irbs presentation - general - august 2010
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Safe Harbor & Data PresentedSafe Harbor & Data PresentedStatements about the Company's future expectations, including statements aboutthe potential use and scientific results for the Company's drug candidates, scienceand technology, and all other statements in this presentation other than historicalfacts, 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 asthat term is defined in the Private Securities Litigation Reform Act of 1995. TheCompany intends that such forward-looking statements be subject to the safeharbors 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 anduncertainties. The Company's actual results could differ materially from expectedresults as a result of a number of factors, including the uncertainties inherent in
research and development collaborations, pre-clinical and clinical trials and productdevelopment programs (including, but not limited to the fact that future results orresearch and development efforts may prove less encouraging than current resultsor cause side effects not observed in current pre-clinical trials), the evaluation of
potential opportunities, the level of corporate expenditures and monies available forfurther 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 ExchangeCommission. There are no guarantees that any of the Company's proposed
products will prove to be commercially successful. The Company undertakes noduty to update forward-looking statements.
Data presented in this presentation may not be comprehensive; please contact
ImmuneRegen for additional information.
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MissionMission
We are a biotechnology company, focused onWe are a biotechnology company, focused onadvancing products that regenerate or strengthen theadvancing products that regenerate or strengthen thehuman immune system, in part, through stimulationhuman immune system, in part, through stimulationof adult stem cells.of adult stem cells.
We are working to capitalize on our drug candidatesWe are working to capitalize on our drug candidatesby continuing our own development programs andby continuing our own development programs andsimultaneously seeking to license product use forsimultaneously seeking to license product use forspecific indications to Industry partners.specific indications to Industry partners.
To be recognized for developing safeand effective therapeutics and for drivingvalue through drug development
programs that attract licensing andcollaborative partnerships.
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PipelinePipeline
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Idiopathic PulmonaryFibrosis
Influenza Therapeutic
Cancer Therapeutic
Vaccine Adjuvant
Biological and ChemicalAgents
Radiation Damage(Neutropenia)
Wound Healing
Oral Administration
Solid dosage form
provides compoundingflexibility
No additional devicesneeded for administration
Ships formulated formaximum stability, noliquid additions
Solid may preclude needfor cold chain
May enable remotestockpiling
May provide environment-insensitive stability
ral Bioavailability Study shows oral or intra-duodenal Homspera administration results inmeasurable and pharmacologically relevant plasma and pulmonary drug concentrations.
Indications Oral administrationIndications Oral administration
Potential Benefitsof
Oral Administration
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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 LeuLeu Met(OMet(O22))-NH-NH22))
(Arg Pro Lys Pro Gln Gln Phe Phe Gly Leu Met-NH2)
HomsperaHomspera vs. Substance Pvs. Substance P
Homspera NK-1 Receptor SpecificHomspera NK-1 Receptor Specific
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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
HomsperaHomspera
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Homspera - Resistant to enzymaticHomspera - Resistant to enzymatic
degradationdegradation
HomsperaHomspera vs. Substance Pvs. Substance P
Arg Pro Lys Pro Gln Gln Phe Phe Gly Leu Met NH21 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)
Homsperamodificatio
ns
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Roosterman D et al. PNAS 2007;104:11838-11843
ECE-1 regulates NK1 recyclingECE-1 regulates NK1 recycling
Homspera Resistant to ECE-1Homspera Resistant to ECE-1
degradationdegradation
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NK1-R links to MAPK and ERK1/2NK1-R links to MAPK and ERK1/2
(1) SP binding to the NK1R leads torecruitment of -arrestin to the receptor,assembly of a MAPK signalosome, andERK1/2 activation.
(2) Degradation of SP by ECE-1 inacidified endosomes disrupts theSP/NK1R/arr/MAPK signalosome.
(3) NK1R recycles to the plasmamembrane for resensitization.
(4) Inhibiting ECE-1 activity causessustained ERK1/2 activation and SP-induced cell death.
From Murphy JE, Padilla BE, Hasdemira B, Cottrell GS and Bunnett NW (2009) PNAS
Endosomal ECE-1 regulates SP-induced ERK activation andEndosomal ECE-1 regulates SP-induced ERK activation and
cell deathcell death
NK1-R internalization coupled tobeta-arrestin scaffolding triggers
kinase cascade. Substance Pdegradation recyclesreceptor/terminates signal.Homspera resistance to ECE-1alters intracellular signal fordiscordant membrane / intra-cellular signals (published byothers)
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Mechanism of ActionMechanism of Action
Summary of Underlying NK1-RMechanisms Increased hematopoietic progenitor cells from both the
myeloid and lymphoid lineages
Direct stimulation of immune cells includingmacrophages and neutrophils AND antigen presentingcells
Augmentation of the innate immune response dependentupon the status of the local microenvironment
Direct stimulation of dermal fibroblasts, keratinocytesand epidermal cells
Distinct antagonist and intracellular activity profilescompared to SP
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CellD
ifferentiati o
n
Primitive
Stem Cell
Specialized Cells
Hematopoiet
ic Stem Cell
CFU-GEMM
CommonLymphoidProgenitor
CommonMyeloid
Progenitor
Granulocytes
Megakaryocyte
Erythrocyte
CFU-GM
Platelets
NK cellT cellB cell
Macrophage
Monocyte
Adult Hematopoietic Stem Cells (HSCs)Adult Hematopoietic Stem Cells (HSCs)
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HSCs -HSCs - Homspera stimulates progenitorsHomspera stimulates progenitors
Methodology: Colonyforming assays wereperformed under bothoptimal and sub-optimalcytokine/growth factorconditions. The sub-optimal conditions were1/50th the concentration ofthose considered optimaland were concentrations
known to support stem cellgrowth and differentiation.Culturing the cells undersub-optimal growthconditions is an importantcontrol often used toexamine a compoundsstimulatory effect on HSCs.If the cells in culture arealready maximallystimulated (as they could
be under optimalconditions), there is areduced chance ofdetecting a compoundsstimulatory activity.Likewise, if an experimentalcompound merelysubstitutes for a deficientgrowth factor, it would onlybe effective under sub-
optimal conditions. Therefore, it is useful tocompare results under both
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Colony forming assays were performed under optimal cytokine/growth factor conditions.
HSCs -HSCs - Homspera stimulates progenitorsHomspera stimulates progenitors
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Increases stem cell differentiation into cells that are requiredto regenerate or strengthen the human immune system
Enhances production of the following precursors:
1. White blood cellsa. 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
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Radiation & NeutropeniaRadiation & Neutropenia
Homspera Findings Increased survival of small
animals exposed to lethalradiation levels
Treatment is more effectiveafter 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) andUniversity of Arizona (survival)
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Irradiated +Homspera
Irradiated Control
Radiation -Radiation - Homspera findingsHomspera findings
Homspera promotes survival of lethally-irradiatedanimals
Methodology: Sixteen maleC57BL/6 mice (N=8Homspera-treated and N=8radiation-only controls) weregiven a single 7.75 Gy wholebody dose of gammaradiation. The control groupwas administered saline dailyvia nebulizer for 15 min/daywith treatment beginningwithin 2 hours of radiationexposure. The treatmentgroup was administeredHomspera, 50 M solution,15 min/day under the sameconditions.
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Radiation -Radiation - Homspera findingsHomspera findings
Homspera increases WBC counts following radiation
Methodology: 72 Balb/c mice of age5-6 weeks and normal physiologicalstate (Taconic) were separated into 4groups: 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, animalswere placed into the X-ray irradiator(RadSource 2000) for 4 minutes.Non-irradiated controls received noradiation exposure while theirradiated controls were exposed toradiation at the level of 1 Gy/minute.Animals were either treated withvehicle control or Homspera invehicle control solution. The Non-irradiated control group and
Irradiated control group wereadministered 25 L of sterile salineintranasally daily for 7 days followingradiation exposure. Animals treatedwith Homspera pre-radiationexposure were administered 25 L of300 M solution intranasally 1-dayprior to radiation exposure and dailythereafter for 7 days. Animalstreated with Homspera post-radiation
exposure were administered 25 L of300 M solution intranasally daily for7 days following radiation exposure.
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Immune Activity - MechanismsImmune Activity - Mechanisms
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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 increasedexpression of CCL21/SLC, a DC chemoattractant, in lymphaticvessels
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 Cellsexpress NK1 receptors
Bone marrow-derived stem cells express NK1receptors
NK1 receptor expression is upregulated by
TLR agonists
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Ag +
Homspera
AgControl
Figure 1
Enhances humoral antibodyresponses
Increased antigen-specific antibody titersapproximately 10-fold when administeredprior to gene gun-delivered DNA antigen(Figure 1)
In another study intranasally-administered Homspera and antigenrevealed a nearly 10-fold increase ofserum antigen-specific antibodiescompared to antigen-only controls
When administered intranasally while
Ag was administered via IP, a 3-foldincrease in serum antigen-specificantibody titers AND a 2.5-fold increasein heterotypic antibodies (H5N1-derived protein compared to H1N1-derived protein) was observed whencompared to non-Homspera treated
controls
Immune ActivityImmune Activity
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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
Immune ActivityImmune Activity
Survival correlates to 3-fold increases in both homotypic and heterotypicantibody levels observed in mice treated with Homspera intranasally and
antigen intraperitoneally.
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Elevates CD4+ memory T-helper cell
function Enhanced delayed-type hypersensitivity (DTH)
composed of statistically elevated numbers ofCD4+, CD8+ lymphocytes and macrophages tothe vaccination site following epidermalapplication of vaccine antigen along with
Homspera (Figure 2).
By augmenting both innateand humoral immunity,Homspera may also increasethe antibody-dependent cell-mediated cytotoxicity effect,
which limits and containsinfection and controls tumorgrowth.Control Ag
Ag +Homsper
a
Ag + NK1antagonist
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.
Immune ActivityImmune Activity
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Enhanced antigen-specificcytotoxic CD8+ T-cell (CTL)response
Increase the antigen-specific cytotoxicfunction on T-cells by in vivo killing assays(Figure 3).
Induction of a robust CTL response wasalso observed using a more aggressiveimmunization course, which involvedone priming dose, and two boosterdoses. When this immunization
scheme was employed Homspera wasobserved to increase specific cell killingto 92%.
Figure 3
Ag Ag +Homsper
a
P < 0.05
Immune ActivityImmune Activity
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Augments innate immunity and
cytokine expression NK1R activation by Homspera signals through
the NF-B pathway.
Th1-biased immune response.
Ag +Homsper
a
AgControl Ag +Homsper
a
AgControl
Figure 4
IFN- (Figure 4), TNF-, IL-1, IL-2, and GM-CSF productionpredominately influenced. NF-B also regulates the genes encodingthe chemokines Interleukin-8 (IL-8) and macrophage inflammatoryprotein-1 (MIP-1).
Splenic CD4+ T-cells
Splenic CD8+ T-Cells
Immune ActivityImmune Activity
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InfluenzaInfluenza
infects therespiratory 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 thanTamiflu
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-relateddeaths
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Approximately 90% reduction of viral titers
Influenza studies using a cotton rat model of seasonal influenza (Influenza A/Wuhan/359/95) were performed by VirionSystems, Inc.
Influenza Influenza Homspera findingsHomspera findings
Methodology: Young adult (6-8weeks old) cotton rats (SigmodonHispidus) of both genders wereobtained from an inbred colonymaintained at Virion Systems, Inc.(Rockville, MD). A stock of
Influenza/A/Wuhan/359/95 wasprepared by Novavax, Inc.Animals were either treatedintranasally with Homspera orvehicle 1 day before influenzainfection OR given Homsperabeginning 1 hour followinginfluenza infection. Homsperatreatment was continued daily for10 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 x0.1mL).
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Reduction of viral particles and abnormal cilia
Influenza studies using a mouse model performed at University of Arizona
Influenza Influenza Homspera findingsHomspera findings
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 shownormal ciliated epithelial cell (singlearrow) and normal mitochondrialcomplement (double arrows).
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Reduction of pulmonary inflammation
Influenza studies using a cotton rat model of seasonal influenza (Influenza A/Wuhan/359/95) were performed by VirionSystems, Inc.
Influenza Influenza Homspera findingsHomspera findings
Methodology: Young adult (6-8weeks old) cotton rats (SigmodonHispidus) of both genders wereobtained from an inbred colonymaintained at Virion Systems, Inc.A stock ofInfluenza/A/Wuhan/359/95 wasprepared by Novavax, Inc. Animalswere grouped into mock-treated /
infected, oseltamivir (Tamiflu) 10mg/kg / infected, Homspera 0.23mg/kg / infected, oseltamivir(Tamiflu) 10 mg/kg + Homspera0.23mg/kg / infected. Homsperawas administered intranasally andoseltamivir solution wasadministered orally. Treatmentscommenced 1-day prior toinfection. Lung were dissected andinflated, then assessedhistologically. Parametersquantified on 0-4 severity scale:interstitial pneumonia(inflammatory cell infiltration andthickening of alveolar walls), andalveolitis (cells within the alveolarspaces), peribronchiolitis(inflammatory cells clusteredaround the periphery of smallairways), perivasculitis
(inflammatory cells clusteredaround the vesicles).
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More significant reduction of weight loss than
Tamiflu
Influenza studies using a cotton rat model of seasonal influenza (Influenza A/Wuhan/359/95) were performed by VirionSystems, Inc.
Influenza Influenza Homspera findingsHomspera findings
Methodology: Young adult (6-8weeks old) cotton rats (SigmodonHispidus) of both genders wereobtained from an inbred colonymaintained at Virion Systems, Inc.A stock ofInfluenza/A/Wuhan/359/95 wasprepared by Novavax, Inc. Animalswere grouped into mock-treated /infected, oseltamivir (Tamiflu) 10mg/kg / infected, Homspera 0.23mg/kg / infected. Homspera wasadministered intranasally andoseltamivir solution wasadministered orally. Treatments
commenced 1-day prior toinfection. Weights were measureddaily.
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More significant reduction of weight loss than
Tamiflu
Influenza studies using a cotton rat model of seasonal influenza (Influenza A/Wuhan/359/95) were performed by VirionSystems, Inc.
Influenza Influenza Homspera findingsHomspera findings
Methodology: Young adult (6-8weeks old) cotton rats (SigmodonHispidus) of both genders wereobtained from an inbred colonymaintained at Virion Systems, Inc.A stock ofInfluenza/A/Wuhan/359/95 wasprepared by Novavax, Inc. Tamiflu
(oseltamivir, Roche Inc.) wasobtained commercially. Animalswere grouped into mock-treated /infected, oseltamivir (Tamiflu)2mg/kg / infected, Homspera0.23mg/kg / infected, oseltamivir(Tamiflu) 2mg/kg + Homspera0.23mg/kg / infected. Homsperawas administered intranasally andoseltamivir solution wasadministered orally. All treatmentsbegan approximately 1-hourfollowing infection withInfluenza/A/Wuhan/359/95.Homspera was administered oncedaily, whereas oseltamivir wasadministered twice daily, once inthe morning and once in theevening. Treatment was continueddaily for three days. Weights weremeasured daily.
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Reduction of Tamiflu-associated mortality
Influenza studies using a cotton rat model of seasonal influenza (Influenza A/Wuhan/359/95) were performed by VirionSystems, Inc.
Influenza Influenza Homspera findingsHomspera findings
Methodology: Young adult (6-8weeks old) cotton rats (SigmodonHispidus) of both genders wereobtained from an inbred colonymaintained at Virion Systems, Inc.A stock ofInfluenza/A/Wuhan/359/95 wasprepared by Novavax, Inc. from
supernatants of MDCK cells thathad been inoculated 3 dayspreviously at a low multiplicity ofinfection (m.o.i). Tamiflu(oseltamivir, Roche Inc.) wasobtained commercially. Animalswere grouped into mock-treated /infected, oseltamivir (Tamiflu)2mg/kg / infected, oseltamivir(Tamiflu) 2mg/kg + Homspera0.23mg/kg / infected, Homspera0.23mg/kg / infected. Homsperawas administered intranasally andoseltamivir solution wasadministered orally. All treatmentsbegan approximately 1-hourfollowing infection withInfluenza/A/Wuhan/359/95.Homspera was administered oncedaily, whereas oseltamivir wasadministered twice daily, once in
the morning and once in theevening. Treatment was continueddaily for three days.
p = 0.012 (FishersExact Test)
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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 Homespera
10e5 + 2mg Homespera
10e3 Nave Infection
10e5 Nave Infection
Homespera
Days Post Infection
Percentsurvival
Homspera
Homspera Homspera
Influenza studies in Ferrets infected with H5N1 (A/Whooperswan/Mongolia/244/2005) were performed under contractwith the University of Pittsburgh.
Methodology: 20 young adult (20 weeks old) Fitch ferrets of both genders were inoculated with InfluenzaA/Whooperswan/Mongolia/244/2005 (H5N1) with 0, 103 or 105 plaque-forming units (PFU) on Day 0. Uninfectedcontrols were treated with 2 mg/kg Homspera via intranasal administration beginning on Day 1 and continueddaily thru Day 5. Animals infected with 103 PFU were split into 2 groups 1 group received vehicle controltreatment daily for 5 days, the other received 2 mg/kg Homspera treatment intranasally commencing 1 day afterinfection and continuing thru Day 5. Similarly, animals infected with 105 PFU were split into 2 groups 1 groupreceived vehicle control treatment daily for 5 days, the other received 2 mg/kg Homspera treatment intranasallycommencing 1 day after infection and continuing thru Day 5.
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Reduction in tumor metastases using
well-established B16-lung metastasismodel
63% reduction in metastases and 24%increase in survival in animals treated withHomspera for 7 days immediately followingcancer cell injection.
97% reduction in metastases in animalstreated with Homspera for 7 days beginning 7days after cancer cell injection.
Human melanoma cells are not stimulated
A375 and A2058 cell lines were not stimulated following Homsperaexposure.
Chemotherapeutic sensitivity is not affected
OVCAR-3 (human ovarian adenocarcinoma), SK-OV-3 (humanovarian adenocarcinoma), and MDA-MD-231 (human breastadenocarcinoma) sensitivity to chemotherapeutics was not affectedby Homspera exposure.
Oncology -Oncology - Homspera findingsHomspera findings
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Oncology -Oncology - Homspera findingsHomspera findings
Figure 1: Homspera increases cellular immune responses, and reduces and delays the growth ofmelanoma 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 receivingHomspera and TRP2 antigen received either 1 or 2 doses.
Picture of mice treated and sacrificed22d after injection of B16 melanomacells. Mice were geneticallyimmunized with GG encoding themelanoma self-Ag TRP2 in thepresence or absence of Homspera orthe NK1R antagonist L733060 andinjected with B16/F0 malignant
melanoma cells.
Data represents means 1SE of tumor
area (mm2
) of 6 mice per experimentalgroup. Both GG TRP2 plus Homsperatreatments (1 or 2 doses) significantlyinhibit tumor growth compared to GGencoding irrelevant Ag or TRP2 antigenin mice injected with B16/F0 cells(**p
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Oncology -Oncology - Homspera findingsHomspera findings
WO 2009/129498 A2 (patent application)
Preliminary data (August 2010) fromindustry partner Scancell show:
The combination of Homspera with ScancellsImmunoBody DNA immunisation via gene gundelivery enhances both CD8 and CD4 epitopespecific responses in vivo
Data supports previous findings that used adifferent melanoma vaccine (presented on theprevious slide) Follow-up experiments using a melanoma
challenge expected to be completed inSeptember 2010
d h l b ( )
http://v3.espacenet.com/publicationDetails/biblio?CC=WO&NR=2009129498A2&KC=A2&FT=D&date=20091022&DB=&locale=en_ephttp://v3.espacenet.com/publicationDetails/biblio?CC=WO&NR=2009129498A2&KC=A2&FT=D&date=20091022&DB=&locale=en_ep -
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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 MarchFDA review
Orphan Drug and Fast Track designationavailable
50% tax credit on clinical trials and 7 years marketexclusivity
Idi hi P l Fib i
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Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis
Development work supported by Dr. Jacob Finkelstein
Co-Principal Investigator: Center for BiophysicalAssessment and Risk Management Following Irradiation(CBARMFI) 1 of 8 national Centers for MedicalCountermeasures Against Radiation (CMCRs) funded byNIAID Expertise and publications:
Pulmonary fibrosis
Pulmonary effects of radiation exposure Biomarkers of radiation exposure
Development of therapeutics to treat post-radiationexposure sequelae
Research Support:
Eight NIH funded
USOFR funded
EPA funded
NSF funded
CBARMFI (U-19) funding
Professor of Pediatricsand EnvironmentalMedicine andRadiation Oncology(University ofRochester)
d h l bIdi thi P l Fib i
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An interstitial pneumonia leading to diffuse lungscarring and fibrosis
May be linked to alveolar epithelial damage
followed by abnormal repair processes
Redox and immune status may also impactdisease or play causative role
Idiopathic = cause unknown
No effective anti-fibrotic therapies available May 2010 FDA rejected pirfenidone for IPF
Facts
Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis
Idi hi P l Fib iIdi thi P l Fib i
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Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis
Idi thi P l Fib iIdi thi P l Fib i
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Industry-standard bleomycin (intra-tracheal) model 1
2.2 mg/kg bleomycin i.t. (study day 0)
0.02-2.0 mg/kg Homspera p.o. daily
Dosing on study days 1-5 (inflammatory phase); 1-9 (transitional); 10-20
(fibrotic phase)
Homspera p.o. prevented decreased body weight
Homspera p.o. prevented increased lung weight(evidence of inflammatory/fibrotic effects)
1 Chaudhury et al., 2006
Evidence forHomspera
Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis
Idi thi P l Fib iIdi thi P l Fib i
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Whole body gamma irradiation model (mice)
5Gy gamma at 4 days
Homspera (intranasal) 2 mg/kg daily for 10 days
No treatment for 6 weeks allows for developmentof pulmonary sequelae before LPS (endotoxin)challenge
Homspera decreased pulmonary protein exudate inresponse to LPS (TLR 4 agonist)
Evidence forHomspera
Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis
Idi thi P l Fib iIdi thi P l Fib i
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LPS causes pulmonary and hepatic fibrosis
TLR-4 inhibition prevents, whereas activationaccelerates, LPS-induced fibrosis
TGF- plays intermediary role in fibrosis Homspera inhibition of TLR-4 effect suggests
inhibition of fibrosis
Homspera inhibition of bleomycin-induced lung
and weight changes suggests inhibition offibrosis
Discussion
Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis
Idi thi P l Fib iIdi thi P l Fib i
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Fibrosis is dysregulated wound repair1
KGF decreased in fibrosis
KGF expression is anti-fibrotic
KGF accelerates wound healing
Homspera accelerates wound healing
Hematopoietic stem cells (HSCs) protectagainst bleomycin-induced pulmonary
fibrosis2
Homspera induces and mobilizes HSCs
1 Wilson and Wynn, 20092
Aguilar 2010
Rationale for
Homspera
Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis
Idi thi P l Fib iIdiopathic P lmona Fib osis
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Idiopathic Pulmonary FibrosisIdiopathic Pulmonary Fibrosis
Homspera prevents pulmonary injury in chemical-induction
modelsBiomarkers of IPF are critical
Animal models of pulmonary fibrosis are poor correlates of clinicalefficacy IPF Observations Homspera / NK1R effect
Basal Substance P levels reduced NK1-agonist, like Substance P, may amelioratefibrogenesis
TGF-beta levels elevated and plays critical rolein fibrogenesis
Diminished TGF-beta production andpotentially 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 infibrogenesis
Decreased secretion of iNOS
Interleukin-4 (Th2 cytokine; increases TGF-beta) levels elevated
Th1-biasing activity
W d H liWound Healing H Fi diHomspera Findings
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Homspera:Homspera:
Accelerates wound healingAccelerates wound healing in vivoin vivo
Increases proliferation of fibroblastsIncreases proliferation of fibroblasts ininvitrovitro
Stimulates hematopoietic stem cellStimulates hematopoietic stem cellactivityactivity
Activates Dendritic cells and improves T-Activates Dendritic cells and improves T-cell responsescell responses
Data collected by ImmuneRegen under contract with the following laboratories: MIR, HemoGenix, Bio-Quant
Wound Healing Wound Healing Homspera FindingsHomspera Findings
Wo nd He lingWound Healing Hom pe FindingHomspera Findings
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Homspera increases the proliferation of human dermal
fibroblasts in vitro
Performed at Johns Hopkins University
Methodology: Fibroblasts wereseeded in a 96 well plate usingIMDM (media) containing 0.5%FBS. Next day, these serumstarved cells were treated with
various amounts of Homspera orHomspera + antagonist-(Spantide I) for a period of 1 or 3days. Cells were pretreated withHomspera in serum free media(0.5%FBS) for 3 hrs. Cells werethen re-stimulated with serum(5%FBS) or not (0.5%FBS) whilemaintaining the presence ofHomspera. MTT assays wereperformed after 1 and 3 days oftreatment with test article.
These results are indicative oftwo independent experiments.Results are represented as %growth where mean OD of eachsample is normalized to itscontrol.
Wound Healing Wound Healing Homspera FindingsHomspera Findings
Wound HealingWound Healing Homspera FindingsHomspera Findings
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Homspera reduces healing wound area pig
modelMethodology: Two normal, femaleYorkshire pigs three months in age,weighing 15-20 kg, wereanesthetized and wounded. A totalof 20 full-thickness wounds eachwith a 3 cm diameter were createdon each pig using a scalper, 2 cmapart and 10 per side of the animal.8 tattoo labels were made aroundsurrounding the wound for
measuring purposes. Pigs wereobserved daily for morbidity andtoxic signs for 21 days after woundinduction. Homspera (at 10-4M, 10-6M, 10-8M and 10-10 M) and control(DPBS) articles were appliedtopically intra-wound. On each pig,2 ml of Homspera at the testconcentration or control solutionwas applied to fill the wound and
covered it with saline-moistened(not wet) non-adherent Telfa gauze.Sterile techniques were performedas much as possible during thesurgery to minimize the risk ofinfection on wound area. Dressingswere changed every 5 days andHomspera was re-applied at eachdressing change. Wound healingwas evaluated by measuring thediameters of wound closure in 4
different directions on designatedtime point at Days 7, 10, 14, 17, 21,
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Wound Healing Wound Healing Homspera FindingsHomspera Findings
Wound HealingWound Healing
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Wound HealingWound Healing
Wound HealingWound Healing
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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
Wound HealingWound Healing MechanismMechanism
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Coagulation
Inflammation
Cell Migration /
Proliferation
Re-vascularization
Epithelial growth
Wound contraction
Fibrous tissue growth
Maturation
Homspera modulates cytokine (Th1-biased)
responses in macrophages
Homspera enhances the production of both myeloidand lymphoid progenitor cells
Substance P increases neutrophil adhesion toendothelial cells
Substance P increases microvascular permeability
Tachykinins are required for platelet thrombusformation
Tachykinins regulate the function of platelets
Literature references available upon
Wound Healing -Wound Healing - MechanismMechanism
Wound HealingWound Healing MechanismMechanism
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Coagulation
Inflammation
Cell Migration /
Proliferation
Re-vascularization
Epithelial growth
Wound contraction
Fibrous tissue growth
Maturation
Wound Healing -Wound Healing - MechanismMechanism
Substance P induces the proliferation of smooth musclecells and dermal fibroblasts
Substance P stimulates keratinocyte proliferation andmigration
Substance P stimulates, via NK1, endothelial cellmitogenesis and neovascularization, and the formation ofvascular-like tubules in vivo
Topical application of Substance P significantlydecreased wound areas on wound days 1, 2, 6,and 8
Exogenous administration of substance P enhanceswound healing in a genetic diabetic mouse model
Substance P administration elicited a doubling in therate of wound healing and was accompanied byvasodilation in aged rats
Exogenous administration of substance P increased therate of healing in bisected rat medial collateral
Literature references available upon
Research ConclusionsResearch Conclusions
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The stimulatory effects
observed on adulthematopoietic stem cells lead
Management to believe
Homspera regenerates and
strengthens the immune
system, thereby contributingto the effectiveness oftreatment in the following
indications:
HematopoieticHematopoietic
stem cellsstem cells
HomsperaHomspera
stimulationstimulation
Immune cellImmune cellactivationactivation
Increasedsurvival
andenhancedimmunesystem
Idiopathic PulmonaryFibrosis
Immune / Stem CellStimulant
OncologyVaccine AdjuvantInfluenzaBiological / Chemical
Agents
Radiation Damage
Research ConclusionsResearch Conclusions
PartnersPartners
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PartnersPartners
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Management TeamManagement Team
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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 memberof the Board of Directors since co-founding ImmuneRegen BioSciences, Inc., our wholly-ownedsubsidiary, in December 2002. Mr. Wilhelm has served as Managing Director of Foresight CapitalCorporation since July 1996, a company he founded to consult and assist early-stage companies infurthering their growth and development. Mr. Wilhelm holds a Bachelors of Finance degree fromSUNY Buffalo.
John N. Fermanis, Chief Financial Officer
Mr. Fermanis has served as our Chief Financial Officer since December 2004. From May 2001 toOctober 2004 Mr. Fermanis served as Chief Financial Officer of AMPS Wireless Data, Inc., a privatelyheld Arizona corporation which he co-founded in 1998. From 1997 to 2001, Mr. Fermanis held theposition of Treasury Manager for Peter Piper, Inc., a national restaurant chain headquartered inScottsdale, Arizona. Mr. Fermanis has over 18 years of financial management experience with boththe American Express Corporation and Citigroup in New York City. Mr. Fermanis holds a Bachelor ofArts degree from the S.U.N.Y. at Stony Brook and attended Pace University's Graduate School ofManagement 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 ChiefScientific 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 servedas Acting General Manager and Vice President Regulatory and Scientific Affairs for ZilaBiotechnology, Inc. from 2004 to October 2006. In addition, since 2001, Dr. Siegel has providedconsulting services for Siegel Consultancy LLC, which has been providing strategic and tacticalexpertise to life science companies, helping them meet FDA requirements from pre-clinical studiesthrough the regulatory submission process and into the post-approval marketplace. Dr. Siegel holdsdegrees from Rensselaer Polytechnic Institute and SUNY Buffalo, where he earned his Ph.D., inBiochemical Pharmacology.
Outside Board MembersOutside Board Members
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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 andReconstructive Surgery Center, a company which he founded in 1978. Dr. Staahl's professional training was received at theUniversity of Illinois and the University of Wisconsin and is board certified by the American Board of Facial, Plastic andReconstruction Surgeons, the Board of Cosmetic Surgeons and the American Board of Head and Neck Surgeons. Dr. Staahl haspresented 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 onhuman 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 itssupporting 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 CornellUniversity Medical College Cornell University Graduate School of Medical Sciences. He has also played a prominent medical roleat Cornell University Medical College, The New York Hospital-Cornell Medical Center and The Jamaica Hospital-Cornell TraumaCenter. 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 ofCelgene 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 atSandoz Research Institute from 1994 to 1995 and Janssen Research Institute from 1995 to 1997 in both clinical research andmedical development. He has been a Board member of a few start-up biotechnology companies and is currently on the Boardof the Semorex Corporation, the N.J. Chapter of the Arthritis Foundation, and the Castlemans 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 ImmunoBiologicsCorporation, 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 joiningVaxGen, Dr. Gordon was Executive Director of North America for Acambis plc. and a member of the Companys Board ofDirectors from 1999 to 2001. Previously, he served as President and CEO of OraVax, Inc. from 1990 to 1999, prior to itsacquisition by Peptide Therapeutics to form Acambis. Before joining OraVax, he served as the CEO of North American Vaccinefrom 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 ofAllergy and Immunology, Washington University Medical School, St. Louis. He currently serves on the DHHS National VaccinesAdvisory Committee and on the Board of Trustees of the Sabin Vaccine Institute.
Scientific Advisory BoardScientific Advisory Board
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Scientific Advisory BoardScientific Advisory Board
John Dann, M.D., D.D.S., Graduate of Harvard University Dental School andGraduate of Harvard University Dental School andWashington University Medical School, Board Certified maxillofacial and craniofacial surgeon.Washington University Medical School, Board Certified maxillofacial and craniofacial surgeon.
Jacob Finkelstein, Ph.D.,a professor in the departments of Pediatrics, Radiation Oncology anda professor in the departments of Pediatrics, Radiation Oncology andEnvironmental Medicine at the University of Rochester Medical School, recognized for investigations into the effects ofEnvironmental Medicine at the University of Rochester Medical School, recognized for investigations into the effects ofradiation on cells and functions of the lung.radiation on cells and functions of the lung.
Jeffrey Friedman, M.D.,Diplomat, American Board of Cosmetic Surgery, American Board of OtolaryngologyDiplomat, American Board of Cosmetic Surgery, American Board of OtolaryngologyHead and Neck Surgery, Fellow of the American Academy of Cosmetic Surgery.Head and Neck 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 theUniversity of Pittsburgh School of Medicine faculty member of theDermatology and Immunology departments and director of Cutaneous Biology Laboratories and Education, publishedDermatology and Immunology departments and director of Cutaneous Biology Laboratories and Education, publishedextensively on the role dendritic cells and their precursors play in stimulating immune responses.extensively on the role dendritic cells and their precursors play in stimulating immune responses.
Susan E. Leeman, Ph.D, Professor in the Department of Pharmacology and Experimental Therapeutics atProfessor in the Department of Pharmacology and Experimental Therapeutics atthe Boston University School of Medicine. One of the first scientists to isolate substance P in the central nervous andthe Boston University School of Medicine. One of the first scientists to isolate substance P in the central nervous andgastrointestinal systems. She was elected to the National Academy of Sciences in 1991.gastrointestinal systems. She was elected to the National Academy of Sciences in 1991.
K.A. Kelly McQueen, M.D., M.P.H., Anesthesiologist and Public Health Consultant; Infectious DiseaseAnesthesiologist and Public Health Consultant; Infectious Diseaseand Disaster Planning for U.S. Army and US Northern Combatant Command.and Disaster Planning for U.S. Army and US Northern Combatant Command.
Pranela Rameshwar, Ph.D.,Professor in the Department of Medicine, Division of Hematology/Oncology atProfessor in the Department of Medicine, Division of Hematology/Oncology atthe University of Medicine and Dentistry of New Jersey; research areas include Substance P, stem cells and cancer.the University of Medicine 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.
Current StatusCurrent Status
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Eight issued U.S. and foreign patents
At least 67 pending patent applicationsincluding:
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
Recent EventsRecent Events
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Recent EventsRecent Events
August 4, 2010 ImmuneRegen BioSciences Completes Successful Reduction of Debt
April 27, 2010 ImmuneRegen BioSciences(R) Announces Collaboration With theDepartment of Tumor Immunology of the Radboud University Nijmegen Medical Centre,the Netherlands
April 21, 2010 - ImmuneRegen BioSciences(R) Initiates Strategic Collaboration With MPIResearch to Accelerate Clinical Development of Lead Indications
March 4, 2010 - ImmuneRegen BioSciences Submits Homspera(R) for FDA Orphan DrugProduct Designation for the Treatment of Idiopathic Pulmonary Fibrosis
February 10, 2010 - Fred Hutchinson Cancer Research Center Initiates Studies onImmuneRegen BioSciences' Cancer Therapy Candidate
January 27, 2010 - National Cancer Institute Initiates Studies on ImmuneRegen
BioSciences' Vaccine Adjuvant Candidate
January 5, 2010 - ImmuneRegen BioSciences(R) Reports Additional Positive Results FromStudy of Homspera(R) in Treating Highly Pathogenic Influenza
December 14, 2009 - ImmuneRegen BioSciences'(R) Drug Candidate Homspera ConfirmsEfficacy as Cancer Vaccine Adjuvant
Questions & AnswersQuestions & Answers
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For any questions, please contact:For any questions, please contact:
Michael Wilhelm, [email protected]
Dr. Hal Siegel, CSO
Chris [email protected]
Dr. Dan [email protected]
Questions & AnswersQuestions & Answers