Document


UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
Washington, D.C. 20549
FORM 8-K

CURRENT REPORT
Pursuant to Section 13 OR 15(d) of
The Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): January 8, 2018


NewLink Genetics Corporation
(Exact name of registrant as specified in its charter)
 
 
 
Delaware
001-35342
42-1491350
(State or other jurisdiction
(Commission
(IRS Employer
of incorporation)
File Number)
Identification No.)
 
 
 
 
2503 South Loop Drive
Ames, IA
50010
(Address of principal executive offices)
(Zip Code)
 
Registrant's telephone number, including area code: (515) 296-5555
 
Not applicable
(Former name or former address, if changed since last report.)
Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instruction A.2. below):
[ ] Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)
[ ] Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)
[ ] Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))
[ ] Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).
 
Emerging growth company   o
 
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act  o






Section 8 - Other Events

Item 8.01.    Other Events.
 
On January 8, 2018, NewLink Genetics Corporation, a Delaware corporation, or the Company, issued a press release titled "NewLink Genetics Outlines 2018 Business Priorities to Support Phase 3 Pivotal Trial of Indoximod Plus PD-1 Inhibitors."
A copy of the press release and the related presentation are attached hereto as Exhibit 99.1 and 99.2, respectively, and are incorporated herein by reference.






Section 9 - Financial Statements and Exhibits
 
Item 9.01.              Financial Statements and Exhibits.
 
(d)  Exhibits.
 
Exhibit Number
 
Description
99.1
 
Press Release, dated January 8, 2018, entitled “NewLink Genetics Outlines 2018 Business Priorities to Support Phase 3 Pivotal Trial of Indoximod Plus PD-1 Inhibitors”
99.2
 
J.P. Morgan Healthcare Conference Presentation






SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
Dated:    January 8, 2018


 
NewLink Genetics Corporation
 
 
 
 
By:
/s/ John B. Henneman III
 
  John B. Henneman III
Its:
  Chief Financial Officer






INDEX TO EXHIBITS
 


Exhibit Number
 
Description
99.1
 
99.2
 





Exhibit
Exhibit 99.1


http://api.tenkwizard.com/cgi/image?quest=1&rid=23&ipage=11974856&doc=29
NewLink Genetics Outlines 2018 Business Priorities to Support Phase 3 Pivotal Trial of Indoximod Plus PD-1 Inhibitors
NewLink Genetics updates financial and clinical guidance
AMES, Iowa, January 8, 2018 -- NewLink Genetics Corporation (NASDAQ: NLNK) today announced Indigo301, the name of its upcoming Phase 3 trial of indoximod plus PD-1 inhibitors for patients with advanced melanoma, and outlined 2018 business priorities to support this trial. In addition, the company updated clinical and financial guidance and provided preliminary unaudited financial information for year-end 2017.

These updates were made in conjunction with the 36th Annual JP Morgan Healthcare Conference that begins today in San Francisco. NewLink Genetics’ Chairman and Chief Executive Officer, Charles J. Link, Jr., M.D., will discuss the Company’s continued execution of its corporate strategy and 2018 priorities as part of a live presentation on Thursday, January 11, 2018, at 11:00 AM PT/2:00 PM ET. The slide presentation with updated guidance has been posted on the Company’s website and may be found here. The oral presentation will be webcast and available on the NewLink Genetics website under the Investors & Media tab under Events & Presentations.

Indigo301 is a randomized Phase 3 study of indoximod or placebo plus KEYTRUDA® (pembrolizumab) or OPDIVO® (nivolumab) for patients with unresectable or metastatic melanoma. The choice of PD-1 inhibitors will be at the physician’s discretion, mirroring the general clinical setting. The study will consist of a planned 624 patients enrolled at approximately 100 sites in multiple countries and will include co-primary endpoints of Progression-Free Survival (PFS) and Overall Survival (OS), with a secondary endpoint of Objective Response Rate (ORR).

“NewLink has focused its business priorities on the execution of Indigo301 for patients with advanced melanoma,” said Dr. Link. “We will also initiate a randomized Phase 2 trial in collaboration with AstraZeneca for patients with metastatic pancreatic cancer, and we anticipate clinical data from additional development programs.”

To expedite the enrollment of Indigo301, NewLink Genetics has expanded the planned number of trial sites both within and outside of the US and plans several clinical recruitment initiatives to engage with the oncology community with the goal to enroll the majority of patients in 2018. As a result of these clinical planning efforts, NewLink Genetics is accordingly updating its guidance for clinical trials as follows:

Clinical Guidance and Milestones

Enroll the majority of Indigo301 trial by the end of 2018
Phase 2 results for indoximod + PD-1 blockade in advanced melanoma expected in 2018
Phase 2 results for indoximod + gem/nab-paclitaxel in pancreatic cancer expected 1H 2018
Phase 2 randomized AstraZeneca collaboration in pancreatic cancer to initiate 1H 2018




Exhibit 99.1


Financial Guidance and Outlook

“Entering 2018, we have aligned our business and investments to drive Indigo301 and other high-potential development programs,” said Jack Henneman, Executive Vice President and Chief Financial Officer for NewLink Genetics. “As we continue to progress, we remain committed to maintaining the strength of our balance sheet in support of our most promising clinical programs.”

NewLink Genetics ended 2017 with approximately $158 million in cash and cash equivalents. Updated guidance for use of cash is provided in the slide presentation available on the company’s website.

About Indoximod

Indoximod is an investigational, orally available small molecule targeting the IDO pathway. The IDO pathway is one of the key immuno-oncology targets involved in regulating the tumor microenvironment and immune escape. NewLink Genetics is currently evaluating indoximod in multiple combination studies for patients with various types of cancer including melanoma, pancreatic cancer and other malignancies.

About NewLink Genetics Corporation

NewLink Genetics is a late-stage biopharmaceutical company focusing on discovering, developing and commercializing novel immuno-oncology product candidates to improve the lives of patients with cancer. NewLink Genetics’ IDO pathway inhibitors are designed to harness multiple components of the immune system to combat cancer. Indoximod is being evaluated in combination with treatment regimens including anti-PD-1/PD-L1 agents, cancer vaccines, and chemotherapy across multiple indications such as melanoma, pancreatic cancer and other malignancies. For more information, please visit www.newlinkgenetics.com and follow us on Twitter @NLNKGenetics.

KEYTRUDA® is a registered trademark of Merck, Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc.

OPDIVO® is a registered trademark of Bristol-Myers Squibb Company.

Cautionary Note Regarding Forward-Looking Statements

This press release contains forward-looking statements of NewLink that involve substantial risks and uncertainties.  All statements contained in this press release are forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. The words “guidance,” “upcoming,” “will,” “plan,” "anticipate," "approximate," "expect," or the negative of these terms or other similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words.  These forward-looking statements include, among others, statements about NewLink Genetics' financial guidance for 2018; results of its clinical trials for product candidates; its timing of release of data from ongoing clinical studies; its plans related to moving additional indications into clinical development; NewLink Genetics' future financial performance, results of operations, cash position and sufficiency of capital resources to fund its operating requirements; and any other statements other than statements of historical fact.  Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements that NewLink makes due to a number of important factors, including those risks discussed in "Risk Factors" and elsewhere in NewLink Genetics' Annual Report on Form 10-K for the year ended December 31, 2016 and other reports filed with the U.S. Securities and Exchange Commission (SEC).  The forward-looking statements in this press release represent NewLink's views as of the date of this press release. NewLink anticipates that subsequent events



Exhibit 99.1


and developments will cause its views to change.  However, while it may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to do so.  You should, therefore, not rely on these forward-looking statements as representing NewLink Genetics' views as of any date subsequent to the date of this press release.

###

Investor Contact:
Lisa Miller
Director of Investor Relations
NewLink Genetics
515-598-2555
lmiller@linkp.com

Media Contact:
Vivian Ni
Public & Media Relations
LaVoieHealthScience
617-374-8800, ext. 109
vni@lavoiehealthscience.com



jpmorganweek2018final
NewLink Genetics Corporation NASDAQ: NLNK January 8-11, 2018 36th Annual J.P. Morgan Healthcare Conference


 
Forward-Looking Disclaimer This presentation contains forward-looking statements of NewLink that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this presentation are forward-looking statements, within the meaning of The Private Securities Litigation Reform Act of 1995. The words “anticipate,” “believe,” “estimate,” “expect,” “intend,” “may,” “plan,” “target,” “potential,” “will,” “could,” “should,” “seek” or the negative of these terms or other similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. These forward-looking statements include, among others, statements about NewLink Genetics’ financial guidance for 2017 and 2018; results of its clinical trials for product candidates; its timing of enrollment of patients and release of data from ongoing clinical studies; its plans related to moving additional indications into clinical development; NewLink Genetics’ future financial performance, results of operations, cash position and sufficiency of capital resources to fund its operating requirements; and any other statements other than statements of historical fact. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements that NewLink makes due to a number of important factors, including those risks discussed in “Risk Factors” and elsewhere in NewLink Genetics’ Annual Report on Form 10-K for the year ended December 31, 2016 and other reports filed with the U.S. Securities and Exchange Commission (SEC). The forward-looking statements represent NewLink's views as of the date of this presentation. NewLink anticipates that subsequent events and developments will cause its views to change. However, while it may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to do so. You should, therefore, not rely on these forward-looking statements as representing NewLink Genetics’ views as of any date subsequent to the date of this presentation. 2


 
NewLink Genetics Focused on Indoximod, an IDO Pathway Inhibitor  Indoleamine 2,3-dioxygenase (IDO) pathway is a key immuno-oncology target  Our leading IDO pathway inhibitor, indoximod, has a differentiated mechanism of action (MOA)  Indoximod’s unique MOA may allow effectiveness in different combinations and therapeutic settings than direct enzymatic inhibitors  Clinical data suggest indoximod combinations may enhance multiple therapeutic modalities – PD-1 checkpoint inhibitors (advanced melanoma) – Cancer vaccine (metastatic prostate cancer) – Chemotherapy (pancreatic cancer and acute myeloid leukemia)  Indoximod has the potential to improve patient outcomes across a broad range of cancers including both hematologic and solid tumor indications 3 Indoximod has been studied in more than 700 patients


 
 Launching pivotal trial (Indigo301) of indoximod plus PD-1 inhibitors for patients with advanced melanoma  Phase 2 data for indoximod (IDO) plus pembrolizumab (PD-1) suggest potential for improvement of both response rate and PFS for patients with advanced melanoma  Indoximod granted Orphan Drug Designation by the FDA for Stage IIb-IV melanoma  Phase 2 clinical collaboration with AstraZeneca to evaluate indoximod plus durvalumab plus standard-of-care chemotherapy for patients with metastatic pancreatic cancer  First patients dosed with novel salt formulation of indoximod  First patients dosed with NLG802, prodrug of indoximod  Cash and equivalents of approximately $158 million at YE 2017 4 Indoximod program made substantial progress in 2017 NewLink Genetics Highlights


 
Targeting the IDO Pathway  Indoximod – Acts directly on immune cells to reverse IDO pathway-mediated suppression  Other IDO inhibitors – Direct IDO enzymatic inhibitors such as NLG919, epacadostat and BMS-986205 block tryptophan metabolism1,2 5 Indoximod - A Unique Approach To Inhibiting the IDO Pathway IDO, indoleamine 2,3-dioxygenase; Treg, regulatory T cell; MDSC, myeloid-derived suppressor cell; CTL, cytotoxic T lymphocyte. 1Mautino M. AACR 2013. Abstract 491. 2Jochems C. Oncotarget. 2016;7(25):37762-37772. Indoximod has a differentiated mechanism of action


 
IDO Pathway Mediated Immuno-Suppression 6 Treg Activation and Effector Cell Reduction Combination data show potential to enhance multiple different treatment modalities Immuno-suppressive feedback loop dependent on multiple components Munn, D et al. Trends in Immunology. Page 12, Figure 1, March 2012. IDO KYN KYN TRP Effector T cell Regulatory T cell Effector cell suppression/anergy/death Treg activation IDO-expressing cell (DC, Mo, etc) AhR GCN2 AhR GCN2 mTOR mTOR


 
Indoximod is an IDO Pathway Inhibitor with a Differentiated MOA 7 A Proposed Mechanism with a Broad Spectrum of Potential Clinical Utility Combination data show potential to enhance multiple different treatment modalities Indoximod interrupts the IDO mediated immuno-suppressive feedback loop Indoximod MOA 1Metz R. Oncoimmunology. 2012;1(9):1460-1468; 2Holmgaard RB, et al. Cell Reports. 2015;13(2):412-424; 3Sharma MD, et al. Immunity. 2010;33(6):942-954; 4Adapted from Munn, D et al. Trends in Immunology. Page 12, Figure 1, March 2012. IDO KYN KYN TRP Effector T cell IDO-expressing cell (DC, Mo, etc) Regulatory T cell Indoximod  Orally available tryptophan mimetic1  Counteracts immunosuppressive effects of kynurenine1  Activates multiple immune cells (effector cells)2  Prevents activation of regulatory T cells (Tregs)3  Reprograms Tregs into helper T cells3 GCN2 mTOR GCN2 mTOR 4


 
Indoximod is an IDO Pathway Inhibitor with a Differentiated MOA  Orally available tryptophan mimetic1  Counteracts immunosuppressive effects of kynurenine1  Activates multiple immune cells (effector cells)2  Prevents activation of regulatory T cells (Tregs)3  Reprograms Tregs into helper T cells3 8 A Proposed Mechanism with a Broad Spectrum of Potential Clinical Utility Combination data show potential to enhance multiple different treatment modalities Indoximod interrupts the IDO mediated immuno-suppressive feedback loop Indoximod MOA 1Metz R. Oncoimmunology. 2012;1(9):1460-1468; 2Holmgaard RB, et al. Cell Reports. 2015;13(2):412-424; 3Sharma MD, et al. Immunity. 2010;33(6):942-954; 4Adapted from Munn, D et al. Trends in Immunology. Page 12, Figure 1, March 2012. IDO KYN KYN TRP Effector T cell Regulatory T cell Effector cell suppression/anergy/death IDO-expressing cell (DC, Mo, etc) AhR GCN2 AhR GCN2 mTOR mTOR 4


 
Indoximod is an IDO Pathway Inhibitor with a Differentiated MOA  Orally available tryptophan mimetic1  Counteracts immunosuppressive effects of kynurenine1  Activates multiple immune cells (effector cells)2  Prevents activation of regulatory T cells (Tregs)3  Reprograms Tregs into helper T cells3 9 A Proposed Mechanism with a Broad Spectrum of Potential Clinical Utility Combination data show potential to enhance multiple different treatment modalities Indoximod interrupts the IDO mediated immuno-suppressive feedback loop Indoximod MOA 1Metz R. Oncoimmunology. 2012;1(9):1460-1468; 2Holmgaard RB, et al. Cell Reports. 2015;13(2):412-424; 3Sharma MD, et al. Immunity. 2010;33(6):942-954; 4Adapted from Munn, D et al. Trends in Immunology. Page 12, Figure 1, March 2012. IDO KYN TRP Effector T cell IDO-expressing cell (DC, Mo, etc) AhR GCN2 mTOR 4


 
Indoximod is an IDO Pathway Inhibitor with a Differentiated MOA  Orally available tryptophan mimetic1  Counteracts immunosuppressive effects of kynurenine1  Activates multiple immune cells (effector cells)2  Prevents activation of regulatory T cells (Tregs)3  Reprograms Tregs into helper T cells3 10 A Proposed Mechanism with a Broad Spectrum of Potential Clinical Utility Combination data show potential to enhance multiple different treatment modalities Indoximod interrupts the IDO mediated immuno-suppressive feedback loop Indoximod MOA 1Metz R. Oncoimmunology. 2012;1(9):1460-1468; 2Holmgaard RB, et al. Cell Reports. 2015;13(2):412-424; 3Sharma MD, et al. Immunity. 2010;33(6):942-954; 4Munn, D et al. Trends in Immunology. Page 12, Figure 1, March 2012. IDO TRP Regulatory T cell Treg activation IDO-expressing cell (DC, Mo, etc) AhR GCN2 mTOR 4


 
Indoximod is an IDO Pathway Inhibitor with a Differentiated MOA  Orally available tryptophan mimetic1  Counteracts immunosuppressive effects of kynurenine1  Activates multiple immune cells (effector cells)2  Prevents activation of regulatory T cells (Tregs)3  Reprograms Tregs into helper T cells3 11 A Proposed Mechanism with a Broad Spectrum of Potential Clinical Utility Combination data show potential to enhance multiple different treatment modalities Indoximod interrupts the IDO mediated immuno-suppressive feedback loop Indoximod MOA 1Metz R. Oncoimmunology. 2012;1(9):1460-1468; 2Holmgaard RB, et al. Cell Reports. 2015;13(2):412-424; 3Sharma MD, et al. Immunity. 2010;33(6):942-954; 4Munn, D et al. Trends in Immunology. Page 12, Figure 1, March 2012. IDO TRP Regulatory T cell IDO-expressing cell (DC, Mo, etc) Helper T cell KYN AhR GCN2 4


 
Indoximod is an IDO Pathway Inhibitor with a Differentiated MOA  Orally available tryptophan mimetic1  Counteracts immunosuppressive effects of kynurenine1  Activates multiple immune cells (effector cells)2  Prevents activation of regulatory T cells (Tregs)3  Reprograms Tregs into helper T cells3 12 A Proposed Mechanism with a Broad Spectrum of Potential Clinical Utility Combination data show potential to enhance multiple different treatment modalities Indoximod interrupts the IDO mediated immuno-suppressive feedback loop Indoximod MOA 1Metz R. Oncoimmunology. 2012;1(9):1460-1468; 2Holmgaard RB, et al. Cell Reports. 2015;13(2):412-424; 3Sharma MD, et al. Immunity. 2010;33(6):942-954; 4Adapated from Munn, D et al. Trends in Immunology. Page 12, Figure 1, March 2012. IDO KYN KYN TRP Effector T cell Regulatory T cell Effector cell suppression/anergy/death Treg activation IDO-expressing cell (DC, Mo, etc) AhR GCN2 AhR GCN2 mTOR mTOR Helper T cell 4


 
13 Characteristic n = 51* Median age (range), yr 62.9 (27–88) Male, n (%) 34 (67) Race/Ethnicity, n (%) White, non-Hispanic† 50 (98) LDH above ULN, n (%) 12 (24) Disease stage, n (%) III 8 (16) IV 43 (84) M1a 9 (18) M1b 13 (25) M1c 21 (41) Phase 2: Baseline Demographics and Clinical Characteristics ECOG PS, Eastern Cooperative Oncology Group performance status; LDH, lactate dehydrogenase; ULN, upper limit of normal. *Excludes uveal melanoma patients. †One patient declined to answer. Characteristic n = 51* ECOG PS, n (%) 0 38 (75) 1 13 (25) Primary site, n (%) Cutaneous 40 (78) Mucosal or primary unknown 11 (22) Prior therapy, n (%) Radiation 9 (18) Systemic therapy 14 (27) None 28 (55) Indoximod (IDO) plus Pembrolizumab (PD-1) in Advanced Melanoma Zakharia Y, et al. Oral presentation at: Third International Cancer Immunology Conference; September 6-9, 2017; Frankfurt, Germany.


 
14 Phase 2: Impressive Response Rate and Progression Free Survival (N=51) *Patients that progressed due to new non-target lesions. Note: 1 patient was unevaluable for response due to pleural effusion/collapsed left lung; the patient progressed based on several new non-target lesions. Zakharia Y, et al. Oral presentation at: Third International Cancer Immunology Conference; September 6-9, 2017; Frankfurt, Germany. Response N (%) ORR 31 (61) CR 10 (20) PR 21 (41) SD 10 (20) DCR 41 (80) PD 10 (20) Significant depth of response observed in a large number of patients Survival Median PFS 12.9 months PFS at 12 months 56% Indoximod (IDO) plus Pembrolizumab (PD-1) in Advanced Melanoma


 
0 10 20 30 40 50 60 70 80 90 15 Nivolumab1 Pembrolizumab2* Ipilimumab+Nivolumab3 Indoximod+Pembrolizumab4 0 2 4 6 8 10 12 14 ORR PFS CR DCR Comparative anti-PD-1 monotherapy & anti-PD-1 + anti-PD-1 combination data provided for illustrative purposes only; no head-to-head trials conducted. *Data are for Q2W regimen. ORR, overall response rate; CR, complete response; DCR, disease control rate; PFS, progression-free survival. 1Robert C, et al. N Engl J Med. 2015;372(4): 320-330. 2Robert C, et al. N Engl J Med. 2015;372(26): 2521-2532. 3Larkin J, et al. N Engl J Med. 2015;373(1):23-34. 4Zakharia Y. Oral presentation at: Third International Cancer Immunotherapy Conference, September 6-9, 2017; Frankfurt, Germany. P e rc entag e of patient s Mo n th s Indoximod Plus PD-1 Response and Survival in Advanced Melanoma Potential to Improve Outcomes Without Added Toxicity of Ipilimumab + Nivolumab


 
16 Indoximod plus Pembrolizumab Phase 2 Patient Complete Response in Advanced Melanoma Zakharia Y, et al. Oral presentation at: Third International Cancer Immunology Conference; September 6-9, 2017; Frankfurt, Germany. After Treatment (July 2017) Before Treatment (October 2015)


 
17 Adverse Event Profile Appears Comparable to Pembrolizumab Alone Full dose combination generally well tolerated  Combination was generally well tolerated  No treatment-related Grade 4/5 adverse events reported to date  Serious Adverse Events (SAEs) led to discontinuation in only 3 patients  SAEs labelled as possibly related to indoximod reported in 4 patients  Limited immune-mediated adverse events reported regardless of attribution to treatment  No treatment-related deaths were reported Indoximod (IDO) plus Pembrolizumab (PD-1) in Advanced Melanoma Zakharia Y, et al. Oral presentation at: Third International Cancer Immunology Conference; September 6-9, 2017; Frankfurt, Germany.


 
18 • Adults ≥18 years of age with unresectable stage III or IV advanced melanoma • No prior melanoma therapy, except – BRAF/MEK inhibitor – Prior adjuvant or neoadjuvant therapy ≥4 weeks before randomization – Prior adjuvant immunotherapy (no relapse during treatment or ≤6 months of treatment discontinuation) • Stable brain metastases allowed Co-primary endpoints • Progression-free survival • Overall survival Secondary endpoint • Objective response rate • Total planned enrollment: 624 patients • ~100 sites in multiple countries • Randomization (via an interactive web randomization system) stratified by: – Choice of checkpoint inhibitor (pembrolizumab or nivolumab) – Prior BRAF/MEK therapy – M stage at randomization • Treatment until disease progression or unacceptable toxicity *Standard-of-care dosing per country. 1 :1 R a n d o m iz a tio n PD-1 checkpoint inhibitor* + indoximod orally every 12 hours PD-1 checkpoint inhibitor* + placebo orally every 12 hours A Phase 3 Study of Indoximod or Placebo Plus Pembrolizumab or Nivolumab For Patients With Unresectable or Metastatic Melanoma PATIENT POPULATION EFFICACY ENDPOINTS ENROLLMENT


 
Trial Support 19 Broad Set of Initiatives to Drive Enrollment and Expand Awareness  Launching clinical trials initiative – Physician and patient information website – Targeted online and print advertising – Patient advocacy partnerships  Deploying field based medical affairs team in Q1:18 – Work directly with trial sites to accelerate enrollment – Facilitate patient recruitment activities at local and regional levels – Engage Key Opinion Leaders  Enlisting support from multiple industry leading experts – Additional clinical trial specialists targeting Ex US sites – Specialty accrual programs tailored to individual site needs and requirements


 
Phase 2 Randomized, Placebo Controlled Trial* of IDO plus anti-PD-L1 and Chemotherapy for Patients with Metastatic Pancreatic Cancer  Objective: Evaluate 4 drug regimen vs SOC  Planned enrollment of 200 patients  Primary Endpoint: Overall Response  Secondary Endpoints: ̶ Overall Survival ̶ Progression-Free Survival ̶ Safety  Status and Milestones ̶ First Patient 1H:18 ̶ 50/50 Cost Sharing ̶ NewLink to be study sponsor 20 * Clinical collaboration with AstraZeneca


 
Indoximod plus Standard of Care Chemotherapy Phase 1/2 for Indoximod plus Standard of Care Chemotherapy for Patients with Acute Myeloid Leukemia 21 Strong preclinical data and significant unmet need  Patients with newly diagnosed Acute Myeloid Leukemia (AML)  Surrogate efficacy endpoint being explored as potential fast to market strategy  Currently completing initial Phase 1b dose escalation EHA ’17 Abstract E-912, Emadi, et al June 23rd 2017  15 patients enrolled as of June 1, 2017  Indoximod does not appear to add significant toxicity  7/9 patients who completed treatment per protocol (>80% compliance) achieved morphologic CR  7/7 patients with CR had no evidence of minimal residual disease


 
* Burris, H et al. ASCO, June 2017. Abstract 105. ** Mautino, M et al. AACR, October 2013. Abstract 491. 22 Direct IDO1 Enzymatic Inhibitor Significant retained value and clinical development opportunity NLG919  Phase 2 ready asset  Favorable safety profile with no appreciable increase in AEs in combination with PD-L1 blockade*  Peripheral PD showed dose-dependent decreases in plasma kynurenine, consistent with systemic modulation of IDO1*  NLG919 + indoximod preclinical data showed synergistic anti-tumor activity**  NewLink Genetics has worldwide rights to NLG919  Potential for development or licensing opportunities


 
NLG919 & Indoximod 23 NLG919 & Indoximod - Antitumor Activity Alone & Synergy in Combination Control Indoximod NLG919 Indoximod + NLG919 Control: pmel1 cells + gp100 vaccine + CpG + IFA Mautino, M et al; AACR Annual Meeting Poster Presentation, Abstract 491, April 7th, 2013 Indoximod differentiated MOA may demonstrate synergistic activity with direct IDO1 inhibitors


 
NewLink Genetics  Enroll the majority of Indigo301 trial by the end of 2018  Phase 2 results for indoximod + checkpoint blockade in melanoma expected in 2018  Phase 2 results indoximod + gem/nab-paclitaxel in pancreatic cancer expected 1H 2018  AstraZeneca randomized Phase 2 collaboration in pancreatic cancer to initiate 1H 2018 24 Near and Medium Term Catalysts Indoximod offers opportunity to address unmet need in multiple indications


 
Financial Position YE 2017 Cash and Equivalents1 $158 million Debt ~$0.3 million YE 2018 Cash (Projected)2 ~$75 million Forecast Quarterly Cash Use ~$20-22 million Shares Outstanding as of October 31,2017 37.1 million 25 1 Preliminary unaudited cash position at year-end 2017 2 Excludes projections of proceeds, if any, from financings not yet completed Financially well-positioned to execute our business strategy