A New Pill Finally Offers Hope for Pancreatic Cancer

>> NOW TO A MEDICAL BREAKTHROUGH THAT IS DOUBLING THE SURVIVAL TIME FOR PATIENTS WITH ONE OF THE MOST AGGRESSIVE FORMS OF CANCER.

A NEW PILL TAKEN DAILY TO TREAT PANCREATIC CANCER HAS SHOWN POSITIVE FINDINGS IN A STUDY WITH 500 PATIENTS.

SCIENTISTS FOUND THE DRUG REDUCED THE RISK OF DEATH BY 60% COMPARED TO CHEMOTHERAPY.

DR.

MARK GOLDSMITH, THE CEO OF THE BIOTECH COMPANY WHICH FUNDED THIS DEVELOPMENT, JOINS HARI SREENIVASAN TO DISCUSS THE LANDMARK TREATMENT.

>> BIANNA, THANKS.

DR.

MARK GOLDSMITH, THANK YOU SO MUCH FOR JOINING US.

YOU'RE THE CEO OF REVOLUTION MEDICINES.

IT'S A BIOTECH COMPANY.

ACCORDING TO THE AMERICAN CANCER SOCIETY, THE FIVE-YEAR SURVIVAL RATE FOR PEOPLE WITH IMPEACHMENT INQUIRY --PANCREATIC CANCER, IT'S ABOUT 13%.

BEFORE I GET INTO WHAT IS KIND OF INTERESTING AND INTERESTING ABOUT YOUR MEDICINE, TELL US A LITTLE BIT ABOUT WHY PANCREATIC CANCER IS SO DIFFICULT TO BEAT.

>> THANK YOU, HARI.

IT'S REALLY A PLEASURE TO BE ON WITH YOU.

THIS IS A VERY IMPORTANT MOMENT FOR PATIENTS WHO ARE LIVING WITH CANCERS CAUSED BY SOMETHING CALLED RAS PROTEINS.

THEY'RE THE MOST COMMON CAUSE OF HUMAN CANCERS.

AND THE RESULTS THAT WE'RE TALKING ABOUT TODAY ARE OF SUCH SNUGS THAT SIGNIFICANCE THAT IT'S POSSIBLE THROUGH BOLD INNOVATION AND SCIENTIFIC RISK-TAKING TO REVOLUTIONIZE THE TREATMENT FOR PATIENTS LIVING WITH THESE COMMON AND OFTEN DIFFICULT TO TREAT CANCERS.

PANCREATIC CANCER IS ONE OF THOSE.

MOST PEOPLE WHEN THEY ARE DIAGNOSED WITH PANCREATIC CANCER ALREADY HAVE RELATIVELY ADVANCED DISEASE, AND THAT MAKES IT VERY DIFFICULT TO TRY TO UNWIND AND REALLY THE ONLY TREATMENTS FOR THE MOST PART THAT WE'VE HAD FOR MOST PATIENTS WITH PANCREATIC CANCER, PARTICULARLY THOSE WITH METASTATIC PANCREATIC CANCER IS STANDARD CHEMOTHERAPY.

AND IT HAS JUST NOT PERFORMED AT THE LEVEL THAT ANY PATIENT OR THEIR FAMILY OR PHYSICIAN WOULD LIKE.

AND SO THERE'S BEEN AN ENORMOUS PUSH TO TRY TO FIND NEW WAYS TO TACKLE THE UNDERLYING CAUSES OF THE CANCER, NOT JUST TO TRY TO USE CHEMICALS TO KILL TUMORS.

>> SO WHAT DOES THIS PROTEIN DO TO A HEALTHY CELL?

AND I GUESS WHAT DOES YOUR MEDICINE DO TO THAT PROTEIN?

>> YES.

RAS PROTEINS ARE ABSOLUTELY ESSENTIAL TO EVERY NORMAL CELL IN THE HUMAN BODY.

THEY ACT AS A SWITCH.

THEY CONTROL NORMAL CELL GROWTH.

SO WE'RE HAPPY AND FEELING GOOD WHEN RAS PROTEINS ARE DOING WHAT THEY SHOULD DO.

UNFORTUNATELY, IN 20 TO 30% OF HUMAN CANCERS, THAT SWITCH CAN GET STUCK IN THE ON POSITION, MEANING THAT A GENETIC CHANGE IN THE GENE IN CODING FOR A RAS PROTEIN CAUSES THE RAS PROTEIN TO STAY IN THE ON POSITION AND TO HAVE TROUBLE TOGGLING TO OFF.

AND AS A RESULT, IT'S SENDING SIGNALS WITHIN THE CELL TO GROW AND THEN TO GROW UNCONTROLLABLY, AND THAT CAN LEAD TO A MALIGNANCY.

PANCREATIC CANCER IS ONE DISEASE WHICH IS ALMOST ENTIRELY CAUSED BY RAS PROTEINS.

NEARLY EVERYBODY WHO HAS PANCREATIC CANCER HAS ALTERED RAS PROTEINS WITHIN THE TUMOR, AND THEREFORE TRYING TO TARGET THOSE RAS PROTEINS SEEMS LIKE THE MOST LOGICAL WAY TO GO ABOUT THINGS, BUT THAT'S BEEN DIFFICULT OVER MANY DECADES.

>> OKAY.

SO HOW DID YOUR MEDICINE WORK?

WHAT IS THE -- WHAT IS THE SORT OF KEY HERE?

BECAUSE IF THESE PROTEINS ARE IMPORTANT FOR ALL OF US HEALTHY CELLS, HOW DO YOU TARGET THE ONES, JUST THE ONES THAT ARE DEFECTIVE AND KEEP PUSHING THIS ON SWITCH INSTEAD OF GOING ON AND OFF?

>> YES.

THAT'S A REALLY IMPORTANT AND SUBTLE SCIENTIFIC TOPIC THAT YOU'RE RAISING.

FIRST, IT'S BEEN A CHALLENGE TO BIND A SMALL MOLECULE TO ANY RAS PROTEIN.

AND FOR DECADES, SINCE THE 1980s WHEN RAS PROTEINS WERE IDENTIFIED AS THE FIRST CANCER-CAUSING GENE IN PROTEINS, IT'S BEEN VERY DIFFICULT TO DRUG THESE RAS PROTEINS.

IN THE LAST 10 TO 15 YEARS, WE'VE SEEN SOME PROGRESS IN THAT REGARD.

WE'VE FOUND A WAY STANDING ON THE SHOULDERS OF MANY OTHERS WHO CAME BEFORE US TO DESIGN MOLECULES THAT CAN ESSENTIALLY GLUE ON TO SORT OF LIKE VELCRO, BIND ON TO THE SURFACE OF A RAS PROTEIN AND ATTACH IT TO ANOTHER PROTEIN THAT SMOTHERS IT AND KEEPS IT FROM FUNCTIONING WITHIN THE CELL.

NOW YOU'VE ASKED ABOUT CAN WE DIRECT THAT SPECIFICALLY ONLY TO THE MUTANT FORM OR THE GENETICALLY ALTERED FORM THAT DRIVES CANCER.

AND IT IS POSSIBLE TO DO THAT.

WE HAVE A NUMBER OF MOLECULES LIKE THAT IN OUR PIPELINE THAT ARE VERY SPECIFIC FOR THE MUTANT.

THE REASON THAT DARAXONRASIB, THE INVESTIGATIONAL DRUG THAT MIGHT HAVE LED TO THIS DISCUSSION TODAY, THE REASON THAT THAT MOLECULE IS SO DIFFERENT FROM EVERYTHING ELSE IS IT NOT ONLY USES THIS GLUE MECHANISM, BUT IT BINDS TO THE ACTIVE OR ON FORM EFFECTIVELY.

IT DOESN'T BIND TO THE OFF FORM.

IT'S SPECIFICALLY GOING AFTER THE ONCOGENIC FORM FOUND IN THE TUMORS.

IT DOES ATTACK OR BIND OR TARGET ESSENTIALLY ALL FORMS OF RAS, INCLUDING THE NORMAL RAS PROTEINS.

WE NOW KNOW FROM THE RESULT OF THE CLINICAL-BASED TRIAL THAT WERE JUST LED OUT AT ASCO, THIS WAS A GLOBALIZED RANDOM TRIAL OF 500 PATIENTS WHO RECEIVED EITHER DARAXONRASIB OR STANDARD CARE CHEMOTHERAPY, THAT WE SAW SIGNIFICANT UNPRECEDENTED IMPROVEMENTS ACROSS MANY DIFFERENT MEASURES THAT ARE TYPICALLY USED IN STUDIES OF CANCER DRUGS.

THAT INCLUDED A 60% REDUCTION IN THE RISK OF DEATH, WHICH IS OF COURSE THE MOST IMPORTANT THING THAT WE GO AFTER, BUT SIMILAR REDUCTIONS ACROSS A VARIETY OF DIFFERENT MEASURES.

IN FACT, THOSE SAME PATIENTS ACTUALLY REPORTED THAT THEY SAW A STABILIZATION OF THEIR QUALITY OF LIFE AND PRESERVATION OF THAT QUALITY OF LIFE GREATER THAN DID THOSE WHO RECEIVED CHEMOTHERAPY.

SO LONGER LIFE, PRESERVE QUALITY OF LIFE.

IT INDICATES THAT IT IS POSSIBLE TO DO THAT.

>> IN A CLINICAL TRIAL WITH ABOUT 500 PATIENTS, YOUR MEDICINE NEARLY DOUBLED THE LIFE SPAN COMPARED TO SOMEONE WHO WAS JUST TAKING CHEMOTHERAPY THAT AVERAGE ABOUT 6.

7 MONTHS AND WITH YOUR MEDICINE IT WENT UP TO ABOUT 13.

2 MONTHS.

IT ALSO REDUCED THE DEATH BY 60% IN PATIENTS TAKING JUST YOUR MEDICINE VERSUS CHEMOTHERAPY.

WHAT IS THAT QUALITY OF LIFE LIKE?

WHAT IS THIS DOING THAT'S ALLOWING THEM, I DON'T KNOW, SOMETHING BETTER THAN WHAT THE STANDARD OF CARE IS TODAY?

>> WELL, TWO LIMITATIONS OF STANDARD OF CARE CHEMOTHERAPY YOU TOUCHED ON.

ONE IS THAT IT'S NOT AS EFFECTIVE AS IT NEEDS TO BE.

>> YEAH.

>> IT OFTEN PROVIDES VERY SHORT INCREMENTS IN SURVIVAL.

AND THE EXPERIENCE OF TAKING CHEMOTHERAPY, GOING TO AN INFUSION CENTER REGULARLY, THE SEVERE SIDE EFFECTS, OFTEN HOSPITALIZATION, AND SOME PATIENTS EVEN DIE WHILE THEY'RE RECEIVING CHEMOTHERAPY.

WE NEED TO ADDRESS BOTH OF THOSE.

AND WE BELIEVE DARAXONRASIB DOES THAT BASED ON THE RESULTS WE JUST REPORTED.

AND WE KNOW THAT PATIENTS RING DARAXONRASIB IN GENERAL HAVE BEEN ABLE TO TAKE THAT DRUG CONTINUOUSLY.

SOMETIMES THEY REQUIRE SHORT BREAKS, SHORT VACATIONS, MANY HOLIDAYS FROM THE DRUG.

BUT FOR THE MOST PART, HAVE BEEN ABLE TO TAKE IT AND CONTINUED BENEFITTING FROM ITS SUPPRESSION OF THE RAS PROTEIN THAT'S CAUSING CANCER.

WE KNOW IN ADDITION TO THAT SURVEY THAT PATIENTS TAKE DURING THE COURSE OF THE 302 TRIAL WE ALSO KNOW ALASKAN NECK DOTE TALLY FROM MANY PATIENTS, FROM PHYSICIANS WHO HAVE EXPERIENCED TREATING A PATIENT WITH DARAXONRASIB THAT IT IS NOT UNCOMMON FOR PATIENTS WITHIN A FAIRLY SHORT PERIOD OF TIME TO FEEL BETTER AND FOR THEIR LIFE TO BE IMPROVED TO THE POINT WHERE THEY CAN ACTUALLY EXPERIENCE LIFE, BE WITH THEIR FAMILY, TAKE CARE OF SOME THINGS THAT THEY WOULD VERY MUCH LIKE TO TAKE CARE OF WHILE THEY'RE ACTUALLY HAVING A LONGER LIFE.

BUT I ALSO WANT TO ACKNOWLEDGE SOMETHING REALLY IMPORTANT HERE, HARI.

FOR THE MOST PART, DARAXONRASIB DOESN'T CURE MOST PEOPLE'S CANCERS.

SO WE HAVE MORE WORK TO DO, AND WE CONTINUE TO DESIGN, TO IMPROVE UPON DARAXONRASIB IN A VARIETY OF DIFFERENT WAYS AND TO BRING NEW MOLECULES TO THE CLINIC WITH THE HOPE THAT WE WILL CONVERT PANCREATIC CANCER AND OTHER CANCERS CAUSED BY RAS TO MORE CHRONICALLY MANAGED DISEASES AND EVENTUALLY INTO TRUE CURES.

>> SO DOCTOR, IF THESE RAS MUTATIONS SHOWS UP IN COLORECTAL CANCERS, IN SMALL CELL LUNG CANCERS AND THEY ACCOUNT FOR ALMOST A THIRD OR MORE OF THE DEATHS, CAN THIS MEDICINE BE USED IN THOSE OTHER CANCERS AS WELL?

>> YEAH.

THAT'S A GREAT POINT.

MORE THAN 90% OF PANCREATIC CANCERS CAUSED BY A RAS PROTEIN.

50% OF COLORECTAL CANCER IS CAUSED BY A RAS PROTEIN AND 30% OF SMALL CELL LUNG CANCER.

AND THAT'S JUST THE SHORT LIST OF THE MOST COMMON AND DEADLY CANCERS THAT CAN BE CAUSED BY RAS.

SO YOU'RE RIGHT.

AND WE ARE VERY INTERESTED IN AND VERY ACTIVE IN STUDYING DARAXONRASIB IN PATIENTS WITH THESE OTHER TUMOR TYPES.

IN FACT, WE PUBLISHED --WE HAVE REPORTED DATA ON DARAXONRASIB IN LUNG CANCER IN PATIENTS WITH A RAS CANCER DRIVER ENCOURAGING EARLY DATA, AND WE'RE CURRENTLY RUNNING A GLOBAL PHASE 3 TRIAL IN SMALL CELL LUNG CANCER IN THOSE PATIENTS WHO CARRY A RAS -- CARRY A RAS VARIANTS THAT'S CAUSING THEIR TUMOR.

WE'RE ALSO STUDYING COLORECTAL CANCER.

AND WE HAVE AS I ALLUDED TO EARLIER A DEEP PIPELINE OF MOLECULES BASED ON THIS SAME TECHNOLOGY, BASED ON THIS SAME STRATEGY WHERE WE'VE BENEFITTED FROM A VIRTUOUS CYCLE OF OBSERVATION IN THE CLINIC, SCIENTIFIC INNOVATION IN THE LABORATORY, MORE OBSERVATION IN THE CLINIC, IMPROVED INNOVATION IN THE LABORATORY.

AND THIS IS SOMETHING WE'RE DEEPLY COMMITTED TO FOR THE LONG- TERM TO CONTINUE TRYING TO ADDRESS THESE TIMES ON BEHALF OF PATIENTS.

>> YOU'RE TALKING ABOUT DRUG DEVELOPMENT IN GENERAL TAKING ANYWHERE FROM, I DON'T KNOW, LET'S SAY AVERAGE A DOZEN YEARS.

AND MOST PEOPLE, THAT'S PART OF THE HOPELESSNESS THAT THEY FEEL, THAT EVEN IF YOU'VE GOT SOMETHING IN THE LAB TODAY, IT'S GOING TO TAKE FOREVER BY THE TIME IT CAN ACTUALLY IMPACT MY LIFE.

SO IN THIS PARTICULAR CASE, THIS IS A VERY TRUNCATED TIMELINE.

HOW DID THAT HAPPEN?

>> YEAH.

WE FIRST BROUGHT DARAXONRASIB INTO A CLINICAL STUDY IN 2022.

AND HERE WE ARE IN 2026.

AND WE'VE COMPLETED WHAT SHOULD BE -- APPEARS TO BE THE DEFINITIVE STUDY THAT DEMONSTRATES THIS BENEFIT IN PANCREATIC CANCER.

WE'RE ACTIVELY WORKING TO BRING THE INFORMATION FROM THAT TRIAL TO THE FDA SO THAT THEY CAN REVIEW IT AND MAKE A DECISION ABOUT WHETHER IT SHOULD BE MADE MORE WIDELY AVAILABLE THROUGH AN APPROVAL.

THAT'S A VERY SHORT PERIOD OF TIME.

ONCE THE EARLY RESULTS WERE SEEN IN 2023, PATIENTS WERE CLAMORING TO GET ACCESS TO DARAXONRASIB BECAUSE THEY SMELLED WHAT WE SMELLED, WHICH IS A REAL OPPORTUNITY HERE TO MAKE A DIFFERENCE.

DARAXONRASIB WE HOPE WILL BE MADE AVAILABLE BROADLY THAT WILL BE SUBJECT TO THE REVIEW PROCESS THAT WE NEED TO GO THROUGH WITH THE FDA.

IN THE MEANTIME WE HAVE OPENED AN EXPANDED ACCESS PROGRAM THAT ALLOWS PHYSICIANS WHO ARE CARING FOR PATIENTS WITH PANCREATIC CANCER TO APPLY FOR A DRUG ON BEHALF OF THEIR PATIENTS EVEN BEFORE IT IS APPROVED BY THE FDA AND THE FDA HAS ENDORSED THIS EXPANDED ACCESS PROGRAM.

AND WE'RE NOW SHIPPING DRUG TO DOCTORS ON BEHALF OF THEIR PATIENTS.

SECONDLY, RECEIVING DARAXONRASIB MAY BUY PEOPLE TIME TO ALLOW FOR ADDITIONAL INNOVATION.

AND THAT'S ALREADY BEEN OCCURRING THAT PATIENTS NOW SEE REAL OPPORTUNITY TO CONTINUE THEIR LIVES.

WE HOPE TO HAVE LIVES THAT ARE SATISFYING TO THEM AND TO THEIR FAMILIES.

BUT ALSO HOPE THAT THE NEXT GENERATION OF MOLECULES WILL COME ALONG.

AND WE'RE PUSHING THOSE AS FAST AS WE CAN.

>> WE HAVE A THIS EVIDENCE THAT THERE'S A CLASS AND A CATEGORY OF MEDICINES THAT WILL ACTUALLY REALLY HELPFUL TO A VERY LARGE SWATH OF PEOPLE.

AND THE COST IS A SIGNIFICANT HURDLE.

SO HERE YOU ARE.

YOU'VE SPENT THE TIME AND THE RESOURCES, THE MONEY IN DEVELOPING THIS DRUG, AND YOU WANT TO INCREASE ACCESS.

YOU WANT TO MAKE SURE THAT ANYBODY WITH PANCREATIC CANCER OR ANY OF THE OTHER CANCERS IT WORKS ON GETS ACCESS TO IT.

HOW DO YOU BAKE THAT INTO THE PROCESS?

>> WELL, YOU'RE RIGHT.

IT'S VERY EXPENSIVE TO DEVELOP DRUGS.

WE'VE SPENT EVEN AS A SMALL BIOTECH COMPANY, WE SPENT BILLIONS OF DOLLARS ALREADY EVEN BEFORE WE HAD THE KIND OF EVIDENCE THAT WE HAVE WITH THE RASOLUTE 302 TRIAL.

AND WE'RE RUNNING ABOUT TO INITIATIVE NATE ANOTHER SEVEN OF THESE PHASE 3 TRIALS WHICH ARE EXTRAORDINARILY EXPENSIVE.

SO IT DOES COST A LOT OF MONEY TO DO THIS.

THAT'S JUST INHERENT IN PROVIDING GOOD COMPLIANCE, SAFE MANAGEMENT TO PATIENTS DURING THE COURSE OF THE CLINICAL TRIAL, AND IT REQUIRES LARGE TRIALS THAT TAKE SOMETIMES A COUPLE OF YEARS TO DO.

THAT INVESTMENT HAS TO BE RECOUPED SINCE THAT CAPITAL COMES FROM INVESTORS, AND THAT HAS SOMETHING TO DO WITH PRICING.

I THINK THE OTHER ASPECT OF IT IS THAT DRUGS THAT HAVE GREAT EFFECTS PROBABLY DESERVE TO BE PRICED AT A HIGHER PRICE POINT THAN DRUGS THAT DON'T.

AND THAT'S BUILT INTO THE SYSTEM OF PAIRS, INCLUDING THE FEDERAL GOVERNMENT USE THE OUTCOMES OF THE CLINICAL TRIALS AS ONE OF THE WAYS IN WHICH THEY DECIDE WHAT IS AN APPROPRIATE PRICE AND AN APPROPRIATE TRADE-OFF.

BUT THE QUESTION YOU'RE ASKING IS A VERY BIG ONE THAT HAS TO DO WITH HOW DO WE PAY FOR HEALTH CARE IN GENERAL.

DRUGS ARE A RELATIVELY SMALL COMPONENT OF THE OVERALL COST OF MEDICAL CARE, HOSPITALIZATIONS, PHYSICIAN TIME, INFUSION CENTERS.

THERE ARE MANY, MANY THINGS THAT CONTRIBUTE TO THAT HIGH COST OF MEDICINE, AND WE'LL DO OUR BEST TO DELIVER THE DRUG ON BEHALF OF PATIENTS AND MAKE IT POSSIBLE EVEN FOR THOSE WHO CAN'T AFFORD THROUGH VARIOUS MECHANISMS THAT ARE AVAILABLE.

>> YOU KNOW, I SAW A VIDEO FROM ASCO THAT WAS KIND OF INSPIRING.

YOUR TEAM WAS PRESENTING THE PHASE 3 RESULTS TO THIS HUGE AUDITORIUM FULL OF PEOPLE.

AND YOU JUST SAW A STANDING OVATION.

YOU SAW ALL THESE PEOPLE --SOME OF THEM WERE KIND OF IN TEARS.

BUT TELL ME A LITTLE BIT ABOUT WHY THAT KIND OF MOMENT HAPPENS.

>> WELL, I WAS IN THAT ROOM.

I WAS SITTING AT THE FRONT OF THE ROOM AND FELT THAT WHEN SOME PEOPLE BEHIND ME STARTED TO CLAP, AND WE HEARD THEM STAND UP.

AND THEN WITHIN A FEW SECONDS, THE ENTIRE ROOM WAS STANDING.

IT WAS VERY MOVING FOR ALL OF US AND VERY EMOTIONAL FOR EVERYBODY IN THE ROOM.

I THINK IT'S BECAUSE PANCREATIC CANCER HAS BEEN SO DIFFICULT.

THERE HAVE BEEN MANY FAILED ATTEMPTS TO DEVELOP NEW MEDICINES THAT WOULD REALLY CHANGE AND IMPROVE PEOPLE'S LIVES.

AND THIS ACHIEVEMENT IS VIEWED BY MANY AS UNPRECEDENTED, AS HIGHLY DIFFERENTIATED.

AND ALSO AS YOU ALLUDED TO EARLIER IN OUR CONVERSATION, IT OPENS UP THE POSSIBILITY OF TREATING OTHER PATIENTS WITH DIFFERENT CANCERS, DIFFERENT CANCERS CAUSED BY RAS WITH SIMILAR --WITH THIS DRUG OR OTHER DRUGS LIKE IT AND REALLY MAKING A DIFFERENCE.

AND WE HEARD FROM MANY PEOPLE DURING THE CONFERENCE ONE-ON-ONE, IN LARGE GROUPS, AND OF COURSE IN THAT AUDITORIUM HOW THEY VIEW THIS AS A WATERSHED MOMENT, AND WE'RE SO PROUD TO BE A PART OF THAT.

>> YEAH.

>> AND AT THE SAME TIME, WE HAVE A REALLY DEEP RESPONSIBILITY TO KEEP INNOVATING ON BEHALF OF PATIENTS.

AND WE'RE UNIQUELY POSITIONED TO DO THAT AT REVMED, AND WE WILL CONTINUE.

>> AS A RESEARCHER, WHEN YOU LOOK OUT AT WHAT'S HAPPENED TO A LOT OF DIFFERENT GRANTS THAT GO TO UNIVERSITIES, HOW DOES THAT AFFECT WHAT YOU DO AND WHAT OTHER PRIVATE COMPANIES DO?

IS SOME OF THE TECHNOLOGY OR THE RESEARCH THAT YOU ARE BUILDING ON SOMETHING THAT HAPPENED IN ONE OF THOSE EARLY DISCOVERY LABORATORIES THAT WAS GOVERNMENT FUNDED?

>> ABSOLUTELY.

ABSOLUTELY.

I CAME FROM AN ACADEMIC CAREER IN MEDICINE BEFORE I JOINED THE BIOTECH FIELD WHERE I DID MY WORK BASED ON GRANTS FROM THE FEDERAL GOVERNMENT.

AND I THINK THE IMPACT OF ANY CHANGES IN THAT FUNDING IS SOMETHING THAT WILL BE FELT IN THE FUTURE.

IT DOESN'T ONLY AFFECT THE LIVES OF THOSE WHO ARE ACTUALLY DOING THE RESEARCH AND HAVE A GRANT TRUNCATED, BUT IT REALLY WILL HAVE SIGNIFICANT LONG- TERM IMPACT.

AND I HOPE THAT WE WILL CONTINUE TO INVEST, TO RECOGNIZE THAT THE WORK THAT WE DO TODAY REALLY DOES BUILD ON THE WORK OF YESTERDAY AND THE DAY BEFORE THAT AND THE DAY BEFORE THAT.

AND I FEAR NOT A POLITICAL COMMENT, BUT I FEAR AS WE HAVE COMPETITION FOR RESOURCES THAT THE ACADEMIC WORK MIGHT HAVE IMPACT FOR GENERATIONS TO COME IF WE DON'T MAKE SURE TO SUPPORT IT.

SO WE CERTAINLY ENCOURAGE SUPPORTING IT.

WE'LL DO WHAT WE CAN.

AT REV MED, WE INVEST HEAVILY IN THE SCIENCE.

WE FIND THAT'S THE BEST WAY TO MAKE THE PRODUCTS FOR PATIENTS.

>> CEO OF REVOLUTION DR.

MARK GOLDSMITH.

THANK YOU SO MUCH FOR YOUR TIME.

>> THANK YOU, HARI.

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