- DCC-3116 Selectively Targets ULK Kinase, an
Initiating Protein that Activates Autophagy -
- Company to Host a Webcast on Tuesday, June
18, 2019 at 8 a.m. ET to Discuss Autophagy Inhibition and the
Treatment of Mutant RAS Cancers -
Deciphera Pharmaceuticals, Inc. (NASDAQ:DCPH) today announced
the addition of a new candidate to its pipeline, DCC-3116, a
potential first-in-class small molecule designed to inhibit cancer
autophagy, a key tumor survival mechanism. DCC-3116, discovered
using the Company’s novel switch control inhibitor platform, is
designed to inhibit autophagy by inhibiting the 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, 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 as well as with direct inhibitors of mutant RAS.
Based on pre-clinical studies, DCC-3116 selectively inhibits ULK
kinase, believed to be the initiating factor that activates
autophagy. Autophagy is a cell survival pathway in which cells
respond to stress by recycling their own components and/or clearing
damaged organelles and proteins from the cell. Mutant RAS cancers,
including KRAS, NRAS, and HRAS cancers, are reported to have high
basal levels of autophagy, which they use to maintain nutrient
supply, regulate cancer cell metabolism, and mitochondria
surveillance.1 In multiple in vitro and in vivo models of mutant
RAS cancers, autophagy inhibition combined with inhibition of MAPK
signaling using MEK inhibitors or ERK inhibitors has demonstrated
synergistic anti-tumor effects.2,3 When used in pre-clinical in
vitro and in vivo studies in combination with inhibitors of the
MAPK pathway, DCC-3116 synergized with these inhibitors to inhibit
mutant RAS cancer growth. Cellular studies in mutant RAS cancers
have demonstrated that MAPK pathway inhibitors further activate
autophagy as a compensatory survival mechanism. Such activation of
autophagy is seen with RAF, MEK, and ERK inhibitors as well as with
direct inhibitors of mutant KRAS G12C. As an inhibitor of ULK,
DCC-3116 is designed to address mutant RAS cancers by inhibiting
the basal and compensatory autophagy that mutant RAS cancer cells
use for their survival.
“We are very excited to announce our new development candidate,
DCC-3116, a potential first-in-class agent aimed at treating mutant
RAS cancers through the inhibition of autophagy,” said Steve
Hoerter, President and Chief Executive Officer of Deciphera.
“Recent efforts in the fight against cancer have focused on direct
approaches targeting mutant RAS, which comprise approximately 30%
of all cancers and that we believe represents one of largest unmet
medical needs in oncology. We believe that as a highly selective
inhibitor of ULK kinase, DCC-3116 may offer a new and complementary
approach to targeting mutant RAS cancer through suppression of
autophagy.”
“Our new clinical candidate, DCC-3116, is a potent and selective
inhibitor of ULK kinase generated using our proprietary switch
control inhibitor platform. Inhibition of ULK has potential
application in a very wide range of cancers and is an exciting
addition to our pipeline,” said Daniel Flynn, Executive Vice
President, Chief Scientific Officer and Founder of Deciphera.
Deciphera is currently conducting IND-enabling studies for
DCC-3116 and, pending favorable results, expects to file an IND in
mid-2020.
DCC-3116 Event and Webcast Information
Deciphera will host a live event and webcast to discuss the new
program on Tuesday, June 18, 2019 at 8 a.m. ET. The event will
feature members of the Deciphera management team and Channing Der,
Ph.D., Sarah Graham Kenan Distinguished Professor, Department of
Pharmacology, UNC School of Medicine, who is a leading expert in
mutant RAS cancers and autophagy.
A live audio webcast of the event and accompanying slides may be
accessed through the Investors section of Deciphera’s website at
www.deciphera.com. A replay of the webcast will be available for 30
days following the event.
About Deciphera Pharmaceuticals
Deciphera Pharmaceuticals is a clinical-stage biopharmaceutical
company focused on improving the lives of cancer patients by
tackling 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, such
as macrophages. We have used our platform to develop a diverse
pipeline of tumor-targeted and immuno-targeted drug candidates
designed to improve outcomes for patients with cancer by improving
the quality, rate and/or durability of their responses to
treatment.
Availability of Other Information About Deciphera
Pharmaceuticals
Investors and others should note that Deciphera Pharmaceuticals
communicates with its investors and the public using its company
website (www.deciphera.com), including but not limited to investor
presentations and scientific presentations, Securities and Exchange
Commission filings, press releases, public conference calls and
webcasts. The information that Deciphera Pharmaceuticals posts on
these channels and websites could be deemed to be material
information. As a result, Deciphera Pharmaceuticals encourages
investors, the media and others interested in Deciphera
Pharmaceuticals to review the information that it posts on these
channels, including Deciphera Pharmaceuticals’ investor relations
website, on a regular basis. This list of channels may be updated
from time to time on Deciphera Pharmaceuticals' investor relations
website and may include other social media channels than the ones
described above. The contents of Deciphera Pharmaceuticals' website
or these channels, or any other website that may be accessed from
its website or these channels, shall not be deemed incorporated by
reference in any filing under the Securities Act of 1933, as
amended.
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 DCC-3116 program, our expectations for and the
possibility of our DCC-3116 candidate to inhibit ULK and autophagy
and possibly treat or provide therapeutic benefit for a wide range
of cancers, and the timing of and our plans to conduct IND-enabling
studies, file an IND and develop DCC-3116 for mutant RAS cancers.
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 designation of
DCC-3116 as a new clinical candidate, the expected benefits and
development of DCC-3116, delay of any current or planned
pre-clinical, IND-enabling and/or clinical studies or the
development of our drug candidates, including ripretinib,
rebastinib, DCC-3014 and DCC-3116, our advancement of multiple
early-stage and later-stage efforts, 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 efforts to scale up and
manage drug product manufacturing, our ability to implement
commercial readiness, actions of regulatory agencies, any or all of
which may affect the initiation, timing and progress of clinical
studies and other risks identified in our SEC filings, including
our Quarterly Report on Form 10-Q for the quarter ended March 31,
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.
References:1. Guo, Jessie Yanxiang et al. “Activated Ras
requires autophagy to maintain oxidative metabolism and
tumorigenesis.” Genes & Development
2011; 25: 460-470.2. Bryant, Kirsten L. et al.
“Combination of ERK and autophagy inhibition as treatment approach
for pancreatic cancer.” Nature Medicine 2019; 25: 628-640.3.
Kinsey, Conan G. et al. “Protective autophagy elicted by RAF
→ MEK → ERK inhibition suggests a treatment strategy
for RAS-driven cancers.” Nature Medicine 2019; 25: 620-627.
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version on businesswire.com: https://www.businesswire.com/news/home/20190610005187/en/
Investor Relations:Jen RobinsonDeciphera Pharmaceuticals,
Inc.jrobinson@deciphera.com781-906-1112
Media:Gina Nugent, The Yates
Networkgina@theyatesnetwork.com617-460-3579
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