BIO CEO & Investor Conference

February 14, 2012

This presentation includes forward-looking statements and predictions, including statements about potential revenue-bearing transactions, the market potential of

CBLI’s technologies and product candidates, and the potential value of pipeline products. These statements represent CBLI’s judgment as of the date of this

presentation and are subject to risks and uncertainties that could cause actual results to differ materially from those expressed in such forward-looking

statements. In particular, CBLI faces risks and uncertainties that it may not be able to sustain its business model, that revenues may be lower or expenses higher than

projected, that product sales may not increase, that development of product candidates in the Company’s pipeline may not succeed or that commercial

transactions may not go forward as planned.

The factors that could cause actual results to differ are discussed in more detail in CBLI’s filings with the Securities and Exchange Commission, including its latest

Annual Report on Form 10-K, Quarterly Reports on Form 10-Q and Current Reports on Form 8-K. These reports are available under the “Investors” tab on CBLI’s website

at www.cbiolabs.com.

Safe-Harbor

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• Broad pipeline of 9 drug candidates with multiple applications • 8 proprietary oncology products • Dual application for lead candidate as radiation countermeasure

• Opportunity for accelerated commercialization through biodefense

• Open IND for oncology trials

• Strategic partnerships with Cleveland Clinic and Roswell Park Cancer Institute

• Track record of non-dilutive grants and contracts (~$100M, including $30M conditional purchase for ARS countermeasure)

• Strong IP portfolio with over 20 patent applications worldwide, including composition of matter (granted patents in USA, Europe, Asia)

Investment Highlights

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CBLI Corporate Structure

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Basic Proprietary Concepts Behind CBLI’s Drugs

organism

Apoptosis

TumorNormal tissues

radiation

Imitating tumor antiapoptoticmechanisms: inhibition of p53

(Pifithrins) and activation of NF-kB (Protectans)

• Komarov et al., 1999. Science 285, 1733 • Burdelya et al., 2008. Science 320: 226

Necrosis, senescence, mitotic catastrophe

p53

NF-kB

bone marrow

lymphoid organs

small intestine

hair follicles

Restoring apoptosis in tumor cells by simultaneous activation of p53 and

inhibition of NF-kB (Curaxins)

• Gasparian et al., 2011. ScienceTransl Med 3(95): 95ra74

Understanding tumor mechanisms leads to new innovative approaches to cancer treatment and

normal tissue protection 5

Product Pipeline - CBLI Corporate

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Product

Research Pre-Clinical

Ph I Pivotal BLA

Protectan CBLB502

Radiation Countermeasure

Product Research Pre-

clinical Ph I Ph II Ph III

Protectan CBLB502

Direct anticancer (companion diagnostic) Supportive care in oncology

Protectan CBLB612

HSC* induction & mobilization

*HSC: hematopoietic stem cells

Product Pipeline - Incuron, LLC

Product Research Pre-

clinical Ph I Ph II Ph III

Curaxin CBLC102 (non-proprietary)

Liver cancer

Curaxin CBLC137 (proprietary)

Broad anticancer

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Product Pipeline - Panacela Labs, Inc.

Product Research Pre-

clinical Ph I Ph II Ph III

Revercom Chemo adjuvant

Mobilan Immunotherapy

Arkil Androgen Receptor Inhibitor

Antimycon Inhibitor of Myc

Oncogene

Xenomycins Anti-bacterial & Anti-fungal

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Protectan CBLB502 Radiation Countermeasure

Immunotherapy against cancer Supportive care against cancer therapy side effects

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Radiation Countermeasure Opportunity

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• Nuclear attack identified by US and global leaders as number one security threat as evidenced by Reauthorization of Pandemic All Hazards Preparedness Act

• Fukushima disaster highlights risk of nuclear industry

• Drug Profile:

• 1 intramuscular injection

• Up to 48 hrs. post exposure

• Ideal for stockpile & distribution

• There are no FDA licensed countermeasures for ARS

CBLB502 uniquely positioned as therapeutic against ARS

CBLB502 as Medical Radiation Countermeasure Origin & Mechanism of Action

• Protein of bacterial origin (flagellin) pharmacologically optimized to improve stability, decrease immunogenicity and improve production yield

• Acts through multiple mechanisms mediated by activation of pro-survival NF-kB signaling pathway via highly specific interaction with innate immunity receptor TLR5

• Selectively protects normal tissues (but not malignant tumors) from radiation induced injury

• Increases survival of stem cells and early progenitors of hematopoietic system and stimulated regeneration of different HP lineages

• Reduces radiation damage to and stimulates regeneration of crypts, villi and lamina propria of GI tract

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Unique Regulatory Process - FDA’s Animal Rule

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• Efficacy in animal models that mimic human disease, with relevant end-points

• Human safety in healthy volunteers

• Well understood mechanism of action to justify selection of objective biomarkers of efficacy

• Well understood correlation of biomarker response between animal models and human volunteers to calculate dose conversion

• Fast Track and Orphan Drug Status granted

• Robust manufacturing process with 100,000s of dose equivalents on hand

FDA pathway to approve drugs where efficacy is unethical to test in humans

Days after 6.5 Gy gamma-TBI0 10 20 30 40

% o

f su

rviv

ors

0

20

40

60

80

100

vehicle (PBS), n=8

CBLB502 @ +16h, n=12

CBLB502 @ +25h, n=10

CBLB502 @ +48h, n=12

CBLB502 Efficacy

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• N= >900 non-human primates (“NHP”s) over ~ 30 studies

• Multiple strains of mice over ~ 180 studies

• Improved survival (~20% to ~80%)

• CBLB502 reduced damage to HP and GI systems, spleen, thymus and lymph nodes = increased survival and improved quality of life

Mitigation

CBLB502 Safety in Humans

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• 150 healthy volunteers received 2-50 µg in 2 studies

• Adverse event profile is predictable and directly related to mechanism of action (short-lasting “flu-like” syndrome):

• Activation of TLR5 in cell types distinct from those targeted by agonists of other TLRs, that produce a uniquely safe, though powerful, spectrum of cytokines (G-CSF, IL-6, IL-8, IL-10)

• No induction of cytokine storm-generating cytokines

• Methodology established to determine projected human efficacious dose (based on biomarkers)

Projected efficacious dose in humans below DLT

CBLB502 Countermeasure Path to Licensure

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Completed Remaining steps

CMC

GMP process developed and tested, drug suitable for clinical trials released, 100,000s

dose equivalents on hand

Additional consistency runs

Efficacy

Data from ~1,000 primates demonstrates dramatic survival benefits and accelerated

recovery

Pivotal animal studies

Human safety

Two trials: 50-subject dose-escalation and 100-subject study completed Definitive safety study

FDA process

Open IND, Fast Track Status,

Orphan Drug Status Package preparation and

BLA submission

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Protectan CBLB502 Medical Applications

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Direct Anti-tumor Effects of CBLB502 (summary)

healthy

TLR5- tumors in liver

TLR5+ tumors in liver

TLR5+ tumors

TLR5- tumors

CB

LB5

02

No toxicity

Tumor suppression

Tumor suppression

Tumor suppression

No antitumor effect

TLR5-negative tumors

TLR5-positive tumors

CBLB502 is active against TLR5+ tumors and against TLR5+/- liver metastases

Companion diagnostic

assay in development

Direct Anticancer Efficacy of CBLB502*

Time (Days)

Me

an T

um

or

We

igh

t (m

g)

0 4 8 12 16 20 24 28 32 36 40 44 48 52Me

an

Tu

mo

r W

eig

ht

(mg

)

200

500

2000

5000

100

1000

10000

Indivadual rat bearing advanced Ward colorectal carcinoma

response to CBLB502 0.2 mg/kg/day by i.p. daily x 5

Time (Days)

0 4 8 12 16 20 24 28 32 36 40 44 48 52

Me

an

Bo

dy

We

igh

t (%

)

90

95

100

105

110

115

Rat # 1

Rat # 2

Rat # 3

Rat # 4

"Toxicity"

"Antitumor Activity"

0

CBLB502, x3 daily, 0.2 mg/kg

200

500

2000

5000

1000

10000

Control (mean)

Treated (individual animals)

* * *

CBLB502 3xdaily 0.2 mg/kg

CBLB502 as a single agent can cause complete tumor regression of Wart colon tumors in Fisher rats *

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* unpublished data

Intact

Anti-Fas

CBLB502 + anti-Fas

con

tro

l C

BLB

50

2

• CT26, TLR5-negative syngeneic colon cancer was grown as liver metastases in Balb/c mice

• Tumor growth was monitored using luminometer imager (tumors express luciferase)

CBLB502 Against Liver Metastases of Colon Cancer *

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* unpublished data

Control (no drug) CBLB502, 5hrs post injection

immunocyte infiltration

0 10 20 30 400.0

0.5

1.0

Intact (n=5)CBLB502+anti-Fas (n=9)

days

Tum

or-

free

frac

tio

n

Tumor suppressive effect of a single injection of CBLB502 is associated with tumor infiltration with immunocytes

CBLB502 Against Radiotherapy Side Effects

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Toll-like Receptor 5 Agonist Protects Mice from Dermatitis and Oral Mucositis Caused by Local Radiation: Implications for Head and Neck Cancer Radiotherapy 2

Hair follicle

Epidermis

euthanasia required at 25% weight loss

Cross sections at day 14

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CBLB502 Competitive Landscape*

Radiation Mitigation Cellerant (CLT-008) - myeloid progenitor cells targeting hematopoietic system

Aeolus (AEOL 10150) - small molecule antioxidant targeting lung and GI

Neumedicines (HemaMax) - recombinant human IL-12 targeting hematopoietic system

Onconova (ExRad) - modulator of DNA repair pathways targeting overall survival

Araim (ARA290) - short peptide interacting with tissue protective receptor targeting hematopoietic system

RxBio (Rx100) - small-molecule analog of an endogenous, pro-survival molecule targeting overall survival

MedImmune (Amifostine) – cytoprotective agent targeting xerostomia in head and neck cancer

Solgenix (SGX201) – corticosteroid targeting acute radiation enteritis

CBLB502 only known agonist of TLR5, triggering both pro-survival mechanisms & innate immune response

* Sampling compiled from public data

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Protectan CBLB612 Mobilizer of Hematopoietic Stem Cells

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CBLB612 Overview

• Synthetic proprietary derivative of Mycoplasma lipopeptide 5

• TLR2/6 agonist

• Powerful inducer and mobilizer of hematopoietic stem cells (HSCs)

• Works synergistically with G-CSF (Neupogen®) and AMD3100 (Mozobil®)

• Potential clinical applications: • mitigation of neutropenia (compromised immune system) • stem cell transplantation without aphaeresis

Synergistic effect of CBLB612, G-CSF, and AMD3100 on HSC mobilization*

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To

tal C

FC

nu

mb

er

pe

r 1

ml o

f P

B, x 1

00

0

* unpublished data

Principle efficacy assessment in Phase I = potential partnering

CBLB612 Product Development Strategy

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A Phase I safety study in healthy volunteers should enable accurate estimates of induction

and mobilization of stem cells in peripheral blood, a direct predictor of efficacy of the drug

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Curaxins Small Molecule Anticancer Therapeutics

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Curaxins

• Synthetic small molecules with proprietary structure

• Unique molecular target (FACT): simultaneous modulation of four signal transduction pathways commonly deregulated in cancer:

• Suppression of NF-kB • Activation of p53 • Suppression of Heat Shock Factor 1 • Suppression of Hypoxia Inducible Factor a

• Efficacious in a broad spectrum of preclinical tumor models

• In vivo anti-cancer efficacy demonstrated for IV and oral routes

• Lack of genotoxicity suggests safe applications including cancer prophylaxis

• $5 million prestigious Russian government Skolkovo grant awarded September 2011

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Recent Peer Review of Curaxins

• Science Translational Medicine (2011)6

“These results introduce FACT as a novel target for anticancer therapy. The

broad anti-tumor activity of curaxins, their previously unidentified mechanism

of action – which apparently does not rely on the induction of DNA damage –

and their ability to affect multiple pathways fully justify a continued effort in

evaluating them as anticancer agents that could possibly hit the clinic.”

- excerpt from accompanying Perspective by Giulio Draetta (Dana

Farber Cancer Institute) and Ronald DePinho (President, Univ. of Texas

MD Anderson Cancer Center)

• Journal of Virology (2010)7

• Cell Cycle (2009)8

• Oncogene (2009)9

Anti-tumor effect of CBLC137 in multiple human cancer xenografts in mice 6

Caki-1: renal cell carcinoma DLD-1: colon carcinoma Mel-7: melanoma PDA: pancreatic ductal adenocarcinoma * - indicates statistical significance

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Synergy of CBLC137 and known anticancer therapeutic: Activity against aggressive tumor in mice*

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CBLC137 alone

known anticancer drug alone

CBLC137 + known anticancer drug

* unpublished data

Pe

rce

nt

surv

ival

Time to Medium palpable tumor

Vehicle

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Incuron, LLC – JV for Curaxin Development

• Joint venture with BioProcess Capital Partners LLP, Moscow

• ~$15M to reach inflection points for primary molecules

• CBLI oversees mechanistic studies and formal development

• Ongoing dosing of Phase Ib trial for prototype CBLC102 in gastrointestinal and liver cancer patients in Russia

• Phase I trial with oral formulation of next generation CBLC137 in solid tumors planned for 2012 in Russia

• Optimization of IV formulation of next generation CBLC137 for future trial in US underway

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Anticancer Therapeutics & Anti-Infectives

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Panacela Labs, Inc.

• Joint venture with Open Joint Stock Company “RUSNANO”, $10B Russian Federation fund

• IP Partners: Roswell Park Cancer Institute, Cleveland Clinic, Children’s Cancer Institute Australia

• Commitment from RUSNANO: $9M received, 17M over four years, based on milestones

• Portfolio of five compounds entering formal pre-clinical development or hit-to-lead optimization

• Strategy – to accelerate human data and licensure in Russian market

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CBLI Milestones CBLB502 Defense (all in discussion) • BARDA development contract • Start of pivotal animal efficacy studies • Start of definitive safety/dose validation trial in healthy volunteers

CBLB502 Medical • Trial as single agent in advanced cancer patients (enrollment open) • Trial as supportive care in head and neck cancer patients (protocol in

development)

CBLB612 • Complete formal pre-clinical development (in process)

Incuron • Complete dosing of CBLC102 trial in Russia (enrolling) • Phase I trial of CBLC137 in Russia (IND filed) • IV formulation and pre-clinical development of CBLC137 in US (in process)

General • High profile peer reviewed publications (some submitted, others in process)

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Financial Summary

• Shares Outstanding: 35M common, 52M fully diluted

• Government Grants & Contracts support CBLB502 for defense and limited medical applications:

– Continually seeking new grants and contracts as well as modifications to existing grants and contracts to maximize availability of non-dilutive financing

• Pro forma cash at September 30, 2011: $34 million

– Recognizes $9 million investment made by Rusnano in majority owned subsidiary Panacela Labs, Inc. on October 4, 2011

• Other: – $5 million Russian government Skolkovo grant to Incuron, LLC subsidiary – $7 million milestone investment into Incuron, LLC subsidiary, pending

opening of Russian IND for clinical study of CBLC137

Yakov Kogan, PhD, MBA

Interim Chief Executive Officer

• SVP of Basic Science, Roswell Park Cancer Institute

• Former Chair, Dept. Molecular Biology at Cleveland Clinic

• 30+ issued patents

• 150+ research publications

Andrei Gudkov, PhD, D.Sci

Chief Scientific Officer

• 30 years of financial and operations management and accounting experience

• 6 years as CFO of a public biotech company

• 15 years experience in federal contracting

Michael Fonstein, PhD

President

Neil Lyons, CPA

Chief Financial Officer

Senior Management Team

• 25 years global oncology drug development experience

• Senior positions in clinical operations at CROs

• Led clinical development in several publicly traded biotech companies

Michael Kurman, MD

Chief Medical Officer

• Over 20 years of regulatory experience at large and small pharma

• Multiple successful NDAs, MAAs, sNDAs, advisory committees

Ann Hards, PhD

Executive Vice President, Regulatory Affairs and Quality Assurance

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• Former Director of Business Development at Integrated Genomics, Inc.

• Expert in technical sales and contract negotiations

• Scientist and entrepreneur

• Founder of The Fellowship for Interpretation of Genomes (FIG)

• Founder and Former CEO of Integrated Genomics, Inc. (‘97-03)

Scientific Advisory Board

George R. Stark, PhD Chairman of SAB, Member of NAS, Former Director of Lerner Research Institute of Cleveland Clinic, Scientific Advisor to Amersham and Genentech, pioneered numerous major research technologies

Inder Verma, PhD Member of NAS, Professor of Salk Institute, Founder and Scientific Advisor to Cell Genesys, Signal Pharmaceuticals, UroGenesys, Ventana Pharmaceuticals, Quark Biotech. Internationally recognized leader in cancer biology and inflammation

Bruce Blazar, MD Professor, Chair in Transplantation Immunology of University of Minnesota. Member of the FDA Advisory Committee, SAB member of BioMarin Pharmaceutical, Seattle Genetics, etc.

Board of Directors

Independent Directors

Bernard L. Kasten, MD Former CEO, SIGA Technologies David Hohn, MD Former President of Roswell Park Cancer

Institute James Antal, CPA, MBA Former CFO and CIO of Experian

Paul DiCorleto, PhD Chairman Lerner Research Institute,

Cleveland Clinic

Management

Yakov Kogan, PhD, MBA Interim CEO, Cleveland BioLabs, Inc. Michael Fonstein, PhD President, Cleveland BioLabs, Inc. Andrei Gudkov, PhD, DSci CSO, Cleveland BioLabs, Inc.

Boards

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Bibliography

1. Burdelya, et al. (2008) An agonist of toll-like receptor 5 has radioprotective activity in mouse and primate models. Science 320(5873): p. 226-230

2. Burdelya, et al. (2011) Toll-like Receptor 5 Agonist Protects Mice from Dermatitis and Oral Mucositis Caused by Local Radiation: Implications for Head-and-Neck Cancer Radiotherapy. Int. J. Radiat. Oncol. Biol. Phys., Oct.14 (e-pub ahead of print)

3. Fukuzawa et al. (2011) A TLR5 agonist inhibits acute renal ischemic failure. J Immunol. 187: 3831-9

4. Yoon et al. (2012) Structural basis of TLR5-flagellin recognition and signaling. Science (in press)

5. Singh et al. (2011) CBLB613: A TLR 2/6 Agonist, Natural Lipopeptide of Mycoplasma arginini , as a Novel Radiation Countermeasure. Radiat Res. Dec 16

6. Gasparian et al. (2011) Curaxins: Anticancer Compounds that Simultaneously Suppress NH-kB and Activate p53 by Targeting FACT. Science Transl Med 3(95):95ra72

7. Gasparian et al. (2010) Inhibition of encephalomyocarditis virus and poliovirus replication by quinacrine: implications for the design and discovery of novel antiviral drugs. J.Virol. 84 (18): 9390-7

8. Neznanov et al. (2009) Anti-malaria drug blocks proteotoxic stress response: anti-cancer implications. Cell Cycle 8(23):3960-70

9. Guo C. et al. (2009) 9-Aminoacridine-based anticancer drugs target the PI3K/AKT/mTOR, NF-kappaB and p53 pathways. Oncogene 28(8): 1151-61

10. Draetta GF, Depinho RA. (2011) Cancer drug discovery faces the FACT. Science Transl Med. 3(95):95ps34

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