2Combinations: Chemotherapy, epigenetic modulator, CD20 mAb, HPV vaccine, CART, PD-L1, BTK, Herceptin, modified CD8+ T cells, IL-2, CSF1R, LAG-3, bispecific w/ HER-2, two co-stimulators (w/ OX40)  OX40  MedImmune, GSK, Incyte, Genentech, Pfizer, AbbVie, Bristol Myers, Alligator Bio   Phase 1/2OX-40 prior to surgery. Other combinations: PD-1, PD-L1, CTLA4, axitinib, 41BB, smoothened inhibitor Anti-CD33, azacitidine, TLRs, bi-specifics of OX40 and CTLA-4  GITR  Novartis, Incyte-Agenus, MedImmune, Leap Therapeutics, BMS, OncoMed  Phase 1Combinations: PD-1, Fc disabled co-stimulation, hexameric GITR ligand, IDO inhibitor, CTLA-4, GITR ligand-fusion  CD27  Celldex-BMS, Merck-Aduro  Phase 1/2Combinations: PD-1/L-1, sunitinib, CD20, melanoma vaccine, TL3 agonist  ICOS  Celgene-Jounce, GSK  Phase 1/2Combinations: PD-1, CTLA4, docetaxel  TNFRSF25  Heat (under Pelican)  Filing IND in Q2 2019 in advanced solid tumors. Combination studies being planned  TNFRSF25 is a potential best-in-class T cell co-stimulator due to its preferential specificity to ‘memory’ CD8+ T cells Pelican is the only company with a disclosed program targeting TNFRSF25  

 TNFRSF25 agonist + ImPACT Significantly Increases Survival in Mice   OX40  GITR  4-1BB  TNFRSF25  Schreiber T. et al. SITC 2014  Control4-1BBImPACTImPACT + 4-1BB  ControlOX40ImPACTImPACT + OX40  ControlGITRImPACTImPACT + GITR  ControlTNFRSF25ImPACTImPACT + TNFRSF25  39  Nine-day B16-F10 melanoma model 

 Preferential CD8+ T-cell Induction with TNFRSF25 in MicePre-clinical studies with murine agonist antibody shows TNFRSF25 preferentially ‘boosts’ CD8+ T-cells, whereas OX40 is preferential to CD4+ T-cells  The frequency of antigen-specific memory CD4+ or memory CD8+ T-cells following treatment of mice with ImPACT™ alone, or in combination with OX40 or TNFRSF25 antibodies  Schreiber et al. J Immunol 2012:189(7);3311-8  % AntigenSpecific Memory CD8+ T-cells  TNFRS25  OX40  ImPACT + + + +  40 

 TNFRSF25 is preferentially expressed on CD8+ T-cellscompared to other T-cell co-stimulators  Genomics Institute of the Novartis Research Foundation Su et al. PNAS 2004:101(16);6062-7  (red = high expression)  41 

 Management and Advisors  Jeff WolfFounder & CEO  Ann RosarVP of Finance  Janice McCourtVP of Business Devt.  Lori McDermottVP of Clinical Dev.  Gary VinsonVP of Manufacturing  Jeff Hutchins, Ph.D.CSO/COO  George Peoples, MDChief Medical Advisor  Management   Scientific Advisors      Robert Levy, Ph.D.University of Miami    Roger Cohen, MDUniversity of Pennsylvania  Robert Negrin, MDStanford University    Llew Keltner, MD, Ph.D.Epistat  Anthony Tolcher, MDNext Oncology    Gary Acton, MDAdvisor  Board of Directors  Jeff WolfFounder, Chairman and CEO  John Prendergast, Ph.D.Lead Independent Director  John Monahan, Ph.D.Director  Edward SmithDirector  42