IGNYTA, INC. (NASDAQ:RXDX) Files An 8-K Regulation FD Disclosure

Item7.01 Regulation FD Disclosure

On April4, 2017, Ignyta, Inc., (the Company) announced
preclinical data on RXDX-106 which represents a novel class of
immunomodulatory agents that appears to restore innate immunity
in preclinical models via potent inhibition of the TYRO3, AXL and
MER (or TAM) family of receptors presented at the 2017 Annual
Meeting of the American Association for Cancer Research (AACR) in
Washington D.C. In addition, the Company will also showcase its
first ever data in hematological malignancies for entrectinib an
orally available, CNS-active tyrosine kinase inhibitor targeting
tumors that harbor TRK, ROS1 or ALK fusions in molecularly
defined acute myeloid leukemia (AML). The press release, dated
April4, 2017, announcing the new data is attached hereto as
Exhibit 99.1.

The information contained in this Item7.01 and in Exhibit 99.1 of
this Current Report on Form 8-K shall not be deemed filed for
purposes of Section18 of the Securities Exchange Act of 1934, as
amended (the Exchange Act), or incorporated by reference in any
filing under the Securities Act of 1933, as amended, or the
Exchange Act, except as expressly set forth by specific reference
in such a filing.

Item8.01 Other Events

On April4, 2017, the Company announced preclinical data on
RXDX-106 which represents a novel class of immunomodulatory
agents that appears to restore innate immunity in preclinical
models via potent inhibition of the TAM family of receptors
presented at the 2017 Annual Meeting of the AACR in Washington
D.C. In addition, the Company will also showcase its first ever
data in hematological malignancies for entrectinib an orally
available, CNS-active tyrosine kinase inhibitor targeting tumors
that harbor TRK, ROS1 or ALK fusions in molecularly defined AML.

In the presented RXDX-106 data, researchers studied the activity
of RXDX-106 in a
commonly studied syngeneic mouse colon carcinoma model in matched
immunocompetent and immunocompromised mice, finding that RXDX-106
had greater tumor growth inhibition in the immunocompetent
animals, which suggested that RXDX-106 effects in this system
were modulated by the immune system. Immuno-phenotypic modulation
by RXDX-106 was also observed in the mouse model, including an
increase in tumor infiltrating lymphocytes (TILs), an increase in
the ratio of M1/M2 macrophages, and an increase in expression of
CD69 and PD-1 on
CD8 T Cells. In another syngeneic mouse model, RXDX-106 inhibited
tumor growth as a single agent and demonstrated further tumor
growth inhibition in combination with anti-PD-1 or anti-CTLA-4
antibodies, which was accompanied by increased levels of IFN in
the blood. In a separate preclinical investigation of RXDX-106
targets, AXL and MER fusion proteins were shown to independently
act as oncodrivers and, therefore, may be viable therapeutic
targets for patients harboring such molecular alterations. The
preclinical data to be presented at the AACR Annual Meeting
suggest that RXDX-106 can act as both an anti-tumor
immuno-modulator and TAM oncodriver inhibitor and support
clinical development of RXDX-106 in a wide variety of
cancers.