Catalyzing Precision Medicine with Integrated Rx/Dx in Oncology

March 2015

Exhibit 99.2

Safe Harbor Statement

2

This document contains forward-looking statements, as that term is defined in Section 27A of the Securities Act of 1933 

and Section 21E of the Securities Exchange Act of 1934, about Ignyta, Inc. (“us” or the “Company”). Statements that are

not purely historical are forward-looking statements. These include statements regarding, among other things: the clinical 

and/or non-clinical data or plans underlying entrectinib or any of our other development programs; our ability to design 

and conduct development activities for entrectinib and our other development programs; our ability to develop or access 

companion diagnostics for our product candidates; our ability to obtain and maintain intellectual property protection for our 

product candidates; our ability to adequately fund our development programs; the Teva transaction serving as a 

transformative event for us and the development and market potential of the acquired assets; our ability to obtain 

regulatory approvals in order to market any of our product candidates; and our ability to successfully commercialize any 

approved products. 

Forward-looking statements involve known and unknown risks that relate to future events or the Company’s future 

financial performance, some of which may be beyond our control, and the actual results could differ materially from those 

discussed in this document.  Accordingly, the Company cautions investors not to place undue reliance on the forward-

looking statements contained in, or made in connection with, this document. 

Important factors that could cause actual results to differ materially from those indicated by such forward-looking 

statements, include, among others, the potential for results of past or ongoing clinical or non-clinical studies to differ from 

expectations or previous results; the interpretation of data from our clinical and non-clinical studies; our ability to initiate 

and complete clinical trials and non-clinical studies; regulatory developments; the potential advantages of our product 

candidates; the markets any approved products are intended to serve; and our capital needs; as well as those set forth 

under the headings “Special Note Regarding Forward-Looking Statements,” “Risk Factors” and “Management’s 

Discussion and Analysis of Financial Condition and Results of Operations” contained in the Company’s Form 10-K filed 

with the Securities and Exchange Commission (“SEC”) on March 12, 2015, and similar disclosures made in the 

Company’s Form 10-Q filings and other SEC filings and press releases. 

The forward-looking statements contained in this document represent our estimates and assumptions only as of the date 

of this document, and we undertake no duty or obligation to update or revise publicly any forward-looking statements 

contained in this document as a result of new information, future events or changes in our expectations.

Third-party information included herein has been obtained from sources believed to be reliable, but the accuracy or 

completeness of such information is not guaranteed by, and should not be construed as a representation by, the 

Company.

Contents

Ignyta and entrectinib overview

Teva transaction overview and vision

Ignyta’s acquired oncology R&D programs

Use of proceeds and milestones

3

Company History and Financial Highlights

San Diego based biotechnology company (NASDAQ: RXDX), incorporated in 2011

~60 employees: more than half with M.D.’s, Ph.D.’s or other graduate degrees

Licensed from Nerviano Medical Sciences exclusive worldwide rights to entrectinib in Oct.

2013 and RXDX-103 in Aug. 2014

Lead program entrectinib granted FDA orphan drug designation for

NSCLC, CRC and

neuroblastoma, and rare pediatric disease designation for neuroblastoma

Acquired oncology R&D pipeline of 4 clinical and preclinical assets from Teva in Mar. 2015

CLIA certified, QSR compliant diagnostic lab with multi-modality assay capabilities

Raised over $140mm between Nov. 2013 and Sept. 2014, and another

$42mm in the

transaction announced on Mar. 17, 2015

Cash, cash equivalents & marketable securities of ~$77mm at 2014YE

4

Ignyta’s vision is to catalyze precision medicine for the benefit of cancer patients

everywhere, with an integrated approach to "Rx/Dx" in oncology

Ignyta’s team has the breadth and depth of experience to successfully develop

targeted therapeutics and companion diagnostics

Ignyta’s Team

5

Senior

management

team

with

key

experience:

-

Operational performance in pharma and biotech

-

Public company corporate governance, investor relations and fundraising

-

Driving sustained increases in stockholder value

Discovery/development

teams

responsible

for

multiple

successful

programs:

-

Discovery, drug development and preclinical activities delivering programs to

the clinic

-

Clinical

programs

leading

to

regulatory

approvals

and

compelling

commercial

success

Diagnostic

team

on

the

leading

edge

of

molecular

testing:

-

QSR compliant, CLIA-registered lab

-

Support of Rx products and programs, including through the development of

novel tests using multiple platforms

Jonathan

Lim,

M.D.,

Chairman,

CEO,

and

Co-Founder.

Former

Chair,

CEO

of

Eclipse;

CEO

at

Halozyme; McKinsey; NIH post-doc at Harvard; Surgical resident at NYH-Cornell.

Jacob

Chacko,

M.D.,

Chief

Financial

Officer.

Former

Vice

President

at

TPG

Capital;

McKinsey;

Marshall Scholar at Oxford University; UCLA Med; Harvard Business School.

Zachary

Hornby,

Chief

Operating

Officer.

Former

Senior

Director

of

Business

Development

at Fate

Therapeutics; Director of BD at Halozyme; L.E.K. Consulting; Harvard Business School.

Pratik

Multani,

M.D.,

Chief

Medical

Officer.

Former

CMO

at

Fate;

VP,

Clinical

Development

at

Kalypsys; CMO at Kanisa; VP, Clinical Development at Salmedix (sold to Cephalon); Sr. Director of

Medical Research at Biogen Idec; MD, MS at Harvard; Residency, MGH; Oncology, Dana Farber.

Robert Wild, Ph.D., Chief Scientific Officer.

Former CSO, Oncology Research/Drug Discovery at Eli

Lilly; Sr. Dir., Oncology Research at OSI Pharma; BMS; SUGEN. Has contributed to multiple

discovery/preclinical/translational programs, including Tarceva,

Erbitux, Sprycel and Sutent.

Matt

Onaitis,

General

Counsel

and

Secretary.

Former

GC

at

Trius

and

Somaxon;

Associate

GC

at

Biogen Idec; Director of Legal Affairs at Elan; Stanford Law School.

Senior Management Team

6

Ignyta’s Pipeline

Pre-Teva Transaction

7

1

In-licensed from Nerviano Medical Sciences (NMS)

Entrectinib

Next Generation Kinase Inhibitor

Potent

inhibitor

of

5

oncogenic

driver

targets:

In

two

Phase

1/2

studies

(Ph

1

dose

escalation

ongoing)

with

multiple

future “pipeline in a product”

opportunities

Licensed

from

Nerviano

Medical

Sciences,

former

Pharmacia

oncology

discovery site with 40 year history in kinase inhibitors

Composition

of

matter

patent

issued

in

the

US

and

allowed

in

Europe,

with commercial protection out to 2029 (excluding patent term

extension)

8

Target

TrkA

TrkB

TrkC

ROS1

ALK

IC50 (nM)

1.7

0.1

0.1

0.2

1.6

Entrectinib Clinical Development Overview: STARTRK Program

(“Studies

Targeting

Alterations

Responsive

to

Targeted

Receptor

Kinase”

inhibition)

9

Global Phase 1/2 study in U.S., EU and Asia

Note: RP2D = Recommended Phase 2 Dose

NTRK3+

cohort

ALKA-372-001

Phase 1 dose

escalation study of

intermittent dosing

schedule in Italy:

20-30 cancer

patients with TrkA,

ROS1 or ALK

alterations

ROS1+

cohort

ALKi

naive

cohort

NTRK1+

cohort

ALKi

treated

cohort

NTRK2+

cohort

STARTRK-2 and Beyond

STARTRK-1

“Basket trial”

expansion cohorts in 100

patients with NTRK1, NTRK2, NTRK3, ROS1

or ALK molecular alterations, treated with

RP2D

Dose escalation of daily continuous dosing

schedule in 6-24 patients with Trk, ROS1 or

ALK molecular alterations

Accelerated approval

and/or breakthrough

therapy designation

possible

Pivotal registration

studies in most

promising tumor

types and targets

Entrectinib: Ongoing Clinical Development

10

Note: RP2D = recommended phase 2 dose

Data as of ESMO September 2014

Dose

Break

1

2

3

4

Week

Schedule A: PO, QD (4 on, 3 off) x 3 weeks, fasting

Dose

Break

1

2

3

4

Week

Schedule C: PO, QD (4 on, 3 off) x 4 weeks, fed

Dose

1

2

3

4

Week

Schedule B: PO, QD, fed

ALKA Study

STARTRK-1 Study

Dose

1

2

3

4

Week

Schedule A: PO, QD, fed

Dose Cohorts

(mg/m²):

100->200->400->

800->1200->1600

(no longer enrolling)

200->…

(ongoing)

400->…

(ongoing)

100->…

(ongoing)

RP2D

Tumor type

(Alteration)

Dose

(mg/m²)

Treatment Cycles / Months

Best

Response

2

4

6

8

10

12

14

16

18

20

22

24

Neuroblastoma

(ALK)

200

400

800

1200

PR

NSCLC

(ALK)

200

400

800

SD

Pancreatic

(ROS1)

400

800

SD

NSCLC

(ALK)

1200

800

PR

NSCLC

(ROS1)

1200

PR

CRC

(TrkA)

1600

PR

NSCLC

(ROS1)

400**

PR

NSCLC

(ROS1)

400***

CR*

PD at C11

PD at C4

11

*  Unconfirmed / **  All PRs were Sch. A except 1 patient with ROS1+ NSCLC in Sch. C / ***  CR was Sch. C

Note: 17 patients had progressive disease, 3 of whom were dosed at 100 mg/m

2

(sub-therapeutic), 3 of whom had

gene deletions (not thought to be tumor-activating), and 1 of whom did not have a relevant molecular alteration

Timing of PR

Timing of CR

Observed Clinical Responses in Patients with Each of TrkA, ROS1

and ALK, in Each of CRC, NSCLC and Neuroblastoma

Note: Data as of ESMO September 2014 poster discussion

12

Clinical Sites

Specimens

•

GXP

•

CLIA

Platforms

Output

FFPE

Fresh Tissue

FISH

IHC

PCR

NGS

Oncolome®

Trial Enrollment

CDx

Ignyta’s Dx Capabilities Enable Leadership

in Precision Medicine

Central

Lab

•

CNVs

•

Splice variants

•

Mutations

•

Overexpression

•

Rearrangements

Ignyta’s Two-Pronged Approach to Generating Value from

Novel Targets and Repositioned Assets

Oncolome Mining & Pathway Mapping

13

Target Prioritization by Ignyta Oncology Team

Compound Database Screen

Drug Developer Outreach

Program /Company Selection

External Targets

Engage in discussions with

biopharma companies with

existing programs for

potential in-licensing (e.g.,

Nerviano)

Internal Targets

If no attractive clinical or

preclinical stage programs

exist for target of interest,

then initiate Spark discovery

program (e.g., Spark-1)

Drug Candidate Diligence

Deprioritized Clinical Assets

Oncology assets developed

without a biomarker strategy;

failed due to lack of sufficient

efficacy; or were deprioritized

for strategic reasons

Asset(s) repositioned by

Ignyta with biomarker

strategy(ies)

Ignyta and entrectinib overview

Ignyta’s acquired oncology R&D programs

Use of proceeds and milestones

14

Teva transaction overview and vision

Contents

Teva Transaction:

Ignyta Has Acquired Additional Oncology R&D Assets to

Transform Precision Oncology Pipeline

15

•

Teva kicked off process in late 2014 to sell or spin

out Oncology R&D assets

•

Ignyta emerged as Teva’s preferred option due to

breadth and depth of precision oncology expertise

•

Parties signed and announced Ignyta’s acquisition

of the bulk of Teva’s Oncology R&D franchise on

Tue., 3/17/15

Ignyta Deal Rationale:

Pipeline Synergy -

Closing the Strategic Loop

16

•

Compelling, long-

term

•

Senior team and key

employees assembled

•

Build critical mass of

assets with strong

strategic alignment

•

Rx R&D and CLIA Lab

in place

Vision

People

Resources

Assets

Teva’s Oncology R&D Assets Acquired by Ignyta

Asset

Description

Stage

RXDX-105

(CEP-32496)*

Potent small molecule inhibitor of BRAF, EGFR and RET,

with multiple FIC and BIC targeted opportunities in mCRC,

NSCLC, and other solid tumors

Phase I/II

dose

escalation

RXDX-106

(CEP-40783)*

Potent, highly selective pseudo-irreversible inhibitor of AXL

and cMET with FIC/BIC opportunities in NSCLC failing EGFR

inhibitor therapy; pseudo-irreversibility enables prolonged

target inhibition

Late-stage

preclinical

RXDX-107

(CEP-40125)

Nanoformulation of a modified bendamustine with potential

activity in solid tumors

Late-stage

preclinical

RXDX-108

(TEV-44229)**

FIC potent, selective inhibitors of the atypical kinase PKCiota,

enabling targeting of PKCiota amplified squamous NSCLC, K-

RAS mutant CRC, NSCLC and PDAC

Preclinical

17

*  Originally a Cephalon/Ambit program

** Collaboration with Cancer Research Technology (UK)

NOTE:

BIC = best-in-class

FIC = first-in-class

mCRC = metastatic colorectal cancer

NSCLC = non-small cell lung cancer

PDAC = pancreatic ductal adenocarcinoma

Ignyta –

Teva Transaction (1 of 2)

Ignyta has acquired bulk of Teva’s Oncology R&D portfolio:

-

BRAF/EGFR/RET inhibitor

-

AXL/cMET inhibitor

-

Nanobendamustine

-

atypical PKCiota inhibitor program

Teva making concurrent minority equity investment in Ignyta to align

incentives

Ignyta will fund development and commercialization of these

oncology assets using existing balance sheet and proceeds from

this concurrent investment by Teva and institutional investors

No ongoing milestone or royalty obligations to Teva

18

Ignyta –

Teva Transaction (2 of 2)

1.5mm common shares

19

Ignyta

Teva

All assets relating to RXDX-105 (CEP-32496),

RXDX-106 (CEP-40783), RXDX-107 (CEP-

40125), RXDX-108 (TEV-44229)

Asset

Purchase

1.5mm common shares issued at

$10 per share

$15mm equity investment

Stock

Purchase

Equity

Financing

Ignyta raised ~$42mm total in

equity financing (including Teva’s

investment)

Post

Trans-

action

~25.2mm shares outstanding

Incremental $42mm cash

All assets relating to CEP-32496, CEP-40783,

CEP-40125, TEV-44229

3mm shares of Ignyta                    

(11.9% equity stake)

Ignyta’s Pipeline

Post-Teva Transaction

20

1

In-licensed

from

Nerviano

Medical

Sciences

(NMS);

2

Acquired

from

Teva

Pharmaceutical

Industries

Ignyta’s Precision Oncology Vision Realized:

A CRx for Each Oncogene Driver Identified by Our CDx

21

Ignyta’s Trailblaze™

Companion Diagnostic (CDx):

Multiplex assay(s) for identifying actionable oncogenes in various solid tumors

that can then be targeted with Ignyta’s pipeline of companion therapeutics (CRx)

NTRK1+

Entrectinib

ROS1+

mBRAF

RET+

cMET+

mKRAS

EGFR+

RXDX-105

RXDX-108

NTRK2+

NTRK3+

AXL+

RXDX-106

ALK+

Teva’s oncogene targets and programs

Ignyta’s first-in-class and best-in-class CRx’s

Ignyta Pipeline Now Has Potential to Address

More than 80% of Known Oncogenic Drivers in NSCLC

22

entrectinib

RXDX-105

RXDX-106

RXDX-108

Gerber et al., 2014 ASCO Educational Book.

Ignyta’s Targeted Agents Have Potential Activity in

Majority of Genetic Alterations in NCCN Guidelines for NSCLC

23

Note: NCCN Guidelines Version 4.2015 states that ALK positive NSCLC patients intolerant to crizotinib may be switched to ceritinib

Ignyta Targeted Agent

RXDX-105, RXDX-106

entrectinib

--

RXDX-105

RXDX-106

entrectinib

RXDX-105

Driver Oncogenes in Just 2 Solid Tumor Indications Represent

Substantial Market Opportunities for Two Lead Programs

>30,000 NSCLC or CRC patients

in the US each year have a newly detected known oncogenic

fusion kinase or activating mutation that may be targeted by entrectinib or RXDX-105

24

NTRK1

fusions

NTRK2

fusions

NTRK3

fusions

ROS1

fusions

ALK

fusions

RET

fusions

BRAF

fusions

BRAF

mutations

Total

Patients

NSCLC

~1%

<1%

<1%

1-2%

4-7%

2%

<1%

1-3%

12,400

Colorectal

~1%

<1%

<1%

~1%

~1%

~1%

5-10%

18,000

Total

2,300

500

1,500

2,100

6,400

3,200

1,900

12,500

30,400

entrectinib:

12.8k pts

RXDX-105:

17.6k pts

Source: NCI; NHS; Shaw et al., Nature Reviews Cancer 2013; Gerber et al., 2014 ASCO Educational Book; Stransky et al., Nature

Communications

2014;

Wiesner

et

al.,

Nature

Communications

2014;

Lipson

et

al.,

Nature

Medicine

2012;

unpublished communications with

study authors

Note: Estimates above based on US incidence only; assumed midpoint of incidence ranges multiplied by published incidence data for each indication.

Indication

|

Alteration

Driver Oncogenes in Just 2 Solid Tumor Indications Represent

Substantial Market Opportunities for Two Lead Programs

25

NTRK1

fusions

NTRK2

fusions

NTRK3

fusions

ROS1

fusions

ALK

fusions

RET

fusions

BRAF

fusions

BRAF

mutations

Total

Patients

NSCLC

~1%

<1%

<1%

1-2%

4-7%

2%

<1%

1-3%

4,200

Colorectal

~1%

<1%

<1%

~1%

~1%

~1%

5-10%

7,300

Total

2,300

500

1,500

700

1,400

3,200

1,900

-

11,500

entrectinib:

6.4k pts

RXDX-105:

5.1k pts

We

estimate

over

11,000

patients

in

11

biomarker

positive

cohorts

of NSCLC and

CRC

represent

potential

FIC

opportunities

for

entrectinib

or

RXDX-105

Source: NCI; NHS; Shaw et al., Nature Reviews Cancer 2013; Gerber et al., 2014 ASCO Educational Book; Stransky et al., Nature

Communications

2014;

Wiesner

et

al.,

Nature

Communications

2014;

Lipson

et

al.,

Nature

Medicine

2012;

unpublished

communications

with

study

authors

Note: Estimates above based on US incidence only; assumed midpoint of incidence ranges multiplied by published incidence data for each indication.

FIC opportunity

Indication | Alteration

Driver Oncogenes in Just 2 Solid Tumor Indications Represent

Substantial Market Opportunities for Two Lead Programs

26

FIC opportunity

BIC upside opportunity

BIC BRAF-mutant metastatic CRC doubles the addressable market with upside

of

>10,000

patients

for

RXDX-105,

or

>22,000

patients

for

entrectinib

and RXDX-105

NTRK1

fusions

NTRK2

fusions

NTRK3

fusions

ROS1

fusions

ALK

fusions

RET

fusions

BRAF

fusions

BRAF

mutations

Total

Patients

NSCLC

~1%

<1%

<1%

1-2%

4-7%

2%

<1%

1-3%

4,200

Colorectal

~1%

<1%

<1%

~1%

~1%

~1%

5-10%

18,000

Total

2,300

500

1,500

700

1,400

3,200

1,900

10,700

22,200

entrectinib:

6.4k pts

RXDX-105:

15.8k pts

Source: NCI; NHS; Shaw et al., Nature Reviews Cancer 2013; Gerber et al., 2014 ASCO Educational Book; Stransky et al., Nature

Communications

2014;

Wiesner

et

al.,

Nature

Communications

2014;

Lipson

et

al.,

Nature

Medicine

2012;

unpublished

communications with study authors

Note: Estimates above based on US incidence only; assumed midpoint of incidence ranges multiplied by published incidence data for each indication.

Indication | Alteration

Ignyta Clinical Development Plan (CDP):

On the Leading Edge of Precision Oncology

Teva transaction is transformative for Ignyta

-

significantly accelerates Ignyta’s goal of catalyzing precision medicine for the benefit

of cancer patients everywhere

Ignyta plans to initiate a master protocol study in NSCLC

-

STARTRK-2

anticipated

in

2H15

to

generate

clinical

POC

data

for

multiple

FIC

and

BIC opportunities in parallel

CDP has a defensible competitive advantage

-

multiple shots on goal based on broad spectrum of actionable oncogenes targeted

by Ignyta’s expanded pipeline

CDP uniquely enabled by Ignyta’s diagnostic expertise and infrastructure

-

ultimate goal is to validate our multiplex assay(s) to support the breadth of

therapeutic

options

in

our

pipeline

(i.e.,

“companion

therapeutic”

paradigm)

27

Patients with advanced NSCLC

Biopsy

Separate by molecular alteration

Molecular profile by Ignyta central lab

NTRK1+

Entrectinib

STARTRK-2 Master Protocol initiated at clinical sites globally

ROS1+

BRAF

RET+

AXL+

cMET+

EGFR+

RXDX-105

RXDX-106

NTRK2+

NTRK3+

FIC opportunities

28

Pan wild type

RXDX-107

BIC opportunities

mKRAS

RXDX-108

tudies   argeting    lterations    esponsive to   argeted    eceptor    inase inhibition in NSCLC

S

T

A

R

T

R

K

Contents

Ignyta and entrectinib overview

Teva transaction overview and vision

Ignyta’s acquired oncology R&D programs

Use of proceeds and milestones

29

Teva’s Lead Program: RXDX-105

First-in-Class BRAF, EGFR and RET Inhibitor

30

Has demonstrated profound and unique-in-class efficacy in preclinical

mBRAF colorectal cancer xenografts and PDX models

Phase 1 study ongoing; Phase 2 (CRC) planned for 2H15, following

recommended Phase 2 dose selection

Target product profile

-

BRAF+ locally advanced or metastatic NSCLC; upside in BRAF+ metastatic

colorectal cancer (mCRC) with EGFR feedback activation

-

RET+ NSCLC, mCRC, and/or other solid tumors

-

Improved safety profile versus currently approved BRAF and EGFR inhibitors

(e.g., QTc, epithelial hyperplasia, ophthalmologic, dermatologic, etc.)

-

Dose-sparing effects in combination regimens (e.g., irinotecan, 5-FU, MEKi)

-

Pharmacoeconomic benefits relative to doublet and triplet combination

therapies

RXDX-105 Targets Multiple Points of Receptor Tyrosine

Kinase (RTK) Oncogenic Signaling Pathways

31

Discovery Medicine; Adapted from “Thyroid carcinoma: molecular pathways and therapeutic targets”, Modern Pathology (2008) 21, S37–S43

RET is an RTK, upstream of cell signaling

pathways such as MAPK & PI3K

Well known EGFR / KRAS / BRAF /

MAPK signaling pathway

RXDX-105

BRAF-EGFR Biology / MOA Rationale

32

CRC

NSCLC

Well documented that blocking

only EGFR or

BRAF is suboptimal

Potential therapeutic value of dual

EGFR / BRAF blockade?

RXDX-105 Has Equivalent Cellular Potency against

BRAF, EGFR and RET, and No Off Target VEGFR2 Activity

33

Ligand-stimulated Kinase Target

Biochemical Target Inhibition in Human Cells

IC

50

(nM) [Cell Line]

B-RAF

V600E

60 [Colo205] –

84 [A375]

EGFR

65 –

80 [A431]

RET

60 [TT-1]

Abl (h); Bcr-Abl (h)

39 –

70 [K562]

VEGF-R2 (h)

>1000

[HUVEC]

VEGF-R1

>5000

[HUVEC]

Lck (h)

800 [Jurkat]

C-KIT (h)

>1000 [A431]

RXDX-105 Demonstrates Superior Anti-Tumor Activity vs. Vemurafenib

in mBRAF and wtBRAF Primary Human Melanoma & CRC Tumorgrafts

34

Significant efficacy against broad range of melanoma and CRC tumorgrafts with varying

BRAF mutations. Superior efficacy versus vemurafenib in 9 of 15 chemo-resistant

melanoma and 7 of 7 CRC tumorgrafts

RXDX-105 treated

Vemurafenib treated

RXDX-105 Demonstrates Superior Efficacy versus

Vemurafenib and Dabrafenib in BRAF-Driven Models of CRC

35

CCR-014: BRAF mt (V600E) CRC PDX model

ST201: BRAF mt (D594G) CRC PDX model

vs. vemurafenib

vs. dabrafenib

Study 1105: Phase 1/2 Study

36

Phase 1/2 Study: Dose escalation to determine RP2D followed by

single cohort expansion

Phase 1: Conventional 3+3 dose escalation to determine

MTD/RP2D

All histologies

No patient selection based on mutational status

Phase 2: Proof-of-concept expansion anticipated to begin in

2H15

Relapsed/refractory,

BRAF

V600E

or

D

colorectal

cancer

BRAF inhibitor naïve

Single stage: n = 33 subjects

RXDX-105 Single Agent Differentiation

37

Features

Benefits

•

Dual MOA

•

PK

•

Response rate

•

Tumor types

•

Adoption

•

Improved AE

profile

•

Fewer complaints

•

Compliance,

Efficacy

•

Dual MOA

•

Lower barrier to

combo therapy

•

Price

•

Access

•

Reimbursement

Behaviors

Zelboraf et al

RXDX-105

Competitive Landscape in BRAF and RET Solid Tumors

38

*Encorafenib Ph 2 in NSCLC has been suspended

Indication

Alteration

Competitive Landscape

RXDX-105 Advantage / Potential

Positioning

NSCLC

BRAF+

•

dabrafenib +/-

trametinib and

vemurafenib single agent in early

Ph 2 for BRAF V600 mutant

NSCLC*

•

FIC in non V600 alterations

•

BIC or FIC as single agent

RET+

•

cabozantinib, vandetanib,

ponatinib, lenvatinib all in Ph 2

for RET fusion+

NSCLC

•

All four have substantial VEGFR

activity, which can be dose-

limiting relative to RET activity

•

BIC as single agent

mCRC

BRAF+

•

vemurafenib (+ panitumumab or

cetuximab and irinotecan or 5-FU)

in Ph 2

•

dabrafenib (+ panitumumab +/-

trametinib) in Ph 2 

•

encorafenib (+ cetuximab +/-

WNT974 or BYL719) in Ph 1 for

BRAF V600 mutant

CRC

•

RXDX-105 single agent could be

BIC vs. dual agent combos; or

•

RXDX-105 dual agent combo

(e.g., with chemo, MEKi, etc.)

could be BIC vs. triple agent

combo

RET+

•

no clinical studies currently

ongoing

•

Opportunity to be FIC

Program Summary: RXDX-106 (or CEP-40783)

Highly Potent, Selective Pseudo-Irreversible AXL and MET Inhibitor

39

Potent, oral and selective pseudo-irreversible Axl and cMet inhibitor with

potential to be first-in-class based on high potency and long duration of

response

Axl and cMet have been identified as key mechanisms of resistance to

EGFR-targeted therapy in NSCLC

Axl and cMet have also been involved as key targets in epithelial-

mesenchymal transition (EMT), cancer stem cell (CSC) expansion and

invasive/metastatic disease progression in multiple cancers

Primary Indications: NSCLC, relapsed or refractory to EGFR inhibitors (as

monotherapy and/or in combination); NSCLC with MET exon 14 partial

deletions

Secondary Indications: mCRC, melanoma, breast, pancreatic, gastric,

esophageal, ovarian, AML

IND targeted for 2H15

Program Summary: RXDX-107 (or CEP-40125)

Nano-Formulation of a Modified Bendamustine for Solid Tumors

40

Nanoformulation of a modified bendamustine that maintains the unique

properties of bendamustine, including non-cross-resistance to other

alkylators

Potential to expand anti-tumor activity to solid tumors due to enhanced

permeability and retention effect (EPR)

-

Preclinical models demonstrate extended plasma half-life with increased

tumor concentration

-

Demonstrates potent anti-tumor activity in multiple solid tumor patient

tumorgraft models, including in NSCLC

Extends the reach of Ignyta’s pipeline to address pan-wild type patients

(i.e., no clear oncogenic driver) across multiple solid tumor types

Potential for IND filing in 1H16

Program Summary: RXDX-108 (or TEV-44229)

First-in-Class Potent, Selective Inhibitor of Atypical Kinase PKCiota

41

Atypical PKCiota is a novel and emerging oncogenic target, essential for

mutant K-RAS signaling as well as RAS/RAF/RAC mediated signaling

downstream of oncogenic receptor TKs (e.g., cMet, EGFR, HER2)

PKCiota

has

also

been

implicated

as

an

important

mediator

of

EMT

and

CSC expansion and self-renewal signals (Notch/Wnt/Hh) driving drug

resistance

RXDX-108 is a first-in-class, oral PKCiota kinase inhibitor with favorable

drug-like properties that meet criteria for rapid candidate nomination

Targeted PKCiota therapy has potential to function as a broad, tractable

precision

medicine

approach

for

patients

with

high

unmet

medical

need

(e.g., PKCiota amplified squamous NSCLC; K-RAS mutant NSCLC, CRC and

PDAC; serous high grade ovarian and esophageal squamous cell

carcinoma)

Contents

Ignyta and entrectinib overview

Teva transaction overview and vision

Ignyta’s acquired oncology R&D programs

Use of proceeds and milestones

42

Use of Proceeds

43

Ignyta, pre-Teva transaction:

-

YE 2014 cash balance (cash, cash equivalents & available-for-sale securities)

of $76.6mm (vs. Q3 ’14 cash balance of $94.7mm)

Includes impact of $10mm milestone paid in December 2014 to NMS for entrectinib;

aside from milestone payment, cash burn of core business in Q4 ‘14 of $8.1mm (vs.

$6.9mm in Q3 ‘14) 

Funds all key 2015 clinical & development activities for entrectinib, RXDX-103 and

Spark programs

Does

not

include

the

benefit

of

$10mm

SVB

delayed

draw

term

loan

facility

available at Ignyta’s discretion after initiation of Phase 2a of STARTRK-1 trial

Ignyta, post-Teva transaction:

-

Total proceeds from current equity raise of ~$42mm

-

New funding provides additional resources for clinical & development activities

related to the Teva assets

-

Ignyta is well capitalized to execute precision oncology strategic plan with

ample runway to achieve anticipated key value inflection points

2015 –

2016 Corporate Milestones

44

2011 –

2015

Advance clinical pipeline

2016 –

2020

Commercialize RXDX

lead

2021 –

2025

Scale pipeline revenue

2026 –

2030

Drive sustainable

profitability

Leading precision

medicine

company

2030 Vision

2015 -

2016 Milestones

Obtain US orphan drug designation for at least one indication

Report clinical data from ALKA-372-001 and STARTRK-1 at ASCO, 2Q15; ESMO and/or ENA, 2H15

Implement internally developed CDx to support STARTRK-1 Ph 2a, mid-15; Dx lab CAP licensure, YE15

Identify RP2D, preferred dosing schedule for entrectinib, mid-2015; FPI in STARTRK-1 Ph 2a, 3Q15

Identify RP2D for RXDX-105, 3Q15; report clinical data at ESMO or ENA, 2H15; FPI in Study 1105 Ph 2

mBRAF mCRC, 2H15

Initiate

STARTRK-2

NSCLC

master

protocol

for

entrectinib,

RXDX-105

+/-

RXDX-106,

2H15

File

IND

for

RXDX-106

and/or

RXDX-107,

2H15

–

1H16

Report preliminary POC clinical data from STARTRK-1 Ph 2a, Study 1105 Ph 2 mBRAF mCRC, and

STARTRK-2 Ph 2 NSCLC data at AACR and/or ASCO, 2Q16; ESMO and/or ENA, 2H16

Company Highlights

45

Precision oncology company with integrated approach to Rx/Dx development 

Experienced management team, excellent track record in oncology

Pipeline

with

critical

mass

of

targeted

first-in-class

and

best-in-class

product

candidates under clinical development in oncology

Multiple potential registration-enabling studies initiating in 2015

Comprehensive diagnostic capabilities and biomarker strategies for patient

screening and confirmation

Composition of matter IP for pipeline of development candidates

Strong financial position

20-year vision to be the leading precision oncology company