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THIS IS WHERE
POTENTIAL TURNS
INTO POSSIBLE

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COMMITTED TO ENSURING NO CANCER PATIENT RUNS OUT OF OPTIONS

RAS pathway-driven cancers are highly aggressive and often recur, so patients
rarely experience optimal outcomes. We recognize that too many patients with RAS
pathway mutations have been left behind with advances in cancer treatment, and
we’re committed to pursuing paths that haven’t been fully explored to deliver
better options – and ultimately, more hope for these patients.




RAS PATHWAY MUTATIONS ARE AT THE FOREFRONT OF OUR RESEARCH

Almost 30% of all human cancers are driven by mutations in the RAS family of
genes that includes KRAS, NRAS and HRAS. Patients with a RAS pathway mutation
tend to experience worse outcomes and a more significant impact on their lives
than those without RAS pathway mutations.

FIND OUT MORE





EXPANDING POSSIBILITIES FOR PATIENTS

For many patients with difficult-to-treat cancers, the options have been few.
Verastem Oncology aims to change that by relentlessly pursuing RAS-targeted
treatment combinations with avutometinib (VS-6766). We’re driven to develop
treatments that give patients more choices and the possibility of better
outcomes.

EXPLORE OUR PIPELINE





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© 2021 Verastem, Inc. All Rights Reserved.




MEET FAYE SEYEDI VIDEO TRANSCRIPT

I have always loved the science. I've always liked to do work that is discovery.
It's scientific, and obviously that's interesting to me. But I can do that in a
number of different fields related to chemistry. I can be in Ag-chemicals, for
instance. The fact that, at the end of the day, you think you might have made a
difference in someone's life, in a very impactful way, that's very gratifying.


MECHANISM OF ACTION VIDEO TRANSCRIPT

The RAS pathway can be activated by upstream signaling, RAS mutation, or
additional mutations in the pathway. RAS, which includes KRAS, NRAS, and HRAS,
is the most frequently mutated oncogene driving the growth of approximately 30%
of all human cancers. RAS activates RAF, which includes BRAF, CRAF and ARAF. RAF
then phosphorylates and activates MEK, which, in turn, phosphorylates and
activates ERK to drive tumor growth.

Because cancer has a strong dependence on the RAS pathway, blocking any single
target is thought to be insufficient because the cancer will maintain its growth
and survival through compensatory activation of signaling proteins elsewhere in
the RAS pathway or activation of parallel signaling pathways. For example:

 * Activated ERK suppresses upstream RAF signaling through a negative feedback
   loop. Upon binding of a MEK-only inhibitor, phospho-ERK inhibition attenuates
   this suppressive signal thus activating RAF kinase and stimulating tumor
   growth. MEK-only inhibition also induces phosphorylation and compensatory
   activation of Focal Adhesion Kinase and potentially other parallel pathway
   signaling nodes. Once activated, FAK can drive compensatory signaling through
   PI3K, RhoA and YAP, effectively by-passing RAS pathway blockade by the
   MEK-only inhibitor to drive tumor growth.
 * Phospho-ERK inhibition by BRAF-only inhibitors also attenuates the
   suppressive signal from ERK to RAF, reactivating RAF. BRAF inhibitors also
   induce phosphorylation and compensatory activation of FAK.

VS-6766 is a dual RAF/MEK inhibitor that blocks BRAF, CRAF and MEK signaling and
is thought to be the only agent in development that blocks more than one node in
the RAS pathway. In contrast to MEK-only inhibitors, when VS-6766 blocks MEK and
feedback reactivation of RAF occurs, RAF is now prevented from
re-phosphorylating MEK and reactivating the ERK pathway, leading to more
complete and durable suppression of tumor growth.

Novel combinations may be required to achieve the deepest and most durable
response in RAS-driven cancers. VS-6766 has the potential to become a backbone
of therapy by combining it with inhibitors of other nodes of the RAS pathway,
such as KRAS G12C inhibitors, as well as with inhibitors of key targets in
parallel pathways. For example, the combination of VS-6766 with the FAK
inhibitor, defactinib, blocks both RAF and MEK as well as the compensatory FAK
activation for more complete blockade of signaling and tumor growth.

By better controlling the RAS signaling network, customized RAS-targeted
treatment combinations with VS-6766 have the potential to greatly expand the
number of effective treatments for cancer patients who have limited options
today.


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ABOUT THIRD PARTY LINKS ON OUR SITE

Verastem Oncology offers links to other third party websites that may be of
interest to our website visitors. The links provided in our website are provided
solely for your convenience and may assist you in locating other useful
information on the Internet. When you click on these links you will leave the
Verastem Oncology's website and will be redirected to another site. These sites
are not under the control of Verastem Oncology. Verastem Oncology is not
responsible for the content of linked third party websites. We are not an agent
for these third parties nor do we endorse or guarantee their products. We make
no representation or warranty regarding the accurary of the information
contained in the linked sites. We suggest that you always verify the information
obtained from linked websites before acting upon this information. Also, please
be aware that the security and privacy policies on these sites may be different
than Verastem Oncology policies, so please read third party privacy and security
policies closely. If you have any questions or concerns about the products and
services offered on linked third party websites, please contact the third party
directly.

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