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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. We’re driven to develop treatments
that give patients more choices and the possibility of better outcomes.

EXPLORE OUR PIPELINE





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© 2024 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

RAS, which includes KRAS, NRAS, and HRAS, is the most frequently mutated
oncogene driving Because cancer has a strong dependence on the RAS pathway,
blocking any single target is insufficient because the cancer will maintain its
growth and survival through compensatory activation of signaling proteins
elsewhere in the RAS pathway or in parallel pathways. For example:

1. ERK constantly suppresses upstream RAF signaling. Phospho-ERK inhibition by
MEK-only inhibitors attenuates this suppressive signal to activate RAF kinase
and reinvigorate tumor growth. MEK-only inhibition also induces phosphorylation
and compensatory parallel pathway activation of FAK and potentially other
parallel pathway signaling nodes that can drive tumor growth. Once activated FAK
can drive compensatory signaling through pathways, such as PI3K, RhoA and YAP,
effectively by-passing RAS pathway blockade and driving tumor growth.

2. Phospho-ERK inhibition by BRAF-only inhibitors also attenuates the
suppressive signal from ERK to RAF and induces phosphorylation and compensatory
activation of FAK. Avutometinib, which was previously known as VS-6766, is a
first in class RAF/MEK clamp that blocks RAF and MEK signaling by holding ARAF,
BRAF and CRAF in inactive complexes with MEK, and is the only agent in
late-stage clinical development that blocks more than one node in the RAS
pathway. In contrast to MEK-only inhibitors, when avutometinib blocks MEK and
feedback reactivation of RAF occurs, RAF is now prevented from
re-phosphorylating MEK and reactivating the ERK pathway, leading to a more
pronounced and sustained response.

Novel combinations may be required to achieve the deepest and most durable
response in RAS- mediated cancers. avutometinib has the potential to become a
backbone of therapy by combining it with a variety of other agents targeting the
RAS pathway and parallel pathways. Preclinical data have shown a strong synergy
beween avutometinib in combination with inhibitors of other nodes of the RAS
pathway, such as EGFR, KRAS G12C, SHP2, SOS1 and ERK1/2. Synergy of avutometinib
with inhibitors of parallel pathway targets, including FAK, CDK4/6, PI3K, AKT
and mTOR has also been demonstrated. For example, the combination of
avutometinib 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. Avutometinib has the potential to become the preferred backbone of
therapy for a variety of agents targeting the RAS pathway and parallel pathways
involved in tumor growth and metastases. With improved control over the RAS
signaling network, it is possible to develop customized treatment combinations
using avutometinib. Such combinations have the potential to significantly
broaden the range of effective treatments available to patients with RAS
pathway-driven cancers who currently have limited options.


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IS NOT OPERATED BY VERASTEM ONCOLOGY. WE ARE NOT RESPONSIBLE FOR THE CONTENT OR
AVAILABILITY OF LINKED SITES.


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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