8-K

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): October 28, 2019

DECIPHERA PHARMACEUTICALS, INC.

(Exact name of registrant as specified in its charter)

Delaware	001-38219	30-1003521
(State or other jurisdiction of Incorporation)	(Commission File Number)	(IRS Employer Identification Number)
200 Smith Street Waltham, MA		02451
(Address of registrant’s principal executive office)		(Zip code)

(781) 209-6400

(Registrant’s telephone number, including area code)

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:

☐ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 203.425)

☐ 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))

Title of each class	Trading Symbol	Name of exchange on which registered
Common Stock, $0.01 Par Value	DCPH	The Nasdaq Global Select Market

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 or Rule 12b-2 of the Securities Exchange Act of 1934.

Emerging growth company  ☒

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.  ☒

Item 7.01. Regulation FD Disclosure.

On October 28, 2019, Deciphera Pharmaceuticals, Inc. (the “Company”) issued a press release announcing updated data for two of its programs, namely (1) its Phase 1b/2 study of rebastinib (DCC-2036) in combination with paclitaxel: preliminary safety, efficacy, pharmacokinetics and pharmacodynamics in patients with advanced or metastatic solid tumors and (2) preclinical studies with DCC-3116, an ULK kinase inhibitor designed to inhibit autophagy as a potential strategy to address mutant RAS cancers. The data were presented on October 28, 2019 in poster sessions at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics being held October 26-30, 2019 in Boston, MA (the “Triple Meeting”). A copy of the press release is furnished as Exhibit 99.1 to this Current Report on Form 8-K, and a copy of the presentations are furnished as Exhibit 99.3 and Exhibit 99.4 to this Current Report on Form 8-K.

On October 29, 2019, the Company issued a press release announcing updated data for two of its programs, namely (1) updated results of its phase 1 study of ripretinib (DCC-2618), a broad-spectrum KIT and PDGFRA inhibitor, in patients with gastrointestinal stromal tumor (GIST) by line of therapy (NCT02571036) and (2) its Phase 1 study of DCC-3014, an oral inhibitor of CSF1R, to assess the safety, tolerability, pharmacokinetics, and pharmacodynamics in patients with advanced solid tumors, including diffuse-type tenosynovial giant cell tumor. The data were presented on October 29, 2019 in poster sessions at the Triple Meeting. A copy of the press release is furnished as Exhibit 99.2 to this Current Report on Form 8-K, and a copy of the presentations are furnished as Exhibit 99.5 and Exhibit 99.6 to this Current Report on Form 8-K.

The furnishing of the attached press releases and presentations is not an admission as to the materiality of any information therein. The information contained in the press releases and the presentations is summary information that is intended to be considered in the context of more complete information included in the Company’s filings with the U.S. Securities and Exchange Commission, or the SEC, and other public announcements that the Company has made and may make from time to time by press release or otherwise. The Company undertakes no duty or obligation to update or revise the information contained in this report, although it may do so from time to time as its management believes is appropriate. Any such updating may be made through the filing of other reports or documents with the SEC, through press releases or through other public disclosures. For important information about forward looking statements, see the “Cautionary Note Regarding Forward-Looking Statements” section of the press releases in Exhibit 99.1 and Exhibit 99.2 attached hereto.

The information in this Item 7.01 of this Current Report on Form 8-K and Exhibit 99.1, Exhibit 99.2, Exhibit 99.3, Exhibit 99.4, Exhibit 99.5 and Exhibit 99.6 attached hereto shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended, or otherwise subject to the liabilities of that section or Sections 11 and 12(a)(2) of the Securities Act of 1933, as amended. The information contained in this Item 7.01 and in the press releases attached as Exhibit 99.1 and Exhibit 99.2 to this Current Report and in the presentations attached as Exhibit 99.3, Exhibit 99.4, Exhibit 99.5, Exhibit 99.6 to this Current Report shall not be incorporated by reference into any filing with the SEC made by the Company, whether made before or after the date hereof, regardless of any general incorporation language in such filing, except as expressly set forth by specific reference in such filing.

Item 9.01 Financial Statements and Exhibits.

(d) Exhibits.

Exhibit     No.	Description
99.1	Press Release issued by Deciphera Pharmaceuticals, Inc. on October 28, 2019, furnished herewith.
99.2	Press Release issued by Deciphera Pharmaceuticals, Inc. on October 29, 2019, furnished herewith.
99.3	Presentation from October 28, 2019, furnished herewith.
99.4	Presentation from October 28, 2019, furnished herewith.
99.5	Presentation from October 29, 2019, furnished herewith.
99.6	Presentation from October 29, 2019, furnished herewith.

2

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.

Date: October 29, 2019	DECIPHERA PHARMACEUTICALS, INC.
	By:	/s/ Steven L. Hoerter
		Steven L. Hoerter
		President and Chief Executive Officer

3

EX-99.1

Exhibit 99.1

Deciphera Pharmaceuticals Presents Data from Rebastinib and DCC-3116 Programs at the

AACR-NCI-EORTC International Conference on Molecular Targets and Cancer

Therapeutics

- Combination of Rebastinib and Paclitaxel Exhibited Encouraging Preliminary Anti-tumor Activity

Across Treatment Arms in the Ongoing Phase 1b/2 Clinical Study -

- DCC-3116 Represents a Differentiated Approach to Autophagy Inhibition and a First-in-Class

Opportunity for a New Therapeutic Modality in Mutant RAS Cancers -

Waltham, MA – October 28, 2019 – Deciphera Pharmaceuticals, Inc. (Nasdaq:DCPH), a clinical-stage biopharmaceutical company addressing key mechanisms of tumor drug resistance, today presented data from its ongoing Phase 1b/2 clinical study of rebastinib, an oral TIE2 kinase inhibitor, in combination with paclitaxel at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics in Boston. In addition, the Company also presented data from preclinical studies of DCC-3116, a potential first-in-class autophagy inhibitor to treat mutant RAS cancers.

“Both of these datasets highlight the broad applicability of Deciphera’s kinase switch control platform and our potential to address unmet needs in oncology,” said Matthew L. Sherman, M.D., Executive Vice President and Chief Medical Officer of Deciphera. “We look forward to continuing Part 2 of our Phase 1b/2 study of rebastinib in combination with paclitaxel with the insights garnered from Part 1 of the study. We also look forward to advancing the IND-enabling studies for DCC-3116.”

Rebastinib

The Phase 1b/2 study of rebastinib in combination with paclitaxel is a two-part, open-label, multicenter study assessing the safety, tolerability, anti-tumor activity and pharmacokinetics of multiple doses of rebastinib in patients with advanced or metastatic solid tumors. Data presented today are from 43 patients from Part 1 of the study, including 24 patients from the rebastinib 50 mg oral twice a day (BID) with paclitaxel 80 mg/m² IV cohort and 19 patients from the rebastinib 100 mg oral BID with paclitaxel 80 mg/m² IV cohort. Preliminary results from Part 1 included:

• Encouraging preliminary anti-tumor activity was observed in both dose cohorts, with objective responses seen across a heavily pre-treated patient population, including patients with prior exposure to paclitaxel. Objective responses were seen in eight patients including ovarian (3), breast (2), carcinosarcoma (2), and peritoneal mesothelioma (1), seven of whom had prior therapy with paclitaxel or docetaxel. A best response of partial response (PR) was observed in 5 of 24 patients in the 50 mg BID dose cohort and 3 of 19 patients in the 100 mg BID dose.

• Exposure to rebastinib was dose-proportional at the 50 mg BID and 100 mg BID doses when given in combination with paclitaxel.

• Mean circulating Ang-2 levels increased with exposure to higher doses of rebastinib in combination with paclitaxel, indicating TIE2 inhibition.

• Rebastinib in combination with paclitaxel was generally well-tolerated, with similar frequency of treatment-emergent adverse events (TEAEs) between the two dose cohorts, and most TEAEs were consistent with first-in-human studies of rebastinib or known to be associated with treatment with paclitaxel.

• Based on the observed frequency of muscular weakness in preliminary data from the ongoing Part 2 portion of the study with the 100 mg BID dose, the recommended phase 2 dose (RP2D) was changed to 50 mg BID.

DCC-3116

DCC-3116 is designed as a potential autophagy inhibitor by selectively targeting ULK kinase. Autophagy is a cellular pathway that has been shown to be upregulated in mutant RAS cancers and that also mediates resistance to inhibitors of the RAS signaling pathway. Subject to favorable investigational new drug (IND)-enabling studies and filing and activation of an IND application, Deciphera intends to develop DCC-3116 for the potential treatment of mutant RAS cancers in combination with inhibitors of downstream effector targets including RAF, MEK, or ERK inhibitors (MAPK inhibitors) as well as with direct inhibitors of mutant RAS. Preclinical data presented today included the following:

• DCC-3116 was shown to be a potent, selective, and tight-binding inhibitor of ULK kinase.

• DCC-3116 inhibited phosphorylation of the ULK substrate ATG13 in cancer cells and exhibited synergy in vitro in combination with MAPK inhibitors in inhibiting cancer cell growth.

• Oral doses of DCC-3116 led to sustained inhibition of ULK activity as shown by the inhibited phosphorylation of the ULK substrate ATG13 in vivo.

• DCC-3116 exhibited synergy with MAPK inhibitors in tumor growth inhibition in mouse models.

A copy of each poster presentation is available at www.deciphera.com.

About Rebastinib

Rebastinib is an investigational, orally administered, potent and selective inhibitor of the TIE2 kinase, the receptor for angiopoietins, an important family of vascular growth factors in the tumor microenvironment that also activate pro-tumoral TIE2 expressing macrophages. In a Phase 1 clinical study, biomarker data have demonstrated rebastinib-induced increases in the TIE2 ligand angiopoietin 2, providing evidence of TIE2 inhibition. Rebastinib is currently being evaluated in a Phase 1b/2 clinical study in combination with paclitaxel (NCT03601897) and in a Phase 1b/2 clinical study in combination with carboplatin (NCT03717415).

About DCC-3116

DCC-3116 is a potential first-in-class small molecule designed to inhibit cancer autophagy, a key tumor survival mechanism, by inhibiting the ULK kinase. Subject to favorable investigational new drug (IND)-enabling studies and filing and activation of an IND application, expected in mid-2020, Deciphera intends to develop DCC-3116 for the potential treatment of mutant RAS cancers in combination with inhibitors of downstream RAS effector targets including RAF, MEK, or ERK inhibitors as well as with direct inhibitors of mutant RAS.

About Deciphera Pharmaceuticals

Deciphera Pharmaceuticals is a clinical-stage biopharmaceutical company focused on improving the lives of cancer patients by addressing key mechanisms of drug resistance that limit the rate and/or durability of response to existing cancer therapies. Our small molecule drug candidates are directed against an important family of enzymes called kinases, known to be directly involved in the growth and spread of many cancers. We use our deep understanding of kinase biology together with a proprietary chemistry library to purposefully design compounds that maintain kinases in a “switched off” or inactivated conformation. These investigational therapies comprise tumor-targeted agents designed to address therapeutic resistance causing mutations, immuno-targeted agents designed to control the activation of immunokinases that suppress critical immune system regulators, and agents designed to inhibit reprogramming of cancer cell

metabolism. We have used our platform to develop a diverse pipeline of tumor-targeted, immuno-targeted, and metabolism-targeted drug candidates designed to improve outcomes for patients with cancer by improving the quality, rate and/or durability of their responses to treatment.

Cautionary Note Regarding Forward-Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, including, without limitation, statements regarding our expectations regarding the broad applicability of our kinase switch control platform, the potential of our drug candidates to address unmet needs in oncology, continuation of Part 2 of our Phase 1b/2 study of rebastinib in combination with paclitaxel, advancing DCC-3116 through IND-enabling studies, and the timing of the potential filing of an IND for DCC-3116, subject to favorable IND enabling studies. The words “may,” “will,” “could,” “would,” “should,” “expect,” “plan,” “anticipate,” “intend,” “believe,” “estimate,” “predict,” “project,” “potential,” “continue,” “target” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Any forward-looking statements in this press release are based on management’s current expectations and beliefs and are subject to a number of risks, uncertainties and important factors that may cause actual events or results to differ materially from those expressed or implied by any forward-looking statements contained in this press release, including, without limitation, risks and uncertainties related to the delay of any current or planned clinical studies or the development of our drug candidates, including ripretinib,.our ability to successfully demonstrate the efficacy and safety of our drug candidates including in later-stage studies, the preclinical and clinical results for our drug candidates, which may not support further development of such drug candidates, actions of regulatory agencies, any or all of which may affect the initiation, timing and progress of clinical studies and regulatory development and other risks identified in our SEC filings, including our Quarterly Report on Form 10-Q for the quarter ended June 30, 2019, and subsequent filings with the SEC. We caution you not to place undue reliance on any forward-looking statements, which speak only as of the date they are made. We disclaim any obligation to publicly update or revise any such statements to reflect any change in expectations or in events, conditions or circumstances on which any such statements may be based, or that may affect the likelihood that actual results will differ from those set forth in the forward-looking statements. Any forward-looking statements contained in this press release represent our views only as of the date hereof and should not be relied upon as representing its views as of any subsequent date. We explicitly disclaim any obligation to update any forward-looking statements.

Contacts:

Investor Relations:

Jen Robinson

Deciphera Pharmaceuticals, Inc.

jrobinson@deciphera.com

781-906-1112

Media:

David Rosen

Argot Partners

David.Rosen@argotpartners.com

212-600-1902

EX-99.2

Exhibit 99.2

Deciphera Pharmaceuticals Presents Updated Data from Ripretinib and DCC-3014 Programs at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics

- Median Progression Free Survival (mPFS) of 46 Weeks for the Second-Line Gastrointestinal Stromal Tumors (GIST) Cohort from the Phase 1 Study of Ripretinib in Patients Receiving 150 mg QD as Starting Dose -

- DCC-3014 Phase 1 Data Demonstrated Tolerability, Pharmacokinetics and Biomarker Mechanistic Proof-of-Concept in Patients with Advanced Malignancies -

Waltham, MA – October 29, 2019 – Deciphera Pharmaceuticals, Inc. (Nasdaq:DCPH), a clinical-stage biopharmaceutical company addressing key mechanisms of tumor drug resistance, today announced the presentation of updated results from its ongoing Phase 1 study of ripretinib, a broad-spectrum KIT and PDGFRα inhibitor, in patients with second-line through fourth-line plus GIST, as well as its Phase 1 study of DCC-3014, an oral inhibitor of CSF1R, in patients with advanced solid tumors. The data are being presented today at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics in Boston.

“These updated results continue to underscore the potential of our diverse pipeline of product candidates, all generated using our proprietary kinase switch control inhibitor platform, to improve the lives of cancer patients,” said Matthew L. Sherman, M.D., Executive Vice President and Chief Medical Officer of Deciphera. “Of note, we believe ripretinib continues to demonstrate strong clinical benefit in post-imatinib GIST patients, particularly in the second-line setting. These results bolster our confidence in the ongoing INTRIGUE pivotal Phase 3 clinical study, which is designed to support potential regulatory approvals in patients with second-line GIST.”

Ripretinib

Updated results from the Company’s ongoing Phase 1 study of ripretinib in patients with second-line through fourth-line plus GIST included data from 142 GIST patients receiving 150 mg of ripretinib once daily (QD) as the starting dose, which is the dose being utilized in the Company’s INVICTUS and INTRIGUE registration-enabling studies, as of an August 10, 2019 data cutoff date. The table below includes local, investigator-assessed objective response rate (ORR) by best response as determined by Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1, median duration of response, median progression free survival (mPFS) and mean treatment duration.

Line of Therapy	2nd Line (n=31)			3rd Line (n=28)			³4th Line (n=83)
ORR (confirmed responses only)		19	%		14	%		7	%
Median Duration of Response		80 weeks			NE	(1)		76 weeks
mPFS		46 weeks			36 weeks			24 weeks
Mean Treatment Duration(2)		56 weeks			58 weeks			45 weeks

 (1) NE = not estimable; (2) Includes 64 patients who elected for intra-patient dose escalation from 150 mg QD to 150 mg twice daily (BID).

Data from GIST patients receiving ³ 100 mg of ripretinib daily (n=178) in the ongoing Phase 1 study, as of an August 10, 2019 cutoff date, including 2nd line (n=37), 3rd line (n=31), and ³4th line (n=110) patients were (a) ORR (confirmed responses only): 2^nd line (22%), 3^rd line (13%), ³4^th line (7%); (b) median duration of response: 2^nd line (80 weeks), 3^rd line (NE), ³4^th line (48 weeks); (c) mPFS: 2^nd line (46 weeks), 3^rd line (40 weeks), ³4^th line (24 weeks); (d) mean treatment duration (includes 72 patients who elected for intra-patient dose escalation to 150 mg BID): 2^nd line (53 weeks), 3^rd line (54 weeks), ³4^th line (48 weeks).

Ripretinib was generally well tolerated and the updated adverse events were consistent with previously presented Phase 1 data in patients with GIST. Grade 3 or 4 treatment-emergent adverse events (TEAEs) in >5% of patients were increase in lipase level (n=25; 18%), anemia (n=11; 8%), and abdominal pain (n=11; 8%).

DCC-3014

The Company’s Phase 1 study of DCC-3014 was designed to evaluate the safety, pharmacokinetics and pharmacodynamics of multiple doses of DCC-3014 in patients with advanced solid tumors. The Company expects to present preliminary data from initial tenosynovial giant cell tumor (TGCT) patients at the 2019 Connective Tissue Oncology Society (CTOS) Annual Meeting being held November 13-16 in Tokyo, Japan.

• As of the data cut-off date of September 10, 2019, increasing doses of DCC-3014 were assessed in seven dose cohorts across 36 patients with advanced solid tumor tumors. This included one dose cohort that received 10 mg once daily and six dose cohorts that received a three to five day loading dose regimen at doses of up to 50 mg followed by a schedule of daily, once-weekly or twice-weekly maintenance dosing with DCC-3014.

• Data demonstrated dose-proportional exposure for DCC-3014 and exposure to DCC-3014 was associated with an increase in plasma CSF1 and IL-34, rapid and sustained reduction of CD16+ monocytes in peripheral blood, and substantial decreases in CD163+ macrophages in tumor.

• DCC-3014 was generally well-tolerated, with most treatment-emergent adverse events (TEAEs) Grade 1 or 2. Most common related TEAEs ³10% were fatigue (n=6;17%), diarrhea (n=4; 11%), and nausea (n=4; 11%). Grade 3 or 4 related TEAEs occurred in 4 patients, which were grade 3 aspartate aminotransferase (AST) increase, grade 4 lipase increase, grade 3 amylase increase, and grade 3 colitis. Serious adverse events were reported in 17 patients; none of which were related to DCC-3014.

• The dose escalation evaluation is ongoing to determine a recommended phase 2 dose for advanced solid tumors and diffuse-type TGCT.

A copy of each presentation is available at www.deciphera.com/science/presentation-publications/.

About Ripretinib

Ripretinib is an investigational tyrosine kinase switch control inhibitor that was engineered to broadly inhibit KIT and PDGFRα mutated kinases by using a unique dual mechanism of action that regulates the kinase switch pocket and activation loop. Ripretinib is currently in clinical development for the treatment of KIT and/or PDGFRα-driven cancers, including gastrointestinal stromal tumors, or GIST, systemic mastocytosis, or SM, and other cancers. Ripretinib inhibits initiating and secondary KIT mutations in exons 9, 11, 13, 14, 17, and 18, involved in GIST, as well as the primary D816V exon 17 mutation involved in SM. Ripretinib also inhibits primary PDGFRα mutations in exons 12, 14 and 18, including the exon 18 D842V mutation, involved in a subset of GIST. In June 2019, the U.S. FDA granted Fast Track Designation to ripretinib for the treatment of patients with advanced GIST who have received prior treatment with imatinib, sunitinib and regorafenib. For more information about the Company’s clinical trials with ripretinib, please visit www.clinicaltrials.gov.

Deciphera Pharmaceuticals has an exclusive license agreement with Zai Lab (Shanghai) Co., Ltd. for the development and commercialization of ripretinib in Greater China (Mainland China, Hong Kong, Macau and Taiwan). Deciphera Pharmaceuticals retains development and commercial rights for ripretinib in the rest of the world.

About DCC-3014

DCC-3014 is an investigational, orally administered, potent and highly selective inhibitor of CSF1R. DCC-3014 was designed using the Company’s proprietary switch control kinase inhibitor platform to selectively bind to the CSF1R switch pocket. DCC-3014 has greater than 100-fold selectivity for CSF1R over other closely related kinases and has an even greater selectivity for CSF1R over approximately 300 other human kinases. CSF1R controls the differentiation and function of macrophages including Tumor Associated Macrophages (TAMs) whose density within certain tumors including cancers of the breast, cervix, pancreas, bladder and brain correlates with poor prognosis. Tumors induce TAMs to suppress a natural immune response mediated by cytotoxic T-cells, a type of lymphocyte that would otherwise eradicate the tumor; a process known as macrophage checkpoints. Through inhibition of CSF1R, DCC-3014 has in preclinical studies demonstrated potent macrophage checkpoint inhibition as both a single agent and in combination with PD1 inhibitors. DCC-3014 is currently being evaluated in a Phase 1 clinical study. For more information about the clinical trial design please visit www.clinicaltrials.gov (NCT03069469).

About Deciphera Pharmaceuticals

Deciphera Pharmaceuticals is a clinical-stage biopharmaceutical company focused on improving the lives of cancer patients by addressing key mechanisms of drug resistance that limit the rate and/or durability of response to existing cancer therapies. Our small molecule drug candidates are directed against an important family of enzymes called kinases, known to be directly involved in the growth and spread of many cancers. We use our deep understanding of kinase biology together with a proprietary chemistry library to purposefully design compounds that maintain kinases in a “switched off” or inactivated conformation. These investigational therapies comprise tumor-targeted agents designed to address therapeutic resistance causing mutations and immuno-targeted agents designed to control the activation of immunokinases that suppress critical immune system regulators, and agents designed to inhibit reprogramming of cancer cell metabolism. We have used our platform to develop a diverse pipeline of tumor-targeted, immuno-targeted, and metabolism-targeted drug candidates designed to improve outcomes for patients with cancer by improving the quality, rate and/or durability of their responses to treatment.

Cautionary Note Regarding Forward-Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, including, without limitation, statements regarding our expectations regarding our updated Phase 1 study of ripretinib in patients with GIST to support our pivotal Phase 3 INTRIGUE study in second-line GIST patients, the potential of our pipeline drug candidates to improve the lives of patients with cancer, and the expectation to present additional data from our Phase 1 study of DCC-3014 in patients with diffuse-type tenosynovial giant cell tumor at an upcoming medical meeting. The words “may,” “will,” “could,” “would,” “should,” “expect,” “plan,” “anticipate,” “intend,” “believe,” “estimate,” “predict,” “project,” “potential,” “continue,” “target” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Any forward-looking statements in this press release are based on management’s current expectations and beliefs and are subject to a number of risks, uncertainties and important factors that may cause actual events or results to differ materially from those expressed or implied by any forward-looking statements contained in this press release, including, without limitation, risks and uncertainties related to the delay of any current or planned clinical studies or the development of our drug candidates, including ripretinib, our ability to successfully demonstrate the efficacy and safety of our drug candidates including in later-stage studies, the preclinical and clinical results for our drug candidates, which may not support further development of such drug candidates, our ability to timely complete and prepare the information

required for and file an NDA for ripretinib, our ability to manage and our reliance on third parties such as our third party drug substance and drug product contract manufacturers, actions of regulatory agencies, any or all of which may affect the initiation, timing and progress of clinical studies and the timing of and our ability to obtain regulatory approval, if at all, and make our investigational drugs available to patients, and other risks identified in our SEC filings, including our Quarterly Report on Form 10-Q for the quarter ended June 30, 2019, and subsequent filings with the SEC. We caution you not to place undue reliance on any forward-looking statements, which speak only as of the date they are made. We disclaim any obligation to publicly update or revise any such statements to reflect any change in expectations or in events, conditions or circumstances on which any such statements may be based, or that may affect the likelihood that actual results will differ from those set forth in the forward-looking statements. Any forward-looking statements contained in this press release represent our views only as of the date hereof and should not be relied upon as representing its views as of any subsequent date. We explicitly disclaim any obligation to update any forward-looking statements.

Contacts:

Investor Relations:

Jen Robinson

Deciphera Pharmaceuticals, Inc.

jrobinson@deciphera.com

781-906-1112

Media:

David Rosen

Argot Partners

David.Rosen@argotpartners.com

212-600-1902

EX-99.3

Exhibit 99.3

Phase 1b/2 study of rebastinib (DCC-2036) in combination with paclitaxel: Preliminary safety, efficacy, pharmacokinetics, and pharmacodynamics in patients with advanced or metastatic solid tumors Filip Janku,1 Michael Birrer,2 Debra Richardson,3 Christina Chu,4 Sanjay Goel,5 Gege Tan,6 Bahar Matin,6 Keisuke Kuida,6 Rodrigo Ruiz-Soto,6 Erika Paige Hamilton7 1University of Texas MD Anderson Cancer Center, Houston, TX; 2University of Alabama at Birmingham Comprehensive Cancer Center, Birmingham, AL; 3Stephenson Cancer Center/Sarah Cannon Research Institute at the University of Oklahoma Health Sciences Center, Oklahoma City, OK; 4Fox Chase Cancer Center, Havertown, PA; 5Albert Einstein College of Medicine, Bronx, NY; 6Deciphera Pharmaceuticals, LLC, Waltham, MA; 7Sarah Cannon Research Institute and Tennessee Oncology, PLLC, Nashville, TN Abstract: B055 Circulating Ang-2 significantly increased in both dose cohorts (50 and 100 mg BID) by treatment with rebastinib in combination with paclitaxel (Figure 6) Figure 6. Angiopoietin-2 induction during rebastinib treatment *P<0.05; **P<0.001. P-values are based on Wilcoxon signed-rank test. The Ang-2 level in rebastinib-treated patients was assessed by standard Luminex methods. Plasma samples were collected from patients on the first dose of rebastinib (cycle 1 day 1), cycle 1 day 15, and cycle 2 day 1. The top of the column represents the mean, error bars indicate the standard deviation, and circles and triangles are individual measurements. Ang-2, angiopoietin-2; BID, twice daily; C, cycle; D, day; SD, standard deviation. INTRODUCTION Tunica interna endothelial cell kinase (TIE2) is a cell-surface receptor tyrosine kinase that is expressed in endothelial cells and a subset of macrophages, called TIE2-expressing tumor-associated macrophages (TEMs)1,2 In endothelial cells, the angiopoietin (Ang)/TIE2 signaling axis is a key regulator of angiogenesis and vascular remodeling1,3 TEMs are pro-angiogenic and immunosuppressive and are involved in tumor intravasation and metastasis (Figure 1)2,4 Intravasation occurs at microanatomical vascular sites called the tumor microenvironment of metastasis (TMEM), which are composed of a dedicated tumor cell, a TEM, and an endothelial cell (Figure 1)2,4 Chemotherapy, despite decreasing tumor size, may increase the risk of metastasis through promoting TMEM assembly and increasing the dissemination of tumor cells5 Figure 1. Metastasis-mediated tumor cell intravasation TAM, tumor-associated macrophage; TEM, TIE2-expressing tumor-associated macrophage; TIE2, tunica interna endothelial cell kinase; TMEM, tumor microenvironment of metastasis. Rebastinib (DCC-2036) is a novel tyrosine kinase switch control inhibitor that is a potent and selective picomolar inhibitor of TIE2 kinase activity In preclinical studies, rebastinib blocked the recruitment and function of TEMs and reversed chemotherapy-induced TMEM activity5,6 Rebastinib blocked primary tumor growth, inhibited metastatic growth, and extended survival in combination with paclitaxel or eribulin in a murine breast tumor model6 An investigator-initiated phase 1 study (NCT02824575) of rebastinib in combination with paclitaxel or eribulin mesylate in metastatic breast cancer began in 2016 and is ongoing; rebastinib 100 mg twice daily (BID) was selected as the recommended phase 2 dose (RP2D)7 Two Deciphera-sponsored phase 1b/2 studies are further assessing the safety, tolerability, antitumor activity, and pharmacokinetics of rebastinib in combination with paclitaxel (NCT03601897) or carboplatin (NCT03717415) in patients with advanced or metastatic solid tumors Here, we present data from the dose-escalation phase (Part 1) of the study of rebastinib in combination with paclitaxel METHODS Part 1 enrolled adults with locally advanced/metastatic solid tumors into 1 of 2 rebastinib dose cohorts (50 mg BID or 100 mg BID) using a parallel cohort design (Figure 2; Table 1 and 2) Figure 2. Overall study design Rebastinib 50 mg oral BID Paclitaxel 80 mg/m2 IV on Day 1, 8, and 15 of 28-day cycle 50-mg BID cohort Rebastinib 100 mg oral BID Paclitaxel 80 mg/m2 IV on Day 1, 8, and 15 of 28-day cycle 100-mg BID cohort Parallel cohort design Continue 28-day cycles until progression, toxicity, or withdrawal Determine RP2D At least 15 patients in a cohort have completed 2 cycles Part 1 Part 2a RP2D rebastinib+paclitaxel Triple-negative breast cancer Cohort 1 Inflammatory breast cancer Cohort 2 Ovarian cancer Cohort 3 Endometrial cancer Cohort 4 Enrolling patients with histologically confirmed advanced or metastatic solid tumors for which paclitaxel or (nab-) paclitaxel would be an appropriate treatment ClinicalTrials.gov: NCT03601897 aPart 2 uses a Simon 2-stage design. If >4 responses are seen in a cohort, additional patients will be enrolled for a total of up to 33 patients. If <4 responses are seen in a cohort, the cohort will be terminated. BID, twice daily; IV, intravenous infusion; RP2D, recommended phase 2 dose. Table 1. Key inclusion and exclusion criteria for Part 1 Inclusion criteria 18 years old Histologically confirmed diagnosis of locally advanced or metastatic solid tumor for which paclitaxel is considered an appropriate treatment Progressed despite standard therapies, or for whom conventional therapy is not considered effective or tolerable, as judged appropriate by the investigator 1 measurable lesion per RECIST v1.1 ECOG Performance Status score of 2 Adequate organ function and bone marrow reserve performed 14 days of first dose of study drug Exclusion criteria Prior anticancer therapy or other investigational therapy 28 days or 5x half-life Not recovered from toxicities from prior therapy to grade 1 (or baseline) Grade >1 peripheral neuropathy (any etiology) Known active CNS metastases Use of systemic corticosteroids within 7 days prior to first dose History or presence of clinically relevant cardiovascular abnormalities LVEF <50% at screening CNS, central nervous system; ECOG, Eastern Cooperative Oncology Group; LVEF, left ventricle ejection fraction; RECIST, response evaluation criteria in solid tumors.

EX-99.4

Exhibit 99.4

Preclinical studies with DCC-3116, an ULK kinase inhibitor designed to inhibit autophagy as a potential strategy to address mutant RAS cancers Bryan D. Smith, Lakshminarayana Vogeti, Anu Gupta, Jarnail Singh, Gada Al-Ani, Stacie L. Bulfer, Timothy M. Caldwell, Mary J. Timson, Subha Vogeti, Yu Mi Ahn, Hikmat Al-Hashimi, Chase K. Crawley, Cale L. Heiniger, Cynthia B. Leary, Justin T. Proto, Quanrong Shen, Abstract Hanumaiah Telikepalli, Karen Yates, Wei-Ping Lu, and Daniel L. Flynn B129 Deciphera Pharmaceuticals, LLC, Waltham, MA DCC-3116 Inhibited ULK Kinase in PK/PD Models and Inhibited Tumor Growth in DCC-3116 is a Potent Inhibitor of ULK Kinase and Autophagy in Cellular Assays INTRODUCTION RESULTS Combination with MAPK Inhibitors in Mouse Xenograft Models Figure 4. DCC-3116 Inhibits Both Basal and Trametinib-induced Phosphorylation of Figure 7. DCC-3116 Inhibited ATG13 Phosphorylation in vivo in a PK/PD Model Cancer cells activate autophagy, a catabolic process to resupply nutrients and recycle Autophagy is a Compensatory Survival Mechanism in MAPK Pathway Inhibitor- ULK Substrate ATG13 in RAS- and BRAF-mutant Cell Lines damaged organelles, in order to survive stresses such as limited nutrients and hypoxia, treated RAS Mutant Cancers A549 KRAS G12S LUNG CANCER MIAPACA-2 KRAS G12C PANCREATIC CANCER 250 ATG13 200 MIAPACA-2 PANCREATIC CANCER PK/PD MODEL or chemotherapy treatments. DCC-3116 dose response with 250 nM trametinib DCC-3116 dose response with 100 nM trametinib 200 200 Control) 150 Treatment of a RAS mutant cancer cell line with inhibitors of the MAPK pathway (i.e. DCC-3116 50 mg/kg DCC-3116 25 mg/kg Control) 150 IC 52 nM Control) 150 IC 28 nM 100 RAS mutant cancers, in particular, have been found to require autophagy for tumor of BASAL 50 BASAL 50 Vehicle of 2 hr 6 hr 10 hr 2 hr 6 hr 10 hr RAS, RAF, MEK, or ERK inhibitors) leads to activation of ULK kinase and phosphorylated of (% (% 50 1,2 of 100 100 (% growth and survival. Treating RAS mutant tumors with inhibitors of the downstream phosphorylation of downstream autophagy protein substrates Concentration (nM) 3,016 1,079 243 1,582 581 254 ATG13 ATG13 Levels 0 - MAPK pathway has been largely unsuccessful, as these drugs have been shown to 50 - 50 Veh 2 hr 6 hr 10 hr 2 hr 6 hr 10 hr 2 hr 6 hr 10 hr % pATG13 inhibition 86 71 49 80 63 24 Figure 2. MAPK inhibition leads to increased ATG13 phosphorylation trametinib 1 mg/kg DCC-3116 50 mg/kg + DCC-3116 25 mg/kg + further stimulate autophagy, allowing for tumor cell survival.3,4 Inhibiting autophagy in Phospho 0 Phospho 0 trametinib 1 mg/kg trametinib 1 mg/kg Control Trametinib 10 3.3 1.1 0.37 0.12 0.041 0.014 0.0046 Control Trametinib 10 3.3 1.1 0.37 0.12 0.041 0.014 0.0046 0.0015 combination with MAPK pathway inhibition may represent a possible new treatment DCC-3116 (µM) + Trametinib (250 nM) DCC-3116 (µM) + Trametinib (100 nM) ACTIVATION BY KRAS G12C INHIBITION ACTIVATION BY RAF INHIBITION Figure 8. DCC-3116, in Combination with Trametinib, Inhibited Pancreatic, Lung, paradigm for RAS mutant cancers. mKRAS HCT-116 KRAS G13D COLORECTAL CANCER A375 BRAF V600E MELANOMA AMG-510 MiaPaca-2 cells - AMG-510 dose response A549 cells - LY3009120 dose response 250 150 and Melanoma Xenograft Tumor Growth Control) 200 Control) BASAL DCC-3116 dose response with 100 nM trametinib DCC-3116 dose response with 100 nM trametinib BASAL of 100 250 250 of 150 (% Proof-of-concept for this strategy was obtained in cancer models and in a RAS mutant (% 100 Control) 200 Control) 200 LY3009120 ATG13 ATG13 50 IC 57 nMof IC 40 nM - of 50 50 - pancreatic cancer patient by blocking autophagy with derivatives of chloroquine, in 50 (% 150 (% 150 0 BASAL BASAL Phospho 0 Phospho combination with MAPK inhibitors.3,4 Control 1.1 0.37 0.12 0.041 0.014 0.0046 0.0015 0.0005 Control 10 3.3 1.1 0.37 0.12 0.041 0.014 0.0046 0.0015 0.0005 100 100 AMG-510 (µM) LY3009120 (µM) ATG13 ATG13 - - Trametinib 50 50 ACTIVATION BY MEK INHIBITION ACTIVATION BY ERK INHIBITION Phospho Phospho 0 0 • ULK1/2 kinases initiate autophagy and provide the potential for a targeted approach for Other Pathways A549 cells - Trametinib dose response A549 cells - Ulixertinib dose response Control Trametinib 10 3.3 1.1 0.37 0.12 0.041 0.014 0.0046 0.0015 Control Trametinib 10 3.3 1.1 0.37 0.12 0.041 0.014 0.0046 Can Also 300 200 selectively inhibiting autophagy in RAS mutant cancers. Herein, we describe preclinical Activate ULK DCC-3116 (µM) + Trametinib (100 nM) DCC-3116 (µM) + Trametinib (100 nM) Ulixertinib Control) Control) 150 of 200 of BASAL (% (% 100 studies with the ULK kinase inhibitor DCC-3116, designed as a potential inhibitor of BASAL X ATG13 100 ATG13 - 50 autophagy in RAS mutant cancers. P P P - Figure 5. DCC-3116 Inhibits Autophagosome Formation and Autophagic Flux of LC3 Phospho 0 Phospho 0 LKB1 AMPK ULK Control 1000 500 250 125 62.5 31.3 15.6 7.8 3.9 1.95 Control 10 3.3 1.1 0.37 0.12 0.041 0.014 0.0046 0.0015 P Trametinib (nM) Ulixertinib (µM) METHODS ATG13 AUTOPHAGOSOME FORMATION INHIBITION INHIBITION OF LC3-LUCIFERASE DEGRADATION DCC-3116 dose response with 1 µM PP242 (mTOR inhibitor) DCC-3116 dose response with 250 nM trametinib in HCT-116 in A549 cells – Cyto-ID assay Control cells stably transfected with LC3-Luciferase 300 In vitro kinase assays were performed using cellular levels of ATP (1 mM) and a peptide DCC-3116 is a Potent & Selective ULK Kinase Inhibitor Designed to Inhibit Autophagy 150 Figure 9. DCC-3116, in Combination with MEK Inhibitor Binimetinib or ERK Inhibitor substrate. In cell assays, ULK activity was assessed using an ELISA for phosphorylated 250 IC 29 nM IC 95 nM Ulixertinib, Decreased Pancreatic Xenograft Tumor Growth Figure 3. DCC-3116 Kinome Tree 50 Control) 50 of ATG13 (a cellular ULK substrate). Autophagosome formation was measured using the Potent (IC at 1 mM ATP) 50 200 (% 100 IC50 = 1 M dye, Cyto-ID. Autophagic flux was assessed using cells expressing the autophagy protein IC50 = 100 nM PP242 Units ULK1 4.7 nM; ULK2 36 nM Fluorescence 150 LC3 fused to luciferase. The synergy of DCC-3116 in combination with MAPK inhibitors Tight-binding inhibitor with residency time IC50 = 10 nM was assessed in 2D or 3D cell growth assays. Xenograft models were used to assess Relative 100 Luminescence 50 > 7 hours IC = 1 nM pharmacokinetics (PK) and pharmacodynamics (PD), as well as efficacy in vivo. 50 50 PP242 + Relative 0 0 Control PP242 10 3.3 1.1 0.37 0.12 0.041 0.013 0.043 3116 Control Trametinib 1.1 0.37 0.12 0.041 0.0137 0.0046 0.0015 0.0005 Highly Selective - DCC-3116 (µM) + PP242 (1 µM) DCC DCC-3116 (µM) + Trametinib (250 nM) ULK KINASE: INITIATING FACTOR FOR AUTOPHAGY No off-target kinases within 30-fold of ULK1 Only 6 kinases within 100-fold, inclusive of DCC-3116 Synergizes with MAPK Inhibitors in 2D and 3D Cellular Growth Assays CONCLUSIONS ases initiate autophagy by ULK2 lating and activating other Figure 6. DCC-3116 Exhibits Synergy with Trametinib in Inhibiting Cell Growth of RAS cancers have high basal autophagy, and induce greater autophagy in response to drug treatments pathway proteins (e.g. RAS- or RAF-mutant Cancer Cells Designed to Avoid CNS Exposure ULK kinase inhibitors represent a differentiated approach to autophagy inhibition, and a first-in-class CLIN1, and ATG14) opportunity for a new therapeutic modality in RAS- and RAF-mutant cancers Low Brain:Plasma ratio (4%) to avoid MIAPACA-2 2D PROLIFERATION BXPC3 2D PROLIFERATION MIAPACA-2 3D GROWTH A549 3D GROWTH proteins, organelles, and E inhibition of CNS autophagy DCC-3116 is a potent, selective, and tight-binding inhibitor of ULK kinase Synergy mapped to D-R (BLISS): Synergy mapped to D-R (BLISS): o are targeted to, and DCC-3116 + trametinib DCC-3116 + trametinib DCC-3116 inhibited phosphorylation of the ULK substrate ATG13 in cancer cells, and exhibited synergy in vitro by, autophagosomes in combination with MAPK inhibitors in inhibiting cancer cell growth Optimized Pharmaceutical Properties ULK1/2 Oral doses of DCC-3116 led to sustained inhibition of ATG13 phosphorylation in vivo utophagosomes and In combination with MAPK inhibitors, DCC-3116 exhibited synergy in tumor growth inhibition in mouse models High solubility and oral bioavailability allows for breakdown and combination with pathway Plasma Free Fraction > 10% Selectively blocking autophagy via inhibition of ULK1/2 kinases, in MAPK f metabolic precursors and inhibition, is a promising therapeutic approach for RAS mutant cancers. CYP1A2, 2C9, 2C19, 2D6, 3A4 and DCC-3116 warrants further study as an inhibitor of autophagy, and has been selected as a candidate Trametinib (nM) DCC-3116 (mM) Trametinib (nM) DCC-3116 (mM) hERG IC values >20 µM for potential clinical development in the treatment of RAS mutant cancers 50 Acknowledgments References We would like to acknowledge Waheed Bhatti, Patrick Kearney, Kevin Roesch, Michael 1) Guo et al., Activated Ras requires autophagy to maintain oxidative metabolism and tumorigenesis. Genes and Dev. 2011; 25: 460 2) Yang et al., Pancreatic cancers require autophagy for tumor growth. Genes and Dev. 2011; 25: 717 Kaufman, Arun Mandagere, Randy McCall, Steve Wilson, and Heather Vital for their 3) Bryant et al., Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. Nature Med. 2019; 25: 628 work on this project and input and review of this presentation. 4) Kinsey et al., Protective autophagy elicited by RAF MEK ERK inhibition suggests a treatment strategy for RAS-driven cancers. Nature Med. 2019; 25: 620

EX-99.5

Exhibit 99.5

Updated results of phase 1 study of ripretinib (DCC-2618), a broad-spectrum KIT and PDGFRA inhibitor, in patients with gastrointestinal stromal tumor (GIST) by line of therapy (NCT02571036) Ping Chi,1 Filip Janku,2 Michael C. Heinrich,3 Kristen Ganjoo,4 Hans Gelderblom,5 Michael Gordon,6 Robin L. Jones,7 Albiruni Razak,8 Jonathan Trent,9 Margaret von Mehren,10 Simin Hu,11 Ying Su,11 Rodrigo Ruiz-Soto,11 Suzanne George12 1Memorial Sloan Kettering Cancer Center, New York, New York; 2 The University of Texas MD Anderson Cancer Center, Houston, Texas; 3VA Portland Health Care System and OHSU Knight Cancer Institute, Portland, Oregon; 4Stanford University Medical Center, Palo Alto, California; 5Leiden University Medical Center, Leiden, The Netherlands; 6HonorHealth Research Institute, Scottsdale, Arizona; 7The Royal Marsden NHS Foundation Trust and The Institute of Cancer Research, London, United Kingdom; 8Princess Margaret Cancer Centre, Toronto, Ontario, Canada; 9Sylvester Comprehensive Cancer Center, University of Miami Health System, Miami, Florida; 10Fox Chase Cancer Center, Philadelphia, Pennsylvania; 11Deciphera Pharmaceuticals, LLC, Waltham, Massachusetts; 12Dana-Farber Cancer Institute, Boston, Massachusetts Abstract: C077 Table 2. Efficacy by line of therapy in patients with GIST receiving ripretinib 150 mg QD Safety INTRODUCTION RESULTS 2nd Line 3rd Line 4th Line The most common all grade treatment emergent adverse events (TEAEs) (in >10% of patients) are shown in Table 3 Parameters (n=31) (n=28) (n=83) The most common grade 3 or 4 adverse events (in >5% of patients) were increase in lipase level, 25 (17.6%); Gastrointestinal stromal tumors (GISTs) are the most common soft tissue sarcoma of the gastrointestinal (GI) tract1 Efficacy and safety results from the escalation and expansion phases of the phase 1 study for patients with GIST treated anemia, 11 (7.7%); and abdominal pain, 11 (7.7%) The vast majority (~85%) of GISTs have oncogenic mutations in either KIT or PDGFRA kinases2 at ripretinib 150 mg QD as the starting dose are presented here Best response (confirmed only), n (%) Table 3. All grade TEAEs, regardless of relatedness, in >10% of patients with GIST treated with Despite the clinical benefit provided by the tyrosine kinase inhibitors, imatinib, sunitinib, and regorafenib, patients with • Demographics and baseline characteristics by line of therapy are shown in Table 1 CR 0 0 0 advanced GIST eventually develop drug-resistance PR 6 (19.4) 4 (14.3) 6 (7.2) ripretinib 150 mg QD An unmet need exists well-tolerated treatments that (i) broadly inhibit primary and secondary/drug-resistant mutated 142 patients with GIST in the escalation and expansion phases were treated at 150 mg QD dose for nd rd th Stable disease 21 (67.7) 18 (64.3) 49 (59.0) Grade 1/2, Grade 3/4, All grades, 3 Number of patients by line of therapy were as follows: 31 2 line, 28 3 line, and 83 4 line patients KIT and PDGFRA kinases and (ii) delay disease progression Preferred term n (%) (n=142) n (%) (n=142) n (%) (n=142) 135 patients (95.1%) had KIT-mutant GIST, and 7 patients (4.9%) had PDGFRA-mutant GIST Progressive disease 4 (12.9) 6 (21.4) 22 (26.5) Ripretinib is a novel, tyrosine kinase switch control inhibitor that is designed to broadly inhibit oncogenic KIT and PDGFRA signaling through a unique dual mechanism of action that secures the target kinase into an inactive Not evaluable 0 0 1 (1.2) Alopecia 86 (60.6) 0 86 (60.6) conformation resulting in the inhibition of downstream signaling and cell proliferation3 Fatigue 74 (52.1) 4 (2.8) 78 (54.9) Table 1. Baseline patient characteristics No response assessment 0 0 5 (6.0) Myalgia 68 (47.9) 0 68 (47.9) Ripretinib binds to the switch pocket, preventing access to the switch pocket by the activation loop, thereby locking ORR, n (95% CI) 19.4 (7.5, 37.5) 14.3 (4.0, 32.7) 7.2 (2.7, 15.1) Nausea 64 (45.1) 2 (1.4) 66 (46.5) the kinase into the inactive state 2nd Line 3rd Line 4th Line Total Duration of treatmenta Palmar-plantar erythrodysesthesia syndrome 62 (43.7) 1 (0.7) 63 (44.4) Additionally, ripretinib binds to the activation loop, further preventing its access to the switch pocket and blocking Constipation 57 (40.1) 0 57 (40.1) Characteristics (n=31) (n=28) (n=83) (n=142) Mean, weeks (SD) 56.1 (34.24) 57.5 (32.95) 44.9 (36.58) kinase activity Decreased appetite 46 (32.4) 2 (1.4) 48 (33.8) Age at informed consent, years Median, weeks 64 51 29 Ripretinib was assessed in a phase 1, open-label, first-in-human, dose-escalation study designed to evaluate the safety, Diarrhea 44 (31.0) 3 (2.1) 47 (33.1) tolerability, pharmacokinetics, pharmacodynamics and preliminary antitumor activity of oral ripretinib in adult patients with Mean (SD) 59.8 (11.92) 64.0 (8.33) 59.5 (11.91) 60.4 (11.36) Min, Max 4, 132 8, 124 0.1, 140 Muscle spasms 42 (29.6) 0 42 (29.6) advanced malignancies, including advanced GIST (NCT02571036) Median 60.0 63.5 59.0 60.0 Abdominal pain 28 (19.7) 11 (7.7) 39 (27.5) Duration of response Updated preliminary results presented by George et al4 at ESMO 2018 demonstrated encouraging efficacy Min, Max 32, 80 48, 82 27, 87 27, 87 Lipase increased 14 (9.9) 25 (17.6) 39 (27.5) n 6 4 6 Weight decreased 39 (27.5) 0 39 (27.5) All doses of 100 mg per day were associated with reductions in KIT mutant allele frequency in plasma circulating Age category, n (%), years Number of events 3 1 3 Vomiting 36 (25.4) 1 (0.7) 37 (26.1) tumor DNA, including the KIT mutations least sensitive to ripretinib in vitro Although daily doses of up to 400 mg were tested, a maximum tolerated dose was not determined 18 ≤ Age < 65 18 (58.1) 15 (53.6) 57 (68.7) 90 (63.4) Median, weeks 80 NE 76.1 Headache 35 (24.6) 1 (0.7) 36 (25.4) 65 13 (41.9) 13 (46.4) 26 (31.3) 52 (36.6) Arthralgia 32 (22.5) 0 32 (22.5) Based on preclinical in vivo and in vitro pharmacology studies, 150 mg once daily (QD) is predicted to maintain the 95% CI 24.7, 80.0 52.1, NE 24.1, NE pharmacokinetic exposure above presumed threshold for efficacy in >90% of patients Hypertension 25 (17.6) 7 (4.9) 32 (22.5) Sex, n (%) PFS Dry skin 31 (21.8) 0 31 (21.8) Safety data collected from the phase 1 dose-escalation phase support administration of 150 mg QD as the Male 14 (45.2) 17 (60.7) 52 (62.7) 83 (58.5) Number of censored patients 8 6 12 Anemia 19 (13.4) 11 (7.7) 30 (21.1) recommended starting dose to be used in the expansion phase Female 17 (54.8) 11 (39.3) 31 (37.3) 59 (41.5) Back pain 27 (19.0) 2 (1.4) 29 (20.4) • This presentation reports updated results from the escalation and expansion phases of the phase 1 study for patients Median, weeks 46.4 36.3 23.9 Dyspnea 25 (17.6) 3 (2.1) 28 (19.7) who were treated at 150 mg QD as the starting dose Race, n (%) 95% CI 24.0, 60.0 23.9, 48.4 15.9, 24.3 American Indian or Alaska Native 0 0 3 (3.6) 3 (2.1) Cough 25 (17.6) 0 25 (17.6) Based on the clinical activity observed in heavily pretreated patients with GIST in this phase 1 study, ripretinib at a64 subjects escalated to 150 mg BID among patients with GIST in the 150 mg QD dose group. Dizziness 25 (17.6) 0 25 (17.6) 150 mg QD is being evaluated in two phase 3 studies: Asian 2 (6.5) 1 (3.6) 6 (7.2) 9 (6.3) Rash 23 (16.2) 0 23 (16.2) CI, confidence interval; CR, complete response; NE, not estimable; ORR, objective response rate; PFS, progression-free survival; INVICTUS (NCT03353753) in 4th line patients with GIST, compared with placebo; results reported at ESMO 20195 Actinic keratosis 22 (15.5) 0 22 (15.5) Black or African American 4 (12.9) 2 (7.1) 7 (8.4) 13 (9.2) PR, partial response; SD, standard deviation. Intrigue (NCT03673501) in 2nd line patients with GIST, compared with sunitinib White 25 (80.6) 25 (89.3) 63 (75.9) 113 (79.6) Local (investigator) response assessment. Hypophosphatemia 15 (10.6) 7 (4.9) 22 (15.5) Seborrheic keratosis 22 (15.5) 0 22 (15.5) Other 0 0 4 (4.8) 4 (2.8) Figure 2. Median PFS by line of therapy for patients with GIST treated with Hypokalemia 15 (10.6) 4 (2.8) 19 (13.4) METHODS Eastern Cooperative Oncology Group Rash maculo-papular 19 (13.4) 0 19 (13.4) ripretinib 150 mg QD Blood bilirubin increased 14 (9.9) 4 (2.8) 18 (12.7) (ECOG) performance status, n (%) Pain in extremity 17 (12.0) 1 (0.7) 18 (12.7) The phase 1 study included a dose-escalation phase that tested oral ripretinib QD or twice daily (BID) in 28-day cycles 0 16 (51.6) 13 (46.4) 38 (45.8) 67 (47.2) Insomnia 17 (12.0) 0 17 (12.0) ‒ In this phase, ripretinib dose levels assessed were 20, 30, 50, 100, 150, 200 mg BID or 100, 150, 250 QD 1 15 (48.4) 15 (53.6) 42 (50.6) 72 (50.7) Lines of therapy Median PFS (weeks) 95% CI Pruritus 17 (12.0) 0 17 (12.0) The subsequent expansion phase tested the recommended dose of ripretinib 150 mg QD in 6 cohorts, including 2 0 0 3 (3.6) 3 (2.1) 1.0 Blood creatine phosphokinase increased 13 (9.2) 3 (2.1) 16 (11.3) nd rd th 2 46.4 (24.0, 60.0) Melanocytic nevus 16 (11.3) 0 16 (11.3) cohorts for patients with GIST based on prior lines of therapy (2 , 3 , and 4 line) Primary mutation (determined by 0.9 Local, investigator-assessed Response Evaluation Criteria in Solid Tumors (RECIST 1.1) response assessments were 3 36.3 (23.9, 48.4) Skin papilloma 16 (11.3) 0 16 (11.3) molecular pathology report), n (%) performed every 2 cycles, and patients in the expansion cohorts who progressed per RECIST 1.1 were allowed to dose 4 23.9 (15.9, 24.3) Stomatitis 16 (11.3) 0 16 (11.3) KIT exon 11 26 (83.9) 19 (67.9) 58 (69.9) 103 (72.5) 0.8 Urinary tract infection 14 (9.9) 2 (1.4) 16 (11.3) escalate to 150 mg BID probability Safety and efficacy data are reported from the August 10, 2019, data cutoff KIT exon 9 3 (9.7) 8 (28.6) 15 (18.1) 26 (18.3) 0.7 Peripheral sensory neuropathy 15 (10.6) 0 15 (10.6) KIT other exons 0 1 (3.6) 5 (6.0) 6 (4.2) TEAE, treatment emergent adverse event. Figure 1. Phase 1 dose-escalation (part 1) and expansion (part 2) study design 0.6 PDGFRA 2 (6.5) 0 5 (6.0) 7 (4.9) survival KIT/PDGFRA wild type 0 0 0 0 0.5 CONCLUSIONS SD, standard deviation free 0.4 Part 1: Dose-escalation phase - Ripretinib in escalating dose given orally BID or QD in 28-day cycles Efficacy 0.3 Ripretinib showed encouraging clinical benefit at the recommended dose 150 mg QD, as Participants continued on study drug until discontinuation criteria were met 0.2 measured by median PFS and ORR, in patients with advanced GIST The confirmed-only complete response (CR), partial response (PR), stable disease, and progressive disease are Ripretinib was generally well tolerated in patients with GIST treated in the 2nd line or later presented in Table 2 Progression 0.1 th There were no CRs observed Data from the phase 1 expansion study in 4 line patients supported the phase 3 INVICTUS The objective response rate (ORR; proportion of patients with CR + PR) is as follows: 0.0 study and are consistent with the positive INVICTUS results recently reported at ESMO 2019. 2nd line patients: ORR = 19.4% 0 14 28 42 56 70 84 98 112 INVICTUS evaluated ripretinib as 4th line therapy in 129 patients with advanced GIST Part 2: Expansion phase 3rd line patients: ORR = 14.3% PFS (weeks) (ripretinib, n=85; placebo, n=44), meeting the primary endpoint showing significant Ripretinib 150 mg QD in 28-day cycles 4th line patients: ORR = 7.2% Lines # at risk improvement in median PFS compared with placebo (6.3 vs 1 months, respectively; hazard ratio=0.15 [95% CI, 0.090.25]; P<0.0001)5 Median progression-free survival (PFS) per investigator assessment, by line of therapy, is as follows (Figure 2): 2 n=31 25 18 15 11 7 3 0 0 46.4 weeks in 2nd line patients; 8 patients censored The updated data from the phase 1 study presented here demonstrated a median PFS of 46.4 2nd Line 3rd Line 4th Line 3 n=28 22 15 12 6 4 3 2 0 36.3 weeks in 3rd line patients; 6 patients censored weeks and support the phase 3 study, intrigue, comparing ripretinib to sunitinib in 2nd line GIST GIST GIST 4 n=83 52 28 17 14 9 6 2 0 23.9 weeks in 4th line patients; 12 patients censored patients with GIST Acknowledgments References Presented at AACR-NCI-EORTC International Conference on The investigators would like to thank the patients and their families and caregivers, the investigational site staff of this study, and the medical writing assistance 1. Hemming ML, et al. Ann Oncol. 2018;29: 2037–2045. 2. National Comprehensive Cancer Network (NCCN). Soft Tissue Sarcoma (V2.2019). Available at: Molecular Targets and Cancer Therapeutics, October 26 to 30, 2019 of Akriti Kharbanda, PhD, of ETHOS Health Communications in Yardley, Pennsylvania, which was supported financially by Deciphera Pharmaceuticals, http://www.nccn.org/professionals/physician_gls/pdf/sarcoma.pdf. Accessed October 15, 2019. 3. Smith BD, et al. Cancer Cell. 2019;35:738-751.e9. 4. George S, et al. Oral presentation at: European LLC, Waltham, Massachusetts, in compliance with international Good Publication Practice guidelines. Society for Medical Oncology (ESMO) Annual Meeting; October 19-23, 2018; Munich, Germany. Abstract 16030. 5. von Mehren M, et al. Oral presentation at: European Society for Medical Oncology This study was sponsored by Deciphera Pharmaceuticals, LLC. (ESMO) Annual Meeting; September 27-October 1, 2019; Barcelona, Spain. Abstract 4794.

EX-99.6

Exhibit 99.6

Phase 1 study of DCC-3014, an oral inhibitor of CSF1R, to assess the safety, tolerability, pharmacokinetics, and pharmacodynamics in patients with advanced solid tumors, including diffuse-type tenosynovial giant cell tumor Matthew H Taylor,1 Stephen Leong,2 Gege Tan,3 Cynthia B Leary,3 Xiaoyan Li,3 Keisuke Kuida, 3 Rodrigo Ruiz-Soto,3 Todd Bauer 4 1Oregon Heath & Science University, Portland, OR; 2University of Colorado, Denver, CO; 3Deciphera Pharmaceuticals, LLC, Waltham, MA; 4Sarah Cannon Research Institute and Tennessee Oncology, PLLC, Nashville, TN Abstract: C087 INTRODUCTION Colony stimulating factor 1 receptor (CSF1R) is a receptor tyrosine kinase that is implicated in the recruitment and survival of tumor-associated macrophages (TAMs) through a paracrine interaction with tumor cells in the tumor microenvironment (Figure 1)1-3 CSF1R has 2 known ligands; CSF1 (also known as macrophage-CSF) and interleukin 34 (IL-34)4 CSF1/CSF1R expression in tumors may also contribute to tumor invasiveness through autocrine signaling pathways (Figure 1)3 Figure 1. Role of CSF1R receptor in the tumor invasiveness and growth Tumor-permissive TAMs (CSF1R-dependent) CSF1R Paracrine Loop CSF1 Autocrine Loop CSF1 Tumor Cells T-cell mediated antitumor immune response Angiogenesis Invasiveness CSF1, colony stimulating factor 1; CSF1R, CSF1 receptor; TAMs, tumor-associated macrophages. DCC-3014 is an orally administered, potent, and selective inhibitor of CSF1R that was engineered to bind into the CSF1R switch pocket and inhibit kinase activity5 DCC-3014 potently inhibits CSF1R signaling in cellular assays, as well as functionally blocks macrophage-mediated tumor cell migration, osteoclast differentiation, and proliferation of a CSF1R-dependent cell line DCC-3014 is designed for the inhibition of macrophages that contribute to or are the source of tumor development and dissemination DCC-3014 has >100-fold selectivity for CSF1R relative to closely-related kinases including FLT3, KIT, and PDGFR / and >1,000-fold selectivity vs other kinases5 Tenosynovial giant cell tumor (TGCT) is a rare disease arising from the joint synovia, bursa, and tendon sheath caused by translocation in CSF1 gene resulting in overexpression of CSF1 and recruitment of CSF1R-positive inflammatory cells into the lesion An ongoing phase 1 study (NCT03069469) was initiated to evaluate the safety, preliminary antitumor activity, pharmacokinetics (PK) and pharmacodynamics (PD) of DCC-3014 in advanced solid tumors, including diffuse-type TGCT Here, we report the results from the dose escalation phase of this trial in patients with malignant solid tumors METHODS This is a phase 1 multicenter, open-label, single arm study of DCC-3014 in advanced solid tumors The study consists of 2 parts Part 1 (dose escalation) is designed to determine the recommended phase 2 dose (RP2D) and the maximum tolerated dose (MTD) using a 3+3 dose escalation design with a minimum of 3 patients enrolled at each dose level cohort; starting at a dose of 10 mg once daily (Tables 1–3) Loading doses used from Cohort 2 based on PK profiles observed in Cohort 1 Part 2 (dose expansion) will evaluate the safety, tolerability, preliminary antitumor activity, PK, and PD in 2 expansion cohorts; advanced solid tumors and diffuse-type TGCT Table 1. Dose cohorts in Part 1 (3+3 dose escalation) Loading Doses Dose Cohort 1 None 10 mg QD Cohort 2 10 mg QD x 5 days 10 mg twice a week Cohort 3 20 mg QD x 5 days 20 mg once a week Cohort 4 20 mg QD x 5 days 20 mg twice a week Cohort 5 30 mg QD x 5 days 30 mg twice a week Cohort 6 40 mg QD x 5 days 40 mg twice a week Cohort 7 50 mg QD x 3 days 20 mg QD QD, once daily. Table 2. Key inclusion and exclusion criteria for Part 1 Inclusion criteria 18 years old Solid tumorsa that have progressed after treatment with all available therapies known to confer clinical benefit Tumors with known contribution of macrophages or phagocytes Symptomatic diffuse-type TGCT patients for which surgical resection is not an option Exclusion criteria Prior anticancer therapy or other investigational therapy 14 days or <28 days if half-life longer than 3 days Unresolved toxicity according to NCI-CTCAE, >grade 1 or baseline, from previous anticancer therapy, excluding alopecia Known active CNS metastases NYHA class III or IV heart disease, active ischemia, or any other uncontrolled cardiac condition History or presence of clinically relevant cardiovascular abnormalities Major surgery within 2 weeks of first dose Including, but not limited to, metastatic breast or prostate cancer with bone disease, gastric cancer, ovarian cancer, or NSCLC that frequently have malignant CNS, associated central ascites nervous or effusion. system; NCI-CTCAE, National Cancer Institute common terminology criteria for adverse events; NYHA, New York Heart Association; TGCT, tenosynovial giant cell tumor; TKI, tyrosine kinase inhibitor. Table 3. Study endpoints Primary endpoints Safety and tolerability (including occurrence of DLTs and incidence of TEAEsa) RP2D/MTD Pharmacokinetics (including T , C , C , AUC, t ) max max trough 1/2 Relevant exploratory endpoints Pharmacodynamics Levels of CSF1/IL-34 in plasma Levels of circulating CD16+ monocytes in blood by flow cytometry Macrophage content and/or polarization in tumor Tumor response assessment by RECIST version 1.1 aAdverse events graded by NCI-CTCAE, Version 4.03. AUC, area under the curve; C , maximum concentration; CSF1, colony stimulating factor; C , trough concentration; DLT, dose limiting toxicities; IL-34, interleukin 34; MTD, maximum tolerated dose; max NCI-CTCAE, National Cancer Institute common terminology trough criteria for adverse events; RP2D, recommended phase 2 dose; RECIST, response evaluation criteria in solid tumors; TEAE, treatment emergent adverse events; t , half-life; T , time of C . 1/2 max max RESULTS Patient demographics and disposition As of September 10, 2019, 36 patients with advanced solid tumors (not including diffuse-type TGCT patients) were enrolled and treated, of which 97.2% patients discontinued study treatment (Table 4); mainly due to disease progression (60.0%), withdrawal of patient from treatment (17.1%), or adverse events (11.4%) Table 4. Patient disposition Cohort 1 Cohort 2 Cohort 3 Cohort 4 Cohort 5 Cohort 6 Cohort 7 Total (n = 7) (n = 3) (n = 4) (n = 4) (n = 6) (n = 5) (n = 7) (n = 36) On treatment 0 0 0 0 0 0 1 (14.3) 1 (2.8) Discontinued from treatment 7 (100) 3 (100) 4 (100) 4 (100) 6 (100) 5 (100) 6 (85.7) 35 (97.2) Adverse event 1 (14.3) 0 0 1 (25.0) 2 (33.3) 0 0 4 (11.4)a Physician decision 0 0 0 0 1 (16.7) 0 0 1 (2.9) Progressive disease 3 (42.9) 3 (100.0) 3 (75.0) 3 (75.0) 3 (50.0) 3 (60.0) 3 (50.0) 21 (60.0) Withdrawal by patient 2 (28.6) 0 0 0 0 1 (20.0) 3 (50.0) 6 (17.1) Other 1 (14.3) 0 1 (25.0) 0 0 1 (20.0) 0 3 (8.6)b All value n (%). aLipase increased (grade 4), fatigue (grade 3), intestinal obstruction (grade 3), hemorrhage intracranial (grade 4). bOther: clinical progression/decline, hospice (2). The most frequent diagnoses (10%) were colorectal cancer, pancreatic cancer; and ovarian cancer and most patients were heavily pretreated (median of 4 lines of prior treatments) (Tables 5 and 6) Table 5. Baseline demographics and clinical characteristics Cohort 1 Cohort 2 Cohort 3 Cohort 4 Cohort 5 Cohort 6 Cohort 7 Total (n = 7) (n = 3) (n = 4) (n = 4) (n = 6) (n = 5) (n = 7) (n = 36) Age (years), median 64.0 48.0 64.0 70.0 63.5 59.0 67.0 62.0 (min, max) (39, 91) (27, 77) (55, 74) (50, 77) (51, 71) (55 ,63) (46, 74) (27, 91) Female 4 (57.1) 2 (66.7) 3 (75.0) 3 (75.0) 4 (66.7) 4 (80.0) 3 (42.9) 23 (63.9) Race White 6 (85.7) 3 (100) 4 (100) 3 (75.0) 4 (66.7) 5 (100) 6 (85.7) 31 (86.1) Black or African American 0 0 0 0 1 (16.7) 0 0 1 (2.8) Other 1 (14.3) 0 0 1 (25.0) 1 (16.7) 0 1 (14.3) 4 (11.1) Previous regimens, 7.0 2.0 3.5 5.5 3.5 5.0 3.5 4.0 median (min, max) (2, 8) (1, 7) (3, 7) (2, 6) (2, 5) (3, 8) (1, 7) (1, 8) Except Max, maximum; where indicated, min; minimum. values are n (%). Table 6. Types of cancers Total (n = 36) Colorectal cancer 8 (22) Pancreatic cancer 5 (14) Ovarian cancer 4 (11) Prostate 3 (8) Leiomyosarcoma 2 (6) Liver cancer 2 (6) Uterine cancer 2 (6) Othera 10 (28) All values n (%). aAnal cancer, breast cancer, chondrosarcoma, endometrial, gastroesophageal junction, melanoma, uveal melanoma, synovial sarcoma, non-small cell lung cancer, thymus. Safety Most treatment-emergent adverse events (TEAEs) regardless of relatedness were grade 1 or 2 (Table 7) Common (10%) related TEAEs were fatigue (16.7%), diarrhea (11.1%), and nausea (11.1%) Grade 3 related TEAEs occurred in 4 patients (grade 3 aspartate aminotransferase [AST] increased, grade 4 lipase increased, grade 3 amylase increased, and grade 3 colitis) Serious adverse events were reported in 17 patients; none of which were related to DCC- 3014 Table 7. Common (10%) TEAEs regardless of relatedness Cohort 1 Cohort 2 Cohort 3 Cohort 4 Cohort 5 Cohort 6 Cohort 7 Total (n = 7) (n = 3) (n = 4) (n = 4) (n = 6) (n = 5) (n = 7) (n = 36) Any Grade 3 Any Grade 3 Any Grade 3 Any Grade 3 Any Grade 3 Any Grade 3 Any Grade 3 Any Grade 3 Constipation 3 (42.9) 0 2 (66.7) 0 2 (50.0) 0 1 (25.0) 0 2 (33.3) 0 1 (20.0) 0 2 (28.6) 0 13 (36.1) 0 Vomiting 3 (42.9) 0 0 0 1 (25.0) 0 1 (25.0) 0 3 (50.0) 1 (16.7) 3 (60.0) 1 (20.0) 1 (14.3) 0 12 (33.3) 2 (5.6) Diarrhea 3 (42.9) 0 0 0 2 (50.0) 0 0 0 4 (66.7) 0 1 (20.0) 0 0 0 10 (27.8) 0 Nausea 1 (14.3) 0 0 0 3 (75.0) 0 1 (25.0) 0 3 (50.0) 0 2 (40.0) 0 0 0 10 (27.8) 0 Decreased appetite 3 (42.9) 0 0 0 1 (25.0) 0 1 (25.0) 0 1 (16.7) 0 2 (40.0) 1 (20.0) 1 (14.3) 0 9 (25.0) 1 (2.8) Dyspnea 4 (57.1) 0 0 0 0 0 2 (50.0) 0 1 (16.7) 0 0 0 1 (14.3) 0 8 (22.2) 0 Fatigue 0 0 1 (33.3) 0 1 (25.0) 0 1 (25.0) 1 (25.0) 2 (33.3) 0 2 (40.0) 1 (20.0) 1 (14.3) 0 8 (22.2) 2 (5.6) Abdominal pain 2 (28.6) 1 (14.3) 2 (66.7) 1 (33.3) 0 0 1 (25.0) 1 (25.0) 1 (16.7) 0 1 (20.0) 0 0 0 7 (19.4) 3 (8.3) Dehydration 1 (14.3) 0 0 0 1 (25.0) 0 1 (25.0) 0 1 (16.7) 0 2 (40.0) 0 1 (14.3) 0 7 (19.4) 0 Pyrexia 1 (14.3) 0 1 (33.3) 0 1 (25.0) 0 1 (25.0) 0 1 (16.7) 0 1 (20.0) 0 0 0 6 (16.7) 0 Anemia 1 (14.3) 0 0 0 0 0 1 (25.0) 1 (25.0) 1 (16.7) 0 2 (40.0) 0 0 0 5 (13.9) 1 (2.8) Arthralgia 1 (14.3) 0 1 (33.3) 0 0 0 0 0 2 (33.3) 0 0 0 1 (14.3) 1 (14.3) 5 (13.9) 1 (2.8) AST increased 3 (42.9) 1 (14.3) 0 0 0 0 0 0 0 0 1 (20.0) 0 1 (14.3) 0 5 (13.9) 1 (2.8) Asthenia 2 (28.6) 0 0 0 0 0 0 0 1 (16.7) 0 2 (40.0) 0 0 0 5 (13.9) 0 Back pain 2 (28.6) 0 0 0 0 0 0 0 1 (16.7) 0 1 (20.0) 0 1 (14.3) 0 5 (13.9) 0 Pain in extremity 1 (14.3) 0 0 0 0 0 0 0 2 (33.3) 0 0 0 2 (28.6) 0 5 (13.9) 0 Abdominal distension 1 (14.3) 0 0 0 0 0 0 0 2 (33.3) 0 1 (20.0) 0 0 0 4 (11.1) 0 Blood CPK increase 1 (14.3) 0 0 0 0 0 0 0 0 0 1 (20.0) 0 2 (28.6) 0 4 (11.1) 0 Cough 3 (42.9) 0 0 0 0 0 0 0 0 0 0 0 1 (14.3) 0 4 (11.1) 0 Depression 2 (28.6) 0 1 (33.3) 0 0 0 0 0 0 0 1 (20.0) 0 0 0 4 (11.1) 0 Dyspepsia 0 0 0 0 0 0 1 (25.0) 0 1 (16.7) 0 1 (20.0) 0 1 (14.3) 0 4 (11.1) 0 Hypokalemia 2 (28.6) 0 0 0 0 0 0 0 0 0 1 (20.0) 1 (20.0) 1 (14.3) 0 4 (11.1) 1 (2.8) Insomnia 2 (28.6) 0 0 0 0 0 0 0 1 (16.7) 0 0 0 1 (14.3) 0 4 (11.1) 0 Edema peripheral 0 0 1 (33.3) 0 0 0 1 (25.0) 0 0 0 1 (20.0) 0 1 (14.3) 0 4 (11.1) 0 Periorbital edema 0 0 0 0 1 (25) 0 0 0 2 (33.3) 0 0 0 1 (14.3) 0 4 (11.1) 0 Urinary tract infection 2 (28.6) 0 0 0 0 0 1 (25) 0 1 (16.7) 0 0 0 0 0 4 (11.1) 0 AST, aspartate aminotransferase; CPK, creatine phosphokinase; TEAE, treatment-emergent adverse events. There were 2 dose-limiting toxicities (DLTs) in the first cohort (10 mg QD): grade 4 lipase increased and grade 3 hypocalcemia Both DLTs could be explained by the mechanism of action of DCC-3014; therefore, any grade of asymptomatic serum enzyme elevation (except for Hy’s law cases) and grade 3 hypocalcemia were excluded from DLTs for evaluation of subsequent cohorts Dose density of Cohort 2 (a total dose given in Cycle 1) was lowered from that of Cohort 1 (Table 1) and then subsequently increased No further DLTs were reported in the other cohorts Increases in alanine transaminase (ALT) and AST are considered as the mechanism of action of DCC-3014 Preliminary antitumor activity The overall median treatment duration was 36 days There were 5 patients with a best response of stable disease (2 with colorectal cancer and 1 each with prostate cancer, thymoma, and uveal melanoma) Pharmacokinetics and pharmacodynamics DCC-3014 exposure appears approximately dose proportional (Table 8 and Figure 2) Table cohort 8. DCC-3014 geometric mean PK parameters on C2D1 by
Cohort n Dose C (ng/mL) AUC (h*ng/mL) C (ng/mL)
max 0-8 trough
QD Cohort 1 5 10 mg QD 767a 4510a 447
QD Cohort 7 3 20 mg QD 1250 7980 1040
Twice a week Cohort 2 3 10 mg twice a week 149 1030 122
Twice a week Cohort 4 3 20 mg twice a week 642 4300 441
Twice a week Cohort 5 3 30 mg twice a week 953 5420 574
Twice a week Cohort 6 3 40 mg twice a week 1150 7290 570
Once a week Cohort 3 2 20 mg once a week 530 3380 205
an = 3. AUC , area under the concentration curve from 0 to 8 hours postdose; C2D1, cycle 2 day 1; C , maximum concentration; C , trough concentration; 0-8 PK, pharmacokinetic; QD, once daily. max trough DCC-3014 treatment caused a rise in plasma CSF1 and IL-34 that was drug concentration dependent, a rapid and sustained reduction of CD16+ monocytes that was dose dependent, as well as a reduction in CD163+ macrophages in tumors (Figures 3–5) Figure 3. Changes in levels of circulating A) CSF1 and B) IL-34 in plasma 100000 100000 100000 (pg/ml), 10000 10000 10000 SD concentration± mean plasma 1000 1000 1000 CSF1 100 100 100 C1D1 C1D15 C2D1 C1D1 C1D15 C2D1 C1D1 C1D15 C2D1 B) 10000 Visit 10000 Visit 10000 Visit 1000 (pg/ml), 1000 1000 SD 100 ± 100 concentration 100 mean 10 plasma 10 10 IL34 1 0.1 1 1 C1D1 C1D15 C2D1 C1D1 C1D15 C2D1 C1D1 C1D15 C2D1 Visit Visit Visit 10 mg QD 20 mg QD 10 mg twice a week 20 mg twice a week 20 mg once a week 30 mg twice a week 40 mg twice a week Levels Day 15, of and CSF1 Cycle and 2 IL-34 Day 1. in plasma were determined by standard ELISA. Plasma samples were collected from patients on Cycle 1 Day 1, Cycle 1 C, cycle; CSF1, colony stimulating factor 1; D, day; IL-34, interleukin 34; QD, once daily; SD, standard deviation. Figure 4. Changes in levels of whole blood CD16+ monocytes 50 50 50 SD monocyte± 0 0 0 mean CD16+ in changebaseline, -50 -50 -50 %from -100 -100 -100 C1D1 C1D15 C2D1 C1D1 C1D15 C2D1 C1D1 C1D15 C2D1 Visit Visit Visit 10 mg QD 20 mg QD 10 mg twice a week 20 mg twice a week 20 mg once a week 30 mg twice a week 40 mg twice a week Levels and Cycle of CD16+ 2 Day 1. monocytes were assessed by flow cytometry. Whole blood samples were collected from patients on Cycle 1 Day 1, Cycle 1 Day 15, C, cycle; D, day; QD, once daily; SD, standard deviation. Figure 5. Changes in levels of CD163+ macrophages in tumors 0 Patient with Patient with Pancreatic Cancer Colon Cancer baseline -20 cells) -40 from -60 (CD163+ 200 µm Baseline 200 µm Baseline %Change -80 -100 k k k k k D e e e e e Q e e e e e w w w w w g a a a a a m e e e e e 0 i c c i c i c i c 2 w n w w w t o t t t g g g g g m m m m m 0 0 0 0 0 1 2 2 3 4 200 µm C2D15 200 µm C2D15 Changes were processed in CD163+ for IHC macrophage analysis of populations CD163 (10D6) were. Whole assessed tissue in paired image tumor was analyzed biopsies by taken using at the screening Flagship and cTA at platform Cycle 2 Day to quantify 15 (C2D15) CD163. . Samples Pathologist C2D15, cycle reviewed 2 day 15; and QD, approved once daily. final analysis results as stratified representation of positivity of a population of cells in the tissue. CONCLUSIONS Dose-escalation evaluation is ongoing to determine the recommended phase 2 dose for advanced solid tumors and diffuse-type TGCT In this study, DCC-3014 was generally well tolerated in patients with advanced solid tumors Exposure to DCC-3014 was dose proportional and was associated with an increase in plasma CSF1 and IL-34 in plasma; and a rapid, sustained reduction of CD16+ monocytes in peripheral blood, and substantial decreases in CD163+ macrophages in tumor These results support further evaluation of DCC-3014 in advanced solid tumors as single agent or in combination, as well as in diffuse-type TGCT The preliminary results from initial diffuse-type TGCT patients will be presented at Connective Tissue Oncology Society Annual Meeting (Abstract #3241734, November 13–16, 2019, Tokyo, Japan) Presented at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; Boston, MA; October 26–30, 2019 Acknowledgments This study was sponsored by Deciphera, LLC. Medical writing and editorial support were provided by Nicole Seneca, PhD; and Stefan Kolata, PhD, of AlphaBioCom, LLC (King of Prussia, PA). References AACR 1) Lin Y, Annual et al. J Meeting; Hematol April Oncol. 16–20, 2019; 2016; 12:76; New 2) Orleans, Cannarile LA. MA, et al. J Immunother Cancer. 2017; 5:53; 3) Patsialou A, et al. Cancer Res. 2009; 69:9498-506; 4) Droin N, et al. J Leukoc Biol. 2010; 87:745-7; 5) Smith BD, et al.