We need better drugs now Francis Collins

Tony asked for a show of hands how many

people here are over the age of 48 well

there do seem to be a few well

congratulations because if you look at

this particular slide of us life

expectancy you are now in excess of the

average lifespan of somebody who was

born in 1900 but look what happened in

the course of that century if you follow

that curve you’ll see that it starts way

down there there’s that dip there for

the 1918 flu and here we are at 2010

average life expectancy of a child born

today aged 79 and we are not done yet

that’s the good news but there’s still a

lot of work to do so for instance if you

ask how many diseases do we now know the

exact molecular basis turns out it’s

about 4000 which is pretty amazing

because most of those molecular

discoveries have just happened in the

last little while it’s exciting to see

that in terms of what we’ve learned but

how many of those 4,000 diseases now

have treatments available only about 250

so we have this huge challenge this huge

gap you would think this wouldn’t be too

hard that we would simply have the

ability to take this fundamental

information that we’re learning about

how it is that basic biology teaches us

about the causes of disease and build a

bridge across this yawning gap between

what we’ve learned about basic science

and its application a bridge that would

look maybe something like this where

you’d have to put together a nice shiny

way to get from one side to the other

what would it be nice if it was that

easy unfortunately it’s not in reality

trying to go from fundamental knowledge

to its application is more like this

there are no shiny bridges you sort of

place your bets maybe you’ve got a

swimmer in our rowboat and i’ve sailboat

in a tugboat and you set them off on

their way and the rains come and the

lightning flashes and oh my gosh there’s

sharks in the water and the swimmer gets

into trouble and the swimmer drowned and

you know the sail boat capsized

and that tugboat well it hit the rocks

and maybe if you’re lucky somebody gets

across well what does this really look

like well what is it to make a

therapeutic anyway what’s a drug a drug

is made up of a small molecule of

hydrogen carbon oxygen nitrogen and a

few other atoms all cobbled together in

a shape and it’s those shapes that

determine whether in fact that

particular drug is going to hit its

target is it going to land where it’s

supposed to so look at this picture here

a lot of shapes dancing around for you

now what you need to do if you’re trying

to develop a new treatment for autism or

Alzheimer’s disease or cancer is to find

the right shape in that mix that will

ultimately provide benefit and will be

safe and when you look at what happens

to that pipeline you start out maybe

with thousands tens of thousands of

compounds you weed down through various

steps that cause many of these to fail

ultimately maybe you can run a clinical

trial with four or five of these and if

all goes well 14 years after you started

you will get one approval and it will

cost you upwards of a billion dollars

for that one success so we have to look

at this pipeline the way an engineer

would and say how can we do better and

that’s the main theme of what I want to

say to you this morning how can we make

this go faster how can we make it more

successful well let me tell you about a

few examples where this has actually

worked the one that has just happened in

this last a few months is the successful

approval of a drug for cystic fibrosis

but it’s taking a long time to get there

cystic fibrosis had its molecular cause

discovered in 1989 by my group working

with another group in Toronto

discovering what the mutation was in a

particular gene on chromosome 7 that

picture you see there here it is that’s

the same kid that’s Danny Bessette 23

years later because this is the year and

it’s also the year where Danny got

married where we have for the first time

the approval by the FDA of a drug that

precisely targets the defect in cystic

fibrosis based upon all this molecular

understanding that’s the good news the

bad news is this drug doesn’t actually

treat all cases of cystic fibrosis and

it won’t work for Danny and we’re still

waiting for that next generation to help

him but it took 23 years to get this far

that’s too long how do we go faster

well more money to go faster is to take

advantage of

technology and a very important

technology that we depend on for all of

this it’s the human genome the ability

to be able to look at a chromosome to

unzip it to pull out all the DNA and to

be able to then read out the letters in

that DNA code the a C’s GS and T’s that

are our instruction book in the

instruction book for all living things

and the cost of doing this which used to

be in the hundreds of millions of

dollars has in the course of the last 10

years fallen faster than Moore’s law

down to the point where it is less than

ten thousand dollars today to have your

genome sequenced or mine and we’re

headed for the thousand dollar genome

fairly soon well that’s exciting how

does that play out in terms of

application to a disease I want to tell

you about another disorder this one is a

disorder which is quite rare

it’s called hutchinson gilford progeria

and it is the most dramatic form of

premature aging only about one in every

four million kids has this disease and

in a simple way what happens is because

of a mutation in a particular gene a

protein is made that’s toxic to the cell

and it causes these individuals to age

at about seven times the normal rate let

me show you a video of what that does to

the cell the normal cell if you looked

at it under the microscope would have a

nucleus sitting in the middle of the

cell which is nice and round and smooth

in its boundaries and it looks kind of

like that a progeria cell on the other

hand because of this toxic protein

called progeria has these lumps and

bumps in it so what we would like to do

after discovering this back in 2003 is

to come up with a way to try to correct

that

well again by knowing something about

the molecular pathways it was possible

to pick one of those many many compounds

that might have been useful and try it

out in a named experiment done in cell

culture and shown here in a cartoon if

you take that particular compound and

you add it to that cell that has

progeria and you watch to see what

happened in just 72 hours that cell

becomes for all purposes that we can

determine almost like a normal cell well

that was exciting but would it actually

work in a real human being

this is led in the space

of only four years from the time the

gene was discovered to the start of a

clinical trial to a test of that very

compound and the kids that you see here

all volunteered to be part of this 28 of

them and you can see as soon as the

picture comes up that they are in fact a

remarkable group of young people all

afflicted by this disease all looking

quite similar to each other and instead

of telling you more about it I’m going

to invite one of them Sam burns from

Boston who’s here this morning to come

up on the stage and tell us about his

experience as a child affected with

progeria Sam is 15 years old his parents

Scott Burns and Leslie Gordon both

physicians are here with us this morning

as well Sam please have a seat

so Sam why don’t you tell these folks

what it’s like being affected with this

condition called progeria

well progeria limits me in some ways I

cannot play sports or do physical

activities but I have been able to take

interest in things that progeria luckily

does not limit but when there is

something that I really do want to do

that progeria gets in the way of like

marching band or umpiring we always find

a way to do it and that just shows that

progeria isn’t in control of my life so

what would you like to say there

researchers here and in the auditorium

and others listening to this what would

you say to them both about research on

progeria and maybe about other

conditions as well well a research on

progeria has come so far in less than 15

years and that just shows the drive that

researchers can have to get this far and

it really means a lot to myself and

other kids with progeria and it shows

that if that drive exists anybody can

cure any disease and hopefully progeria

can be cured in the near future and so

we can eliminate those 4,000 diseases

that Francis was talking about excellent

so Sam took the day off from school

today to be here and he is he he is by

the way a straight A plus student in the

ninth grade in his school in Boston

please join me in thanking and welcome

Sammy well done

so I just want to say a couple more

things about that particular story and

then try to generalize how could we have

stories of success all over the place

for these diseases as Sam says these

4,000 that are waiting for answers you

might have noticed that the drug that is

now in clinical trial for progeria is

not a drug that was designed for that

it’s such a rare disease it would be

hard for a company to justify spending

hundreds of millions of dollars to

generate a drug this was a drug that was

developed for cancer turned out it

didn’t work very well for cancer but it

has exactly the right properties the

right shape to work for progeria and

that’s what’s happened wouldn’t it be

great if we could do that more

systematically could we in fact

encourage all the companies that are out

there that have drugs in their freezers

that are known to be safe in humans but

have never actually succeeded in terms

of being effective for the treatments

they were tried for now we’re learning

about all these new molecular pathways

some of those could be repositioned or

repurposed or whatever word you want to

use for new applications basically

teaching old drugs new tricks that could

be a phenomenal valuable activity we

have many discussions now between NIH

and companies about doing this that are

looking very promising and you can

expect quite a lot to come from this

there are quite a number of success

stories one can point to about how this

has led to major advances the first drug

for hiv/aids was not developed for

hiv/aids it was developed for cancer it

was AZT didn’t work very well for cancer

but became the first successful

antiretroviral and you can see from the

table there are others as well so how do

we actually make that a more

generalizable effort well we have to

come up with a partnership between

academia government the private sector

and patient organizations to make that

so at NIH we have started this new

National Center for advancing

translational sciences just started last

December and this is one of its goals

let me tell you another thing we could

do would it be nice to be able to test a

drug to see if it’s effective and safe

without having to put patients at risks

because that first time you’re never

quite sure how do we know for instance

whether drugs are safe before we give

them to people we test them on animals

and it’s not all that reliable

and it’s costly and it’s time-consuming

suppose we could do this instead on

human cells you probably know if you’ve

been paying attention to some of the

science literature that you can now take

a skin cell and encourage it to become a

liver cell or a heart cell or a kidney

cell or a brain cell for any of us so

what if you use those cells as your test

for whether a drug is going to work and

whether it’s going to be safe here you

see a picture of a lung-on-a-chip this

is something created by the vist

Institute in Boston and what they have

done here if we can run the little video

is to take cells from an individual turn

them into the kinds of cells that are

present in the lung and determine what

would happen if you added to this

various drug compounds to see if they

are toxic or safe you can see this chip

even breathes it has an air channel it

has a blood channel and it has cells in

between that allow you to see what

happens when you add a compound are

those cells happy or not you can do this

same kind of chip technology for kidneys

for hearts for muscles all the places

where you want to see whether a drug is

going to be a problem for liver and

ultimately because you can do this for

the individual we can even see this

moving to the point where the ability to

develop and test medicines will be you

on a chip what we’re trying to say here

is the individualizing of the process of

developing drugs and testing their

safety so let me sum up we are at a

remarkable moment here for me at NIH now

for almost 20 years there has never been

a time where there was more excitement

about the potential that lies in front

of us we have made all these discoveries

pouring out of laboratories across the

world what do we need to capitalize on

this first of all we need resources this

is research that’s high risk sometimes

high cost the payoff is enormous both in

terms of health and in terms of economic

growth we need to support that second we

need new kinds of partnerships between

academia and government and the private

sector and patient organizations just

like the one I’ve been describing here

in terms of the way which we could go

after repurposing new compounds and

third and maybe most important we need

talent we need the best and the

brightest from many different

disciplines to come and join this effort

all ages all different groups

because this is the time folks this is

the 21st century biology that you’ve

been waiting for and we have the chance

to take that and turn it into something

which will in fact a knockout disease

that’s my goal I hope that’s your goal I

think it’ll be the goal of the poets and

the Muppets and the surfers and the

bankers and all the other people who

join this stage and think about what

we’re trying to do here and why it

matters it matters for now it matters as

soon as possible if you don’t believe me

just ask Sam thank you all very much

you

托尼要求举手,

这里有多少人 48 岁以上,

似乎确实有一些

祝贺,因为如果你看

这张我们预期寿命的特殊幻灯片,

你现在已经超过

了某人的平均寿命 谁

出生于 1900 年,但看看那个世纪发生的事情,

如果你遵循

这条曲线,你会发现它从

那里开始下降,那里

是 1918 年流感的下降,这里是 2010 年

孩子的平均预期寿命

今天出生,79 岁,我们还没有完成

,这是个好消息,但是还有

很多工作要做,例如,如果

你问我们现在知道多少种疾病,

确切的分子基础结果是

大约 4000 种,这非常惊人,

因为 大多数这些分子

发现刚刚发生在

最近一段时间内,令人兴奋的

是,就我们所学到的而言,但是

这 4,000 种疾病中有多少现在

只有大约 250 种可用的治疗方法,

所以我们有这个拥抱 挑战这个巨大的

差距,你会认为这不会

太难,因为我们只是有

能力利用

我们正在学习的基本信息,

了解基础生物学如何教会我们

疾病的原因并建立一座

桥梁 跨越

我们所学到的基础科学知识

及其应用之间的巨大差距

如果这很

容易,不幸的是,实际上并没有

尝试从基础知识

到应用,更像是

这样 没有闪亮的桥梁

你可以下注 也许你有一个

游泳者在我们的划艇上,而我有

帆船 一艘拖船,你把

他们引到路上,雨来了,

闪电闪烁,哦,天哪

,水里有鲨鱼,游泳者

遇到麻烦,游泳者淹死了,

你知道帆船卡西 zed

和那艘拖船很好地撞到了岩石上

,如果你幸运的话,也许有人能

顺利通过这看起来真的

很好吗?无论如何要制作

治疗药物是什么药物药物

是由一个小分子的

氢碳组成的 氧氮和

其他一些原子都拼凑在一起形成

一个形状,正是这些形状

决定了

特定药物是否真的会击中它的

目标,它是否会降落在它

应该到达的地方所以看这张照片这里

有很多形状 现在为你跳舞

如果你正在

尝试开发一种新的治疗自闭症或

阿尔茨海默病或癌症的方法,你需要做的是

在这种混合物中找到合适的形状,

最终会带来好处并且是

安全的,当你看到

你开始的那个管道会发生什么,你可能

会通过各种步骤清除成千上万种化合物

,导致其中许多最终失败,

也许你可以

用四个或 其中五个,如果

在您开始 14 年后一切顺利,

您将获得一个批准,并且

您将为此花费 10 亿美元以上

的成功,因此我们必须

以工程师的方式看待这条管道,

并说出我们如何才能 做得更好,

这就是我

今天早上想对你们说的主题 我们怎样才能让

这件事进展得更快 我们怎样才能让它更

成功 让我告诉你们

几个例子

过去几个月发生的事情是成功

批准了一种治疗囊性纤维化的药物,

但它需要很长时间才能实现

囊性纤维化的分子原因

是我的团队在 1989 年

与多伦多的另一个团队合作

发现了突变的原因

7 号染色体上的一个特殊基因,

你在这里看到的图片就是

23 年后丹尼·贝塞特的同一个孩子,

因为今年也是丹尼结婚的一年

,我们有 f 或者

是 FDA 首次批准一种

基于所有这些分子

理解的精确靶向囊性纤维化缺陷的药物,这是好消息,

坏消息是这种药物实际上并不能

治疗所有囊性纤维化病例,

它不会 不为 Danny 工作,我们仍在

等待下一代来帮助

他,但花了 23 年才走到这一步

,这太长了,我们如何才能更快

更好地更快地获得更多资金,这是利用

技术和一个非常重要的

我们所依赖的技术

是人类基因组

能够查看染色体

解压缩它以提取所有DNA

然后能够读出

该DNA代码中的字母a C的GS 和 T

是我们在

所有生物的指导书中的指导书,

而这样做的成本曾经

是数亿

美元,在过去的 10

年中下降得比摩尔定律快

今天对你

或我的基因组进行测序只需不到一万美元,我们很快就会

走向千美元的基因组

,这令人兴奋

,这在

我想告诉你另一种疾病的应用方面如何发挥作用

这种疾病是一种

非常罕见的疾病,

它被称为哈钦森吉尔福德早衰症

,它是最引人注目的早衰形式,

400 万儿童中只有大约一个患有这种疾病

,简单来说,发生的事情是由于基因中

的一个突变 特定基因

一种对细胞有毒

的蛋白质会导致这些人以

正常速度的七倍左右衰老 让

我给你看一段视频,看看它对细胞有什么

影响 如果你

在显微镜下观察正常细胞会

在细胞中间有一个

细胞核,它的边界很好,圆润,

光滑,另一方面,由于这种有毒蛋白质,它

看起来有点像早衰细胞

所谓的早衰症中有这些肿块和

肿块,所以我们

在 2003 年发现这一点后想做的

是想出一种方法来尝试

通过了解一些

分子途径来再次纠正这种情况,

可以选择其中一个

那些可能有用的许多化合物,并

在细胞培养中进行的命名实验中进行尝试,

如果

您服用该特定化合物

并将其添加到具有

早衰症的细胞中并观察发生了什么,请在卡通图中显示

在短短 72 小时内,该细胞

就可以用于我们可以确定的所有目的,

几乎就像一个正常的细胞井

一样令人兴奋,但它是否

真的在真正的人类身上起作用?

这是在基因被发现

后仅四年的时间里导致的

临床试验开始到对这种

化合物进行测试,你在这里看到的孩子们

都自愿成为这 28 个

孩子中的一员 扮演一群

受到这种疾病折磨的非凡年轻人,他们看起来都

非常相似,

我不会告诉你更多关于它的事情

,我要邀请其中一个来自波士顿的 Sam Burns,

他今天早上在

这里上台 告诉我们他

小时候患有

早衰症的经历 Sam 15 岁 他的父母

Scott Burns 和 Leslie Gordon 两位

医生今天早上也和我们在一起

就像受到

这种称为早衰的疾病的影响,

早衰在某些方面限制了我我

不能参加体育运动或进行体育活动,

但我能够对

早衰没有限制的事情感兴趣,

但是当有

一些我真正想要的东西时 要做到

这一点,早衰就像

军乐队或裁判一样,我们总能找到

一种方法来做到这一点,这只是表明

早衰无法控制我的生活,所以

你想说什么

这里和礼堂里的研究人员

和其他听这个的人

关于

早衰症的研究,也许还有其他

条件,以及

早衰症的研究到目前为止,不到 15

年的时间里,你会对他们说些什么,这只是显示了驱动力

研究人员必须走到这一步,

这对我自己和

其他患有早衰症的孩子来说意义

重大

弗朗西斯所说的 4,000 种疾病非常好,

所以山姆今天请了一天假

来这里,他就是他,顺便说一下,

他是波士顿学校九年级的一名全 A+ 学生,

请和我一起感谢和欢迎

Sammy 做得很好,

所以我只想

对那个特定的故事多说几句,

然后试着概括一下,我们怎么能像 Sam sa 那样

在各地都有成功的故事来

治疗这些疾病 是的,这

4,000 人正在等待答案,您

可能已经注意到,

现在用于早衰症临床试验

的药物并不是专为这种罕见疾病而设计的药物,

一家公司很难证明花费

数亿美元是合理的 美元来

生产一种药物 这是一种

为癌症而开发的药物 结果它对癌症的

效果不是很好,但它

具有完全正确的特性

正确的形状可以为早衰症工作,

这就是发生的事情 不是

很好 如果我们能更系统地做到这一点,

我们实际上是否可以

鼓励所有

在冰箱

中存放已知对人类安全但

从未真正成功

地对其尝试的治疗有效的药物

的公司 现在我们正在

学习所有这些新的分子途径,

其中一些可以重新定位或

重新利用,或者你想在

新应用中使用的任何词,基本上是

教旧药 可能

是一项非常有价值的活动的新技巧 我们

现在在 NIH

和公司之间就这样做进行了许多讨论,这些讨论

看起来非常有希望,你可以

期待从中获得

相当多的成功案例 有很多成功

案例可以指出 关于这

如何导致重大进展 第一种

艾滋病毒/艾滋病药物不是针对

艾滋病毒/艾滋病开发的 它是针对癌症

开发的

表还有其他的,所以

我们如何真正做出更

普遍的努力,我们

必须在

学术界、政府、私营部门

和患者组织之间建立伙伴关系,

以便在 NIH 我们启动了这个新的

国家推进中心

转化科学去年 12 月才刚刚开始

,这是它的目标之一,

让我告诉你另一件我们

可以做的事情,如果能够测试一种

药物,看看是否 它既有效又安全,

无需将患者置于危险之中,

因为第一次你永远无法

确定我们如何

知道药物是否安全,然后再将

它们提供给我们在动物身上进行测试的人,

而且它并不是那么可靠

,它是 成本高且耗时

假设我们可以在人体细胞上进行此操作,

您可能知道,如果您

一直关注一些

科学文献,您现在可以

将皮肤细胞转化为

肝细胞或心脏 细胞或肾

细胞或脑细胞对于我们任何人来说,

如果您使用这些细胞来测试

药物是否有效以及

它是否安全,您会

看到一张肺上的图片 -芯片 这

是波士顿vist研究所创造的东西,

如果我们可以播放这个小视频,他们在这里所做的

就是从一个人身上提取细胞,

把它们变成肺部存在的细胞类型,

然后确定

会发生什么 如果你添加 d 到

各种药物化合物中,看看它们

是否有毒或安全 你可以看到这个芯片

甚至可以呼吸 它有一个空气通道 它

有一个血液通道,它之间有细胞

,可以让你看到

当你添加一个化合物时会发生什么

那些细胞高兴与否,你可以

为肾脏、心脏、肌肉做同样的芯片技术,

所有

你想知道药物是否

会对肝脏造成问题的地方,

最终因为你可以为

我们的个体做这件事 甚至可以看到这

发展到开发和测试药物的能力将是你

在一个芯片上我们在这里想说的

开发药物和测试其

安全性的过程的个性化所以让我总结一下我们是

近 20 年来,

在 NIH

对我来说是一个

非凡的时刻 s the

world 我们需要利用

什么 首先我们需要资源

这是高风险的研究 有时

是高成本 在

健康和经济增长方面的回报是巨大的

我们需要支持第二个 我们

需要新的

学术界和政府以及私营

部门和患者组织之间的各种伙伴关系,

就像我在

这里描述的那样,我们

在重新利用新化合物后可以采取的方式,

第三,也许最重要的是,我们需要

人才,我们需要最好的

来自许多不同学科的最聪明的人

来加入这项工作,

所有年龄段的不同群体,

因为这

是你们一直在等待的 21 世纪生物学的

时候了,我们

有机会把它变成一些东西

这实际上是一种淘汰疾病

那是我的目标 我希望那是你的目标 我

认为这将是诗人

、布偶、冲浪者和

银行家的目标 所有其他

加入这个阶段并思考

我们在这里尝试做什么以及为什么它

现在很重要

如果你不相信我

就尽快问山姆非常感谢你们