Investor Presentation

January 2012 www.myrexis.com

Forward Looking Statements This presentation contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including, but not limited to statements relating to Myrexis’ corporate strategy and the attributes, expected development, and potential efficacy of our product candidates. These "forwardlooking statements" are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by these forward-looking statements. These risks and uncertainties include, but are not limited to those factors discussed under the heading "Risk Factors" contained in Myrexis’ Form 10-K, for the year ended June 30, 2011, which was filed with the Securities and Exchange Commission on September 13, 2011, as well as any updates to those risk factors filed from time to time in its Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this presentation is as of the date of the presentation, and Myrexis undertakes no duty to update this information unless required by law.

2

Investment Highlights  Robust development pipeline • Discovered and developed internally • Unmet medical needs and large market opportunities

 Three programs in development • Novel structures, distinct mechanisms of action • Potential first-in-class/best-in-class

 Active partnering strategy to maximize value  Extensive intellectual property portfolio  Strong cash position • $109.1 M at September 30, 2011 3

Development Pipeline Drug Development Candidate

Hsp90 Inhibitors

Oncology Cancer Metabolism Inhibitor

Anticipated Next Steps

MPC-3100

Completed Phase 1

Initiate Phase 2a study 1H12

MPC-0767 (Prodrug)

IND-Enabling Studies

File IND 1Q12 Conduct Phase 1 relative bioavailability study

MPC-8640

Late Preclinical

Complete IND-enabling studies Prepare IND Filing

Autoimmune Oral AntiLead MPI-0485520 Interferon Optimization Diseases

Complete lead optimization Initiate IND-enabling studies

All drug candidates discovered internally and covered by issued composition of matter patents or patent applications 4

Hsp90 Inhibitor Program Lead Candidate:

MPC-0767, novel prodrug of MPC-31001

Potential for best-in-class Issued composition of matter patent Program attributes: Structurally distinct, fully synthetic Orally bio-available, ~12h half-life Generally safe and well-tolerated Opportunity:

Multiple solid and hematological cancers

Preclinical data:

Active in all cancer models2 Wide therapeutic index

Status:

Completed Phase 1 study (MPC-3100) 3

Next steps:

Initiate Phase 2a, open MPC-0767 IND

1

5

Papac et al., AACR poster presentation 2011

2 Baichwal

et al., AACR poster presentation 2011

3

Samlowski et al., EORTC/NCI/AACR poster 2011

MPC-3100

Superior Hsp90 Inhibitor Her2+ gastric tumor xenograft 500

Tumor Volume (%)

0

44% tumor regression with MPC-3100

400

300

200

1

Vehicle 2

BIIB-021 (125 mg/kg PO)

100

5FU (100 mg/kg IP)

0

n = 10 mice/group 0

MPC-3100 (200 mg/kg PO) 0

5

10

15

20

Days

25 0 No deaths 1 One death 2 Two deaths

6

Wettstein et al., EORTC-NCI-AACR, poster presentation (2008)

MPC-3100 Phase 1 First-in-Human Study  Dose-escalation, safety and tolerability study  Inclusion criteria • Enrolled 26 patients with cancers refractory to available systemic therapies

 Primary objectives • Characterize safety and tolerability (max. tolerated dose) • Determine appropriate dose for Phase 2

 Secondary objectives • Define pharmacokinetics and pharmacodynamics • Assess antitumor activity

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Phase 1 Study Meets Key Objectives Primary  Well-tolerated, most common AEs observed • Grade 1 & 2 diarrhea, nausea, vomiting, fatigue

 Dose for Phase 2 established • AUC and Cmax similar to efficacious doses in mice

Secondary  Confirmed oral bioavailability in humans  Confirmed on-target activity; inhibits Hsp90 in humans  Dose proportional PK; mean ½-life 11.2 hours  Best clinical response was stable disease 8

Samlowski et al., EORTC/NCI/AACR poster presentation 2011

MPC-3100 Inhibits Hsp90 in Humans

400

Increasing Hsp70 induction with increasing dose and duration of MPC-3100 treatment

300 200

Cohorts 1-5

50 mg/m2

100

100 mg/m2 165 mg/m2

0

21 D ay

8 ay D

ho ur s 24

8

Pr eD 9

ho ur s

245 mg/m2

os e

Amount of Hsp70 Induced (ng/mg total protein)

Activity Biomarker: Hsp70 induction in patient PBMCs

Data from Samlowski et al., EORTC/NCI/AACR poster presentation 2011

340 mg/m2

Hsp90 Inhibitor Program: Next Steps  Initiate MPC-3100 efficacy study in 1H12 • Phase 2a in oncogene-addicted tumor population  Open IND for MPC-0767 in 1Q12 • Prodrug of MPC-3100 • Significantly improved aqueous solubility

• Eliminates need for solubilizing agent  Reduced cost  Reduced risk of side effects  Reduced tablet burden

• Anticipate streamlined Phase 1 program  Only the active drug (MPC-3100) detected in plasma  Relative Bioavailability Study to precede Phase 2a 10

Cancer Metabolism Inhibitor (CMI) Program Lead Candidate:

MPC-8640

Unique attributes:

Potent, selective Nampt inhibitor Orally bio-available, flexible dosing schedule1 Niacin enhances therapeutic index2

Opportunity:

Cancers targeted by companion diagnostics

Preclinical Data:

Tumor regression in mice Synergy with variety of chemotherapies3 (e.g. 5-FU, temozolomide, PARP inhibitors)

Status:

Preclinical IND-enabling studies ongoing

Next steps:

IND filing

1

11

Carlson et al., EORTC poster presentation 2011

2 Fleischer

et al., AACR poster presentation 2011

3

Terry-Lorenzo et al., AACR poster presentation 2011

MPC-8640: Cancer Metabolism Inhibitor  Cancer cells have very high energy needs • Survival • Growth • DNA repair

NMN

NAD

Nampt1

primary energy source

Nam

MPC--8640 MPC Inhibits NAD production

 Cancer cells are more susceptible to NAD depletion 1

12

Nicotinamide phosphoribosyltransferase (Nampt)

Striking Anti-tumor Activity Tumor Regression in HT1080 Xenograft Model MPC-8640 once daily dosing for one week 700 median tumor volume (mm3)

vehicle 600

MPC-8640 (36 mg/kg PO)

MPC-8640 causes dramatic tumor regression and durable responses following short treatment period

500 400 300 200 100 0 0

5

10

Treatment period

13

15

20

25

30

time (days)

Carlson et al., AACR-NCI-EORTC poster presentation 2011

MPC-8640: Objective Response and Cure Rates Responses Rates in HT1080 Xenograft Model

Objective Response Cure

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Carlson et al., AACR-NCI-EORTC poster presentation 2011

..................................

MTD

Treatment with MPC-8640 results in high cure rate at well tolerated doses

Potential Biomarkers for Tumor Sensitivity LOW

HIGH

NA = Nicotinic acid, Niacin, Vitamin B3

LOW 15

Development of Companion Diagnostic Niacin (Vitamin B3) Provides Alternative Pathway for NAD Synthesis Naprt1

Niacin

NaMN

NAD

 Naprt1 enzyme required to produce NAD from niacin  ~40% of all tumors are naturally Naprt1-deficient1  Simple companion diagnostic selects patients for treatment • Detects Naprt1 expression in tumors

 Niacin can selectively protect normal cells from damage • Enhances therapeutic index of Nampt inhibitors 1

16

Fleischer et al., AACR poster presentation 2011

MPC-8640: Novel Cancer Metabolism Inhibitor MPC-8640 induces tumor regressions and cures in xenograft models at well-tolerated doses  Potent, selective, orally administered small molecule inhibitor of Nampt  Reduces tumor cell NAD levels and induces cell death  Demonstrated preclinical efficacy as monotherapy or in combination with antimetabolites and alkylating agents1  Biomarkers may identify sensitive tumors

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1Terry-Lorenzo

et al., AACR poster presentation 2011

Small Molecule Oral Anti-interferon (OAI) Program Lead Candidate:

MPI-0485520 First-in-class Oral Anti-interferon

Unique attributes:

Picomolar inhibitor of novel kinases, IKKε and TBK1 Highly selective (relative to > 120 protein kinases) Orally bio-available small molecule

Opportunities:

Autoimmune diseases (RA, Lupus, Psoriasis)

Preclinical data1:

In vivo inhibition of interferon (IFN) response1 Active in rheumatoid arthritis (RA) model2

Status:

Lead optimization ongoing

Next steps:

IND-enabling studies with lead compound

1

Richards et al., ACR poster presentation 2010

2

Richards et al., EULAR poster presentation 2011

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First Small Molecule, Anti-interferon  IFN-α α and -β β • Regulators of chronic inflammation and autoimmunity

 IKKεε and TBK1 • Novel targets for inhibition of IFN-α and -β expression

OAI

 IFN-a mAbs • In development targeting pathway (psoriasis and lupus)

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X

MPI-0485520 Selectively Inhibits IFN Response IFN Pathway: IKKεε

NFκ κB Pathway: IKKα α 1000

100

10

100% Inhibition p=0.007

1

*

0.1

0.01

TNF-α α mRNA (% of Poly I:C median)

100

10

1

0.1

)

)

ly (I: C

C

Po

ly (I:

20

* interferon response gene

m g/ kg 10 0

10 0

m

g/ kg

+

+

Po

) Po ly (I : C

C ) Po ly (I:

ve hi c

le

0.01

Ve hi cl e

ISG56 mRNA (% of Poly I:C median)

1000

MPI-0485520 Efficacious in RA model Collagen-induced Arthritis Model

Disease Severity Score

20

Vehicle 100 mg/kg QD 150 mg/kg QD

15

p