to learn more about our company, please take a look at our

2

Safe Harbor & Data PresentedSafe Harbor & Data Presented

Statements about the Company's future expectations, including statements about the potential use and scientific results for the Company's drug candidates, science and technology, and all other statements in this presentation other than historical facts, are "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, Section 21E of the Securities Exchange Act of 1934, and as that term is defined in the Private Securities Litigation Reform Act of 1995. The Company intends that such forward-looking statements be subject to the safe harbors created thereby. These future events may not occur as and when expected, if at all, and, together with the Company's business, are subject to various risks and uncertainties. The Company's actual results could differ materially from expected results as a result of a number of factors, including the uncertainties inherent in research and development collaborations, pre-clinical and clinical trials and product development programs (including, but not limited to the fact that future results or research and development efforts may prove less encouraging than current results or cause side effects not observed in current pre-clinical trials), the evaluation of potential opportunities, the level of corporate expenditures and monies available for further studies, capital market conditions, and others set forth in the Company's periodic report on Form 10-Q for the three months ended September 30, 2009 as filed with the Securities and Exchange Commission and report on Form 10-K for the year ended December 31, 2008 as filed with the Securities and Exchange Commission. There are no guarantees that any of the Company's proposed products will prove to be commercially successful. The Company undertakes no duty to update forward-looking statements.

Data presented in this presentation may not be comprehensive; please contact ImmuneRegen for additional information.

3

MissionMission

We are a biotechnology company, focused on advancing products We are a biotechnology company, focused on advancing products that regenerate or strengthen the human immune system, in part, that regenerate or strengthen the human immune system, in part, through stimulation of adult stem cells.through stimulation of adult stem cells.

We are working to capitalize on our drug candidates by continuing We are working to capitalize on our drug candidates by continuing our own development programs and simultaneously seeking to our own development programs and simultaneously seeking to license product use for specific indications to Industry partners.license product use for specific indications to Industry partners.

“To be recognized for developing safe and effective therapeutics and for driving value through drug development programs that attract licensing and collaborative partnerships.”

4

PipelinePipeline

5

Idiopathic Pulmonary Fibrosis

Influenza Therapeutic

Cancer Therapeutic

Vaccine Adjuvant

Biological and Chemical Agents

Radiation Damage (Neutropenia)

Wound Healing

Oral Administration

• Solid dosage form provides compounding flexibility

• No additional devices needed for administration

• Ships formulated for maximum stability, no liquid additions

• Solid may preclude need for cold chain

• May enable remote stockpiling• May provide environment-

insensitive stability

Oral Bioavailability Study shows oral or intra-duodenal Homspera administration results in measurable and pharmacologically relevant plasma and pulmonary drug concentrations.

Indications – Oral administrationIndications – Oral administration

Potential Benefits of Oral Administration

6

Homspera

NK-1R (neurokinin-1 receptor)

Substance P

NK-1R NK-3RNK-2R

(Arg Pro Lys Pro Gln Gln Phe Phe (Arg Pro Lys Pro Gln Gln Phe Phe SarSar Leu Leu Met(OMet(O22)) -NH-NH22))

(Arg Pro Lys Pro Gln Gln Phe Phe Gly Leu Met -NH2)

HomsperaHomspera®® vs. Substance P vs. Substance P

Homspera – NK-1 Receptor SpecificHomspera – NK-1 Receptor Specific

7

Alberts, B. et al. (2002) Molecular Biology of the Cell (4th ed.); Koon, H. et al. (2007) PNAS. 104:2013-2018; Koon, H. et al. (2006) J Immunology. 176:5050-5059;Yang, C et al. (2002) Cellular Signaling. 14:913-923; Koon, H. et al. (2005) J Pharmacology & Experimental Therapeutics. 314:1393-1400.

Mechanism of ActionMechanism of Action

Homspera®Homspera®

8

Homspera - Resistant to enzymatic degradationHomspera - Resistant to enzymatic degradation

HomsperaHomspera®® vs. Substance P vs. Substance P

Arg – Pro – Lys – Pro – Gln – Gln – Phe – Phe – Gly – Leu – Met – NH2

1 2 3 4 5 6 7 8 9 1011

Dipeptidyl peptidase IV

Angiotensin converting enzymeNeprilysin

Substance P endopeptidase

Endothelin-converting enzyme - 1

Prolyl endopeptidase

(E.C. 3.5.4.4)

(E.C. 3.4.21.26)

(E.C. 3.4.24.11) (E.C. 3.4.15.1)

(E.C. 3.4.24.71)

Homspera modifications

Homspera modifications

9

Roosterman D et al. PNAS 2007;104:11838-11843

ECE-1 regulates NK1 recyclingECE-1 regulates NK1 recycling

Homspera – Resistant to ECE-1 degradationHomspera – Resistant to ECE-1 degradation

10

NK1-R links to MAPK and ERK1/2NK1-R links to MAPK and ERK1/2

(1) SP binding to the NK1R leads to recruitment of β-arrestin to the receptor, assembly of a MAPK signalosome, and ERK1/2 activation.

(2) Degradation of SP by ECE-1 in acidified endosomes disrupts the SP/NK1R/arr/MAPK signalosome.

(3) NK1R recycles to the plasma membrane for resensitization.

(4) Inhibiting ECE-1 activity causes sustained ERK1/2 activation and SP-induced cell death.

From Murphy JE, Padilla BE, Hasdemira B, Cottrell GS and Bunnett NW (2009) PNAS 106(42) 17615-17622

Endosomal ECE-1 regulates SP-induced ERK activation and cell deathEndosomal ECE-1 regulates SP-induced ERK activation and cell death

NK1-R internalization coupled to beta-arrestin scaffolding triggers kinase cascade. Substance P degradation recycles receptor/terminates signal. Homspera resistance to ECE-1 alters intracellular signal for discordant membrane / intra-cellular signals (published by others)

11

Mechanism of ActionMechanism of Action

Summary of Underlying NK1-R Mechanisms

• Increased hematopoietic progenitor cells from both the myeloid and lymphoid lineages

• Direct stimulation of immune cells including macrophages and neutrophils AND antigen presenting cells

• Augmentation of the innate immune response dependent upon the status of the local microenvironment

• Direct stimulation of dermal fibroblasts, keratinocytes and epidermal cells

• Distinct antagonist and intracellular activity profiles compared to SP

12Image adapted from http://www.isscr.org/public/images/blood_fig_sm.jpg

Cell Differentiation

Primitive Stem Cell

Specialized Cells

Hematopoietic Stem Cell

CFU-GEMM

Common Lymphoid Progenitor

Common Myeloid

Progenitor

GranulocytesMegakaryocyte

Erythrocyte

CFU-GM

Platelets

NK cellT cellB cell

Macrophage

Monocyte

Adult Hematopoietic Stem Cells (HSCs)Adult Hematopoietic Stem Cells (HSCs)

13Data collected by ImmuneRegen under contract with HemoGenix

HSCs - HSCs - Homspera stimulates progenitorsHomspera stimulates progenitors

Methodology: Colony forming assays were performed under both optimal and sub-optimal cytokine/growth factor conditions. The sub-optimal conditions were 1/50th the concentration of those considered optimal and were concentrations known to support stem cell growth and differentiation. Culturing the cells under sub-optimal growth conditions is an important control often used to examine a compound’s stimulatory effect on HSCs. If the cells in culture are already maximally stimulated (as they could be under optimal conditions), there is a reduced chance of detecting a compound’s stimulatory activity. Likewise, if an experimental compound merely substitutes for a deficient growth factor, it would only be effective under sub-optimal conditions. Therefore, it is useful to compare results under both conditions.

14Data collected by ImmuneRegen under contract with University of Medicine and Dentistry of New Jersey

Colony forming assays were performed under optimal cytokine/growth factor conditions.

HSCs - HSCs - Homspera stimulates progenitorsHomspera stimulates progenitors

15

• Increases stem cell differentiation into cells that are required to regenerate or strengthen the human immune system

• Enhances production of the following precursors:

1. White blood cells

a. Granulocytes

b. Macrophages

c. T cells

d. B cells

2. Platelets

3. Red blood cells

Data collected by ImmuneRegen under contract with the University of Medicine and Dentistry, New Jersey (UMDNJ) and HemoGenix

Adult Hematopoietic Stem CellsAdult Hematopoietic Stem Cells

Homspera – Summary of effects

16

Radiation & NeutropeniaRadiation & Neutropenia

Homspera Findings• Increased survival of small animals

exposed to lethal radiation levels

• Treatment is more effective after exposure to radiation

• WBC numbers increase in treated animals

• Data suggest Homspera could resolve the neutropenia often associated with chemotherapy drugs

Radiation studies performed by TD2 (dose-rate study and pre vs. post-exposure efficacy) and University of Arizona (survival)

17Performed at the University of Arizona

Irradiated + Homspera

Irradiated Control

Radiation - Radiation - Homspera findingsHomspera findings

Homspera promotes survival of lethally-irradiated animals

Methodology: Sixteen male C57BL/6 mice (N=8 Homspera-treated and N=8 radiation-only controls) were given a single 7.75 Gy whole body dose of gamma radiation. The control group was administered saline daily via nebulizer for 15 min/day with treatment beginning within 2 hours of radiation exposure. The treatment group was administered Homspera, 50 µM solution, 15 min/day under the same conditions.

18Performed by TD2

Radiation - Radiation - Homspera findingsHomspera findings

Homspera increases WBC counts following radiation

Methodology: 72 Balb/c mice of age 5-6 weeks and normal physiological state (Taconic) were separated into 4 groups: Non-irradiated control (n=12), Irradiated control (n=20), Irradiated / Treated pre-exposure (n=20), and Irradiated / Treated post-exposure (n=20). On Day 1, animals were placed into the X-ray irradiator (RadSource 2000) for 4 minutes. Non-irradiated controls received no radiation exposure while the irradiated controls were exposed to radiation at the level of 1 Gy/minute. Animals were either treated with vehicle control or Homspera in vehicle control solution. The Non-irradiated control group and Irradiated control group were administered 25 μL of sterile saline intranasally daily for 7 days following radiation exposure. Animals treated with Homspera pre-radiation exposure were administered 25 μL of 300 μM solution intranasally 1-day prior to radiation exposure and daily thereafter for 7 days. Animals treated with Homspera post-radiation exposure were administered 25 μL of 300 μM solution intranasally daily for 7 days following radiation exposure.

19

Immune Activity - MechanismsImmune Activity - Mechanisms

20

Immune ActivityImmune Activity

Increases DC trafficking to skin-draining lymph nodes• Dramatic mobilization of Langerhans’ cells observed 24-hours post-treatment• Administration in conjunction with antigen results in the increased expression of

CCL21/SLC, a DC chemoattractant, in lymphatic vessels

Rescues DC from undergoing apoptosis• DC apoptosis is an immuno-compromising effect often observed during viral

infection such as infection with H5N1 influenza 1

• Homspera-stimulated BMDCs found to have increased survival (95% compared to 63% in untreated animals) in vivo

1) Baskin, CR et al., PNAS, 2009; 106: 3455-3460.

Activates dendritic cells (DCs)• CD11+ and CD11- Antigen Presenting Cells express NK1

receptors• Bone marrow-derived stem cells express NK1 receptors• NK1 receptor expression is upregulated by TLR agonists

21

Ag +Homspera

AgControl

Figure 1

Enhances humoral antibody responses• Increased antigen-specific antibody titers approximately

10-fold when administered prior to gene gun-delivered DNA antigen (Figure 1)

• In another study intranasally-administered Homspera and antigen revealed a nearly 10-fold increase of serum antigen-specific antibodies compared to antigen-only controls

• When administered intranasally while Ag was administered via IP, a 3-fold increase in serum antigen-specific antibody titers AND a 2.5-fold increase in heterotypic antibodies (H5N1-derived protein compared to H1N1-derived protein) was observed when compared to non-Homspera treated controls


22

10075H5N1 Ag + H1N1 Ag

00PBS

100100H5N1 Ag + H1N1 Ag + Homspera

100100H1N1 Ag + Homspera

33.3100H1N1 Ag

00PBS + Homspera

100100H5N1 Ag + Homspera

100100H5N1 Ag

H5N1 A/Indo/5/05H5N1 A/VN/1203/04Vaccine Group

Survival determined 14 days after intranasal challenge with 1 x 106 EID50 of H5N1 virus.

Increased antibodies correlate with increased survival


Survival correlates to 3-fold increases in both homotypic and heterotypic antibody levels observed in mice treated with Homspera intranasally and antigen intraperitoneally.

23

Elevates CD4+ memory T-helper cell function• Enhanced delayed-type hypersensitivity (DTH) composed

of statistically elevated numbers of CD4+, CD8+ lymphocytes and macrophages to the vaccination site following epidermal application of vaccine antigen along with Homspera (Figure 2).

• By augmenting both innate and humoral immunity, Homspera may also increase the antibody-dependent cell-mediated cytotoxicity effect, which limits and contains infection and controls tumor growth.

Control Ag Ag + Homspera

Ag + NK1 antagonist

Figure 2

* indicates a p < 0.05 compared with the non-sensitized animals (naive). ** indicates p < 0.05 compared with immunizations alone at each time point.


24

Enhanced antigen-specific cytotoxic CD8+ T-cell (CTL) response

• Increase the antigen-specific cytotoxic function on T-cells by in vivo killing assays (Figure 3).

• Induction of a robust CTL response was also observed using a more aggressive immunization course, which involved one priming dose, and two booster doses. When this immunization scheme was employed Homspera was observed to increase specific cell killing to 92%.

Figure 3

Ag Ag + Homspera

P < 0.05


25

Augments innate immunity and cytokine expression

• NK1R activation by Homspera signals through the NF-κB pathway.

• Th1-biased immune response.

Ag + Homspera

AgControl Ag + Homspera

AgControl

Figure 4

• IFN-γ (Figure 4), TNF-α, IL-1, IL-2, and GM-CSF production predominately influenced. NF-κB also regulates the genes encoding the chemokines Interleukin-8 (IL-8) and macrophage inflammatory protein-1α (MIP-1α).

Splenic CD4+ T-cells Splenic CD8+ T-Cells


26

InfluenzaInfluenza

infects the respiratory tract

LungsLungs• Reduction of virus particles in the lung and nose• Reduction of illness-related symptoms• Reduction of pathology• Increased survival of infected animals

Homspera findings:

Head-to-head greater efficacy than Tamiflu®

• Homspera reduces lung inflammation observed in mock-treated and Tamiflu-treated animals

• Unlike Tamiflu®, Homspera reduces weight loss associated with influenza infection

• Homspera co-therapy reduced Tamiflu dose-related deaths

27

Approximately 90% reduction of viral titers

Influenza studies using a cotton rat model of seasonal influenza (Influenza A/Wuhan/359/95) were performed by Virion Systems, Inc.

Influenza – Influenza – Homspera findingsHomspera findings

Methodology: Young adult (6-8 weeks old) cotton rats (Sigmodon Hispidus) of both genders were obtained from an inbred colony maintained at Virion Systems, Inc. (Rockville, MD). A stock of Influenza/A/Wuhan/359/95 was prepared by Novavax, Inc. Animals were either treated intranasally with Homspera or vehicle 1 day before influenza infection OR given Homspera beginning 1 hour following influenza infection. Homspera treatment was continued daily for 10 days following infection. Homspera doses were equivalent 0.023mg/kg (10uM x 0.1mL), 0.23mg/kg (100uM x 0.1mL), Homspera 1.16mg/kg (500uM x 0.1mL).

28

Reduction of viral particles and abnormal cilia

Influenza studies using a mouse model performed at University of Arizona


Infected control lungs show Influenza virions inside infected cells (left picture, arrow) and the lack of airway cilia in infected lung (right picture. single arrow) and stressed airway epithelial cell with numerous mitochondria (right picture, double arrows).

Homspera treated lungs show normal ciliated epithelial cell (single arrow) and normal mitochondrial complement (double arrows).

29

Reduction of pulmonary inflammation



Methodology: Young adult (6-8 weeks old) cotton rats (Sigmodon Hispidus) of both genders were obtained from an inbred colony maintained at Virion Systems, Inc. A stock of Influenza/A/Wuhan/359/95 was prepared by Novavax, Inc. Animals were grouped into mock-treated / infected, oseltamivir (Tamiflu®) 10 mg/kg / infected, Homspera 0.23 mg/kg / infected, oseltamivir (Tamiflu®) 10 mg/kg + Homspera 0.23mg/kg / infected. Homspera was administered intranasally and oseltamivir solution was administered orally. Treatments commenced 1-day prior to infection. Lung were dissected and inflated, then assessed histologically. Parameters quantified on 0-4 severity scale: interstitial pneumonia (inflammatory cell infiltration and thickening of alveolar walls), and alveolitis (cells within the alveolar spaces), peribronchiolitis (inflammatory cells clustered around the periphery of small airways), perivasculitis (inflammatory cells clustered around the vesicles).

30

More significant reduction of weight loss than Tamiflu®



Methodology: Young adult (6-8 weeks old) cotton rats (Sigmodon Hispidus) of both genders were obtained from an inbred colony maintained at Virion Systems, Inc. A stock of Influenza/A/Wuhan/359/95 was prepared by Novavax, Inc. Animals were grouped into mock-treated / infected, oseltamivir (Tamiflu®) 10 mg/kg / infected, Homspera 0.23 mg/kg / infected. Homspera was administered intranasally and oseltamivir solution was administered orally. Treatments commenced 1-day prior to infection. Weights were measured daily.

31

More significant reduction of weight loss than Tamiflu®



Methodology: Young adult (6-8 weeks old) cotton rats (Sigmodon Hispidus) of both genders were obtained from an inbred colony maintained at Virion Systems, Inc. A stock of Influenza/A/Wuhan/359/95 was prepared by Novavax, Inc. Tamiflu® (oseltamivir, Roche Inc.) was obtained commercially. Animals were grouped into mock-treated / infected, oseltamivir (Tamiflu®) 2mg/kg / infected, Homspera 0.23mg/kg / infected, oseltamivir (Tamiflu®) 2mg/kg + Homspera 0.23mg/kg / infected. Homspera was administered intranasally and oseltamivir solution was administered orally. All treatments began approximately 1-hour following infection with Influenza/A/Wuhan/359/95. Homspera was administered once daily, whereas oseltamivir was administered twice daily, once in the morning and once in the evening. Treatment was continued daily for three days. Weights were measured daily.

32

Reduction of Tamiflu®-associated mortality



Methodology: Young adult (6-8 weeks old) cotton rats (Sigmodon Hispidus) of both genders were obtained from an inbred colony maintained at Virion Systems, Inc. A stock of Influenza/A/Wuhan/359/95 was prepared by Novavax, Inc. from supernatants of MDCK cells that had been inoculated 3 days previously at a low multiplicity of infection (m.o.i). Tamiflu® (oseltamivir, Roche Inc.) was obtained commercially. Animals were grouped into mock-treated / infected, oseltamivir (Tamiflu®) 2mg/kg / infected, oseltamivir (Tamiflu®) 2mg/kg + Homspera 0.23mg/kg / infected, Homspera 0.23mg/kg / infected. Homspera was administered intranasally and oseltamivir solution was administered orally. All treatments began approximately 1-hour following infection with Influenza/A/Wuhan/359/95. Homspera was administered once daily, whereas oseltamivir was administered twice daily, once in the morning and once in the evening. Treatment was continued daily for three days.

p = 0.012 (Fisher’s Exact Test)

33

Influenza – Influenza – H5N1 findingsH5N1 findings

Increased survival – 60% greater than controlsWS/05

0 1 2 3 4 5 6 7 80

20

40

60

80

100

10e3 + 2mg Homespera10e5 + 2mg Homespera

10e3 Naïve Infection10e5 Naïve InfectionHomespera

Days Post Infection

Per

cen

t su

rviv

al

HomsperaHomspera Homspera

Influenza studies in Ferrets infected with H5N1 (A/Whooperswan/Mongolia/244/2005) were performed under contract with the University of Pittsburgh.

Methodology: 20 young adult (20 weeks old) Fitch ferrets of both genders were inoculated with Influenza A/Whooperswan/Mongolia/244/2005 (H5N1) with 0, 103 or 105 plaque-forming units (PFU) on Day 0. Uninfected controls were treated with 2 mg/kg Homspera via intranasal administration beginning on Day 1 and continued daily thru Day 5. Animals infected with 103 PFU were split into 2 groups – 1 group received vehicle control treatment daily for 5 days, the other received 2 mg/kg Homspera treatment intranasally commencing 1 day after infection and continuing thru Day 5. Similarly, animals infected with 105 PFU were split into 2 groups – 1 group received vehicle control treatment daily for 5 days, the other received 2 mg/kg Homspera treatment intranasally commencing 1 day after infection and continuing thru Day 5.

34

• Reduction in tumor metastases using well-established B16-lung metastasis model

• 63% reduction in metastases and 24% increase in survival in animals treated with Homspera for 7 days immediately following cancer cell injection.

• 97% reduction in metastases in animals treated with Homspera for 7 days beginning 7 days after cancer cell injection.

• Human melanoma cells are not stimulated

• A375 and A2058 cell lines were not stimulated following Homspera exposure.

• Chemotherapeutic sensitivity is not affected

• OVCAR-3 (human ovarian adenocarcinoma), SK-OV-3 (human ovarian adenocarcinoma), and MDA-MD-231 (human breast adenocarcinoma) sensitivity to chemotherapeutics was not affected by Homspera exposure.

Oncology - Oncology - Homspera findingsHomspera findings

35

Oncology - Oncology - Homspera findingsHomspera findings

Figure 1: Homspera increases cellular immune responses, and reduces and delays the growth of melanoma in mice genetically immunized with GG encoding the melanoma self antigen, TRP2. Control groups include non-immunized mice and mice immunized with irrelevant transgenic Ag (luc-luciferase) and injected with B16/F0 malignant melanoma cells. Animals receiving Homspera and TRP2 antigen received either 1 or 2 doses.

Picture of mice treated and sacrificed 22d after injection of B16 melanoma cells. Mice were genetically immunized with GG encoding the melanoma self-Ag TRP2 in the presence or absence of Homspera or the NK1R antagonist L733060 and injected with B16/F0 malignant melanoma cells.

Data represents means 1SE of tumor area (mm2) of 6 mice per experimental group. Both GG TRP2 plus Homspera treatments (1 or 2 doses) significantly inhibit tumor growth compared to GG encoding irrelevant Ag or TRP2 antigen in mice injected with B16/F0 cells (**p<0.0001). There was a significant inhibition on the tumor growth in mice treated with GG pCMV-TRP2 plus Homspera 2-times compared to 1-times (*p<0.01).

No Vaccine GG - Luc GG – TRP2

GG – TRP2 +Homspera

2 doses

GG – TRP2 +Homspera

1 dose

GG – TRP2 +NK1

antagonist

GG-Luc

GG-TRP2

GG-TRP2 + Homspera (2 doses)

Survival curve of mice genetically immunized as described. An indefinite survival of 45% and of 50% of mice injected either with one dose or with two doses of Homspera respectively. Data represents number of mice that survived out of 6 mice treated per experimental group. GG-TRP2 plus one or two doses of Homspera prolonged significantly the survival of mice compared to GG-TRP2 alone or with GG encoding irrelevant Ag and non-immunized mice injected with B16/F0 cells.

NaïveHomsperaGG-LucGG-TRP2GG-TRP2 + Homspera (1 dose)GG-TRP2 + Homspera (2 doses)

Naive

WO 2009/129498 A2 (patent application)

36

Homspera:Homspera:• Accelerates wound healingAccelerates wound healing in vivoin vivo

• Increases proliferation of fibroblasts Increases proliferation of fibroblasts in vitro in vitro

• Stimulates hematopoietic stem cell activityStimulates hematopoietic stem cell activity

• Activates Dendritic cells and improves T-cell Activates Dendritic cells and improves T-cell responsesresponses

Data collected by ImmuneRegen under contract with the following laboratories: MIR, HemoGenix, Bio-Quant

Wound Healing – Wound Healing – Homspera FindingsHomspera Findings

37

Homspera increases the proliferation of human dermal fibroblasts in vitro

Performed at Johns Hopkins University

Methodology: Fibroblasts were seeded in a 96 well plate using IMDM (media) containing 0.5% FBS. Next day, these serum starved cells were treated with various amounts of Homspera or Homspera + antagonist-(Spantide I) for a period of 1 or 3 days. Cells were pretreated with Homspera in serum free media (0.5%FBS) for 3 hrs. Cells were then re-stimulated with serum (5%FBS) or not (0.5%FBS) while maintaining the presence of Homspera. MTT assays were performed after 1 and 3 days of treatment with test article. These results are indicative of two independent experiments. Results are represented as % growth where mean OD of each sample is normalized to its control.


38Performed at Bio-Quant

Homspera reduces healing wound area – pig modelMethodology: Two normal, female Yorkshire pigs three months in age, weighing 15-20 kg, were anesthetized and wounded. A total of 20 full-thickness wounds each with a 3 cm diameter were created on each pig using a scalper, 2 cm apart and 10 per side of the animal. 8 tattoo labels were made around surrounding the wound for measuring purposes. Pigs were observed daily for morbidity and toxic signs for 21 days after wound induction. Homspera (at 10-4M, 10-

6M, 10-8M and 10-10M) and control (DPBS) articles were applied topically intra-wound. On each pig, 2 ml of Homspera at the test concentration or control solution was applied to fill the wound and covered it with saline-moistened (not wet) non-adherent Telfa gauze. Sterile techniques were performed as much as possible during the surgery to minimize the risk of infection on wound area. Dressings were changed every 5 days and Homspera was re-applied at each dressing change. Wound healing was evaluated by measuring the diameters of wound closure in 4 different directions on designated time point at Days 7, 10, 14, 17, 21, and 24 post-wounding.


39

Wound HealingWound Healing

40

Phases of Wound Healing

Witte, M.B., Barbul, A. (1997) Surg Clin North Am. 77:509-528.

Coagulation

Inflammation

Cell Migration / Proliferation

Re-vascularization

Epithelial growth

Wound contraction

Fibrous tissue growth

Maturation

Wound HealingWound Healing

41

Coagulation

Inflammation


Re-vascularization

Epithelial growth

Wound contraction


Maturation

•Homspera modulates cytokine (Th1-biased) responses in macrophages

•Homspera enhances the production of both myeloid and lymphoid progenitor cells

•Substance P increases neutrophil adhesion to endothelial cells

•Substance P increases microvascular permeability

•Tachykinins are required for platelet thrombus formation

•Tachykinins regulate the function of platelets

Literature references available upon request

Wound Healing - Wound Healing - MechanismMechanism

42

Coagulation

Inflammation


Re-vascularization

Epithelial growth

Wound contraction


Maturation

Wound Healing - Wound Healing - MechanismMechanism

•Substance P induces the proliferation of smooth muscle cells and dermal fibroblasts

•Substance P stimulates keratinocyte proliferation and migration

•Substance P stimulates, via NK1, endothelial cell mitogenesis and neovascularization, and the formation of vascular-like tubules in vivo

•Topical application of Substance P significantly decreased wound areas on wound days 1, 2, 6, and 8

•Exogenous administration of substance P enhances wound healing in a genetic diabetic mouse model

•Substance P administration elicited a doubling in the rate of wound healing and was accompanied by vasodilation in aged rats

•Exogenous administration of substance P increased the rate of healing in bisected rat medial collateral ligaments AND promoted an increase (nearly 3-fold) in the force-to-failure strength of healed ligaments

Literature references available upon request

43

Idiopathic Pulmonary Fibrosis (IPF)Idiopathic Pulmonary Fibrosis (IPF)

IPF MarketIPF Market• Estimated 218,000 patients with IPF globally

• Only 60% (or about 125,000) have been diagnosed

• Enhanced diagnostics will lead to more diagnoses soon

• Estimated $2B global market

• Five-year survival rate of 20%

• No FDA-approved therapies on market

• InterMune has submitted NDA for Pirfenidone – March FDA review

• Orphan Drug and Fast Track designation available

• 50% tax credit on clinical trials and 7 years market exclusivity

44

Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis

Development work supported by Dr. Jacob Finkelstein

• Co-Principal Investigator: Center for Biophysical Assessment and Risk Management Following Irradiation (CBARMFI) – 1 of 8 national Centers for Medical Countermeasures Against Radiation (CMCRs) funded by NIAID

• Expertise and publications: • Pulmonary fibrosis• Pulmonary effects of radiation exposure• Biomarkers of radiation exposure• Development of therapeutics to treat post-radiation exposure

sequelae

• Research Support:• Eight NIH funded

• USOFR funded

• EPA funded

• NSF funded

• CBARMFI (U-19) funding

Professor of Pediatrics and Environmental Medicine and Radiation Oncology (University of Rochester)

45

Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis

Homspera® prevents pulmonary injury in chemical-induction models

Biomarkers of IPF are critical • Animal models of pulmonary fibrosis are poor correlates of clinical efficacy

IPF Observations Homspera® / NK1R effectBasal Substance P levels reduced NK1-agonist, like Substance P, may

ameliorate fibrogenesis

TGF-beta levels elevated and plays critical role in fibrogenesis

Diminished TGF-beta production and potentially inhibition of TGF-beta

Interleukin-1-alpha (IL-1a) levels elevated Diminished IL-1a production

p53 levels elevated Diminished p53 production

PARP levels elevated Diminished PARP production

NO elevated and plays critical role in fibrogenesis

Decreased secretion of iNOS

Interleukin-4 (Th2 cytokine; increases TGF-beta) levels elevated

Th1-biasing activity

46

The stimulatory effects observed on adult hematopoietic stem cells lead Management to believe Homspera regenerates and strengthens the immune system, thereby contributing to the effectiveness of treatment in the following indications:

Hematopoietic Hematopoietic stem cellsstem cells

Homspera Homspera stimulationstimulation

Immune cell Immune cell activationactivation

Increased survival and

enhanced immune system

•Idiopathic Pulmonary Fibrosis•Immune / Stem Cell Stimulant•Oncology•Vaccine Adjuvant •Influenza•Biological / Chemical Agents•Radiation Damage•Wound Healing

Research ConclusionsResearch Conclusions

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PartnersPartners

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Drug Company Application Target / Relationship Stage / Value

Neupogen Amgen Stem Cell Cytokines, G-CSF Approved

Mozobil Genzyme Stem Cell CXCR4 NDA submitted

QS-21 Antigenics Adjuvant PartnershipsGSK: $2MM initialElan: $1MM initial

Acambis: $0.2MM initial

Pirfenidone InterMune Idiopathic Pulmonary Fibrosis

Anti-fibrotic mechanisms Pending Approval

TLR agonists Coley Adjuvant Buyout Pfizer: $164MM

Provenge Dendreon Cancer Vaccine Prostate Annual sales: $1B (est.)

Comparator Compounds and Companies

Company OverviewCompany Overview

Ticker Symbol (OTCBB) IRBS

Recent Price (Feb. 9, 2010) $0.35

52-Week Range $1.18 - $0.02

Shares Outstanding 13.1 million

Market Capitalization $4.65 million

Average Volume 33,000 (90-day)17,500 (200-day)

Public Market Float 6.6 million

Insiders +5% Owners ~22%

Institutional Ownership ~20%

Recent Financial Data

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Management TeamManagement Team

Michael K. Wilhelm, Chief Executive Officer and Board MemberMichael K. Wilhelm has been our President and Chief Executive Officer and a member of our Board of Directors since July 2003. Mr. Wilhelm has been President and Chief Executive Officer and a member of the Board of Directors since co-founding ImmuneRegen BioSciences, Inc., our wholly-owned subsidiary, in December 2002. Mr. Wilhelm has served as Managing Director of Foresight Capital Corporation since July 1996, a company he founded to consult and assist early-stage companies in furthering their growth and development. Mr. Wilhelm holds a Bachelors of Finance degree from SUNY Buffalo.

John N. Fermanis, Chief Financial OfficerMr. Fermanis has served as our Chief Financial Officer since December 2004. From May 2001 to October 2004 Mr. Fermanis served as Chief Financial Officer of AMPS Wireless Data, Inc., a privately held Arizona corporation which he co-founded in 1998. From 1997 to 2001, Mr. Fermanis held the position of Treasury Manager for Peter Piper, Inc., a national restaurant chain headquartered in Scottsdale, Arizona. Mr. Fermanis has over 18 years of financial management experience with both the American Express Corporation and Citigroup in New York City. Mr. Fermanis holds a Bachelor of Arts degree from the S.U.N.Y. at Stony Brook and attended Pace University's Graduate School of Management in New York City.

Hal Siegel, Ph.D., Chief Scientific Officer and Board MemberDr. Siegel has served on the Board of Directors since June 2006. Dr. Siegel was appointed as Chief Scientific Officer and Vice President in January 2008 after serving as our Senior Director of Product Development and Regulatory Affairs since June 2006. Prior to joining the company, Dr. Siegel served as Acting General Manager and Vice President Regulatory and Scientific Affairs for Zila Biotechnology, Inc. from 2004 to October 2006. In addition, since 2001, Dr. Siegel has provided consulting services for Siegel Consultancy LLC, which has been providing strategic and tactical expertise to life science companies, helping them meet FDA requirements from pre-clinical studies through the regulatory submission process and into the post-approval marketplace. Dr. Siegel holds degrees from Rensselaer Polytechnic Institute and SUNY Buffalo, where he earned his Ph.D., in Biochemical Pharmacology.

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Theodore E. Staahl, M.D.Dr. Staahl has served on our Board of Directors since April 2003. Dr. Staahl is employed at the Cosmetic, Plastic and Reconstructive Surgery Center, a company which he founded in 1978. Dr. Staahl's professional training was received at the University of Illinois and the University of Wisconsin and is board certified by the American Board of Facial, Plastic and Reconstruction Surgeons, the Board of Cosmetic Surgeons and the American Board of Head and Neck Surgeons. Dr. Staahl has presented papers at national and international meetings on hair transplant, rhinoplasty and cleft lip deformities.

Robert J. Hariri, M.D., Ph.D.Dr. Hariri, M.D. has served on our Board of Directors since April 2007. Dr. Hariri has been CEO of Celgene Cellular Therapeutics, a division of Celgene, since 2005. Previously, he had been President of the division from 2002 to 2005. The division focuses on human stem and biomaterial solutions for a range of clinical indications. From 1998 to 2002, prior to joining Celgene Cellular Therapeutics, Dr. Hariri was Founder, Chairman and Chief Scientific Officer for Anthrogenesis Corp./LIFEBANK, Inc., a New Jersey-based privately held biomedical technology and service corporation involved in umbilical cord blood banking and its supporting technology platform. From 1987 to 1994, he was Co-founder, Vice Chairman and Chief Scientific Officer of Neurodynamics, a privately held medical device and technology corporation. Dr. Hariri has held academic positions at Cornell University Medical College Cornell University Graduate School of Medical Sciences. He has also played a prominent medical role at Cornell University Medical College, The New York Hospital-Cornell Medical Center and The Jamaica Hospital-Cornell Trauma Center. While at Cornell, he was the Director of The Center for Trauma Research. He received his Medical Degree and Ph.D. from Cornell University and was awarded a Bachelor of Arts Degree from Columbia College.

Jerome B. Zeldis, M.D., Ph.D.Dr. Zeldis has served on our Board of Directors since November 2007. Dr. Zeldis currently serves as Chief Medical Officer of Celgene Corporation, Warren N.J., a position he has held since 1997. He is also currently, and since 2003, Professor of Clinical Medicine at the Robert Wood Johnson Medical School in New Brunswick, N.J. Prior to working at Celgene, Dr. Zeldis worked at Sandoz Research Institute from 1994 to 1995 and Janssen Research Institute from 1995 to 1997 in both clinical research and medical development. He has been a Board member of a few start-up biotechnology companies and is currently on the Board of the Semorex Corporation, the N.J. Chapter of the Arthritis Foundation, and the Castleman’s Disease Organization.

Outside Board MembersOutside Board Members

Lance K. Gordon, Ph.D.Dr. Gordon has served on our Board of Directors since May 2007. He currently serves as President and CEO of ImmunoBiologics Corporation, a formative biotechnology company that he founded in 2007. Prior to his work at ImmunoBiologics Corporation Dr. Gordon served as President, Chief Executive Officer and as a Director of VaxGen, Inc. from 2001 to 2007. Prior to joining VaxGen, Dr. Gordon was Executive Director of North America for Acambis plc. and a member of the Company’s Board of Directors from 1999 to 2001. Previously, he served as President and CEO of OraVax, Inc. from 1990 to 1999, prior to its acquisition by Peptide Therapeutics to form Acambis. Before joining OraVax, he served as the CEO of North American Vaccine from 1988 to 1990, prior to its acquisition by Baxter International. Dr. Gordon received his Ph.D. in Biomedical Science, Immunology from the University of Connecticut and completed his postdoctoral fellowship as an NIH fellow at the Division of Allergy and Immunology, Washington University Medical School, St. Louis. He currently serves on the DHHS National Vaccines Advisory Committee and on the Board of Trustees of the Sabin Vaccine Institute.

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Scientific Advisory BoardScientific Advisory Board

John Dann, M.D., D.D.S., Graduate of Harvard University Dental School and Washington University Medical School, Board Certified Graduate of Harvard University Dental School and Washington University Medical School, Board Certified maxillofacial and craniofacial surgeon.maxillofacial and craniofacial surgeon.

Jacob Finkelstein, Ph.D., a professor in the departments of Pediatrics, Radiation Oncology and Environmental Medicine at the a professor in the departments of Pediatrics, Radiation Oncology and Environmental Medicine at the University of Rochester Medical School, recognized for investigations into the effects of radiation on cells and functions of the lung. University of Rochester Medical School, recognized for investigations into the effects of radiation on cells and functions of the lung.

Jeffrey Friedman, M.D., Diplomat, American Board of Cosmetic Surgery, American Board of Otolaryngology Head and Neck Surgery, Diplomat, American Board of Cosmetic Surgery, American Board of Otolaryngology Head and Neck Surgery, Fellow of the American Academy of Cosmetic Surgery.Fellow of the American Academy of Cosmetic Surgery.

Adriana T. Larregina, M.D., Ph.D., University of Pittsburgh School of Medicine faculty member of the Dermatology and University of Pittsburgh School of Medicine faculty member of the Dermatology and Immunology departments and director of Cutaneous Biology Laboratories and Education, published extensively on the role dendritic cells and their Immunology departments and director of Cutaneous Biology Laboratories and Education, published extensively on the role dendritic cells and their precursors play in stimulating immune responses. precursors play in stimulating immune responses.

Susan E. Leeman, Ph.D, Professor in the Department of Pharmacology and Experimental Therapeutics at the Boston University School of Professor in the Department of Pharmacology and Experimental Therapeutics at the Boston University School of Medicine. One of the first scientists to isolate substance P in the central nervous and gastrointestinal systems. She was elected to the National Medicine. One of the first scientists to isolate substance P in the central nervous and gastrointestinal systems. She was elected to the National Academy of Sciences in 1991.Academy of Sciences in 1991.

K.A. Kelly McQueen, M.D., M.P.H., Anesthesiologist and Public Health Consultant; Infectious Disease and Disaster Planning for Anesthesiologist and Public Health Consultant; Infectious Disease and Disaster Planning for U.S. Army and US Northern Combatant Command.U.S. Army and US Northern Combatant Command.

Pranela Rameshwar, Ph.D., Professor in the Department of Medicine, Division of Hematology/Oncology at the University of Medicine Professor in the Department of Medicine, Division of Hematology/Oncology at the University of Medicine and Dentistry of New Jersey; research areas include Substance P, stem cells and cancer.and Dentistry of New Jersey; research areas include Substance P, stem cells and cancer.

Ivan Rich, Ph.D., CEO and founder of HemoGenix, a biotechnology company focused on the development of 21CEO and founder of HemoGenix, a biotechnology company focused on the development of 21stst century stem cell assays. century stem cell assays.

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• Eight issued U.S. and foreign patents

• At least 67 pending patent applications including:• 16 pending U.S. utility patent applications

• 2 pending U.S. provisional applications

• 7 pending international patent applications

• 41 pending foreign patent applications

Current StatusCurrent Status

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Recent EventsRecent Events

January 27, 2010 - National Cancer Institute Initiates Studies on ImmuneRegen BioSciences' Vaccine Adjuvant Candidate

January 5, 2010 - ImmuneRegen BioSciences(R) Reports Additional Positive Results From Study of Homspera(R) in Treating Highly Pathogenic Influenza

December 14, 2009 - ImmuneRegen BioSciences'(R) Drug Candidate Homspera Confirms Efficacy as Cancer Vaccine Adjuvant

November 10, 2009 - ImmuneRegen reports Homspera improves survival and reduces symptoms of highly lethal influenza virus infection without any additional treatment

October 22, 2009 - ImmuneRegen to further Homspera research in U.S. Government funded study on reducing the detrimental effects of radiation on lung immune system function

October 12, 2009 - ImmuneRegen initiates Homspera studies against global influenza threat by performing studies for efficacy against highly lethal H5N1 Avian Influenza and to further define the adjuvant efficacy when coupled with a novel vaccine for H5N1

September 22, 2009 - ImmuneRegen enters into a partnership with Bachem, Inc., for manufacturing of Homspera

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For any questions, please contact:For any questions, please contact:

• Michael Wilhelm, CEO [email protected]

• Dr. Hal Siegel, CSO [email protected]

• Chris Romano [email protected]

• Dr. Dan Holterman [email protected]

Questions & AnswersQuestions & Answers

to learn more about our company, please take a look at our

Documents

substance p homspera

homspera resistant

homspera resistance

receptor specific homspera

enzymatic degradation

substance p degradation

mechanism of action

receptor substance p