Filed by Vertex Pharmaceuticals Incorporated
                           Pursuant to Rule 425 under the Securities Act of 1933
                           Subject Company:  Aurora Biosciences Corporation
                           Commission File Number:  000-22669

The following communications contain forward-looking statements within the
meaning of the Safe Harbor Provisions of the Private Securities Litigation
Reform Act of 1995 about Vertex Pharmaceuticals Incorporated and Aurora
Biosciences Corporation. While the management of Vertex and Aurora make their
best efforts to be accurate in making forward-looking statements, any such
statements are subject to risks and uncertainties that could cause actual
results to vary materially. The forward-looking statements herein address the
following subjects: the belief that the field of kinase inhibitors is going
to be a very fruitful field for drug discovery over the next 10 to 15 years
and will be an important field in many pharmaceutical markets in the future;
the belief that the partnership between Vertex and Novartis position Vertex
and Novartis to hold a very significant position in the field of kinase
inhibitors which will allow Vertex and Novartis to capture a portion of
future markets creating drugs for patients, revenues, profits and shareholder
value; the belief that Vertex is on track to deliver to Novartis; the belief
that Vertex's chemogenomics and structure based platforms give Vertex a
significant, competitive advantage in bringing drugs into the clinic; the
belief that more than 10% of the 500 kinases in the humane genome will be
viable drug targets; the belief that most developments regarding kinase
inhibitors will be in connection with the treatment of cancer, which is the
new way to think about the treatment of cancer; the belief that kinase
inhibitors aimed at kinases other than those currently targeted will enter
the clinic over the next few years for the treatment of cancer; the belief
that multiple kinases inhibitors are required to treat various types of
cancers; the belief that Vertex will have a number of drugs that will be
effective Anti-angiogenic agents in the treatment of cancer; the belief that
Vertex will name two development candidates by the end of this year for
treatment of disease; the belief that Vertex will have additional partners
developing kinase inhibitors that Vertex will develop over the next decade;
the expected announcements of new drug candidates developed individually and
with partners, which should expand to greater than two candidates per year;
the belief that Vertex has a potential diabetic kinase which is the best,
most favored diabetes target in any class; the belief that Vertex's drug
development model and intellectual property protection strategies (i) are the
right mechanisms relating to its drugs, (ii) are particularly suited for
looking at large number of related proteins and (iii) will enable Vertex to
be ready to mine the future kinase and protease universes; the belief that
Vertex has major market opportunities in myocardial and neurological
conditions; the belief that Caspase inhibitors have relevance in Sepsis,
Liver distress and other things; the belief that Vertex has great potential
in anti-biotic resistance, HCV and Alzheimer's disease; the belief that
Vertex is developing strong chemistry and intellectual property foundations;
the expectation of having 160+ scientists by the end of 2001; the belief that
the merger of Aurora and Vertex will strengthen Vertex's ability to produce
through-put in enzyme targets and other non-enzyme areas; and the belief that
Vertex is in the process of rejuvenating big pharma companies' product
pipelines creating opportunities for co-promotion.

The following factors, among others, could cause actual results to differ
materially from those described in the forward-looking statements: the
possibility of delays in the research and development necessary to select
drug development candidates and delays in clinical trials, the risk that
clinical trials may not result in marketable products, the risk that the
combined company may be unable to successfully finance and secure regulatory
approval of and market its drug candidates, the development of competing
systems, the combined company's ability to protect its proprietary
technologies, patent-infringement claims, risks of new, changing and
competitive technologies and regulations in the U.S. and internationally,
costs related to the merger, failure of Vertex's or Aurora's stockholders to
approve the merger, Vertex's or Aurora's inability to satisfy the conditions
of the merger, the risk that Vertex's and Aurora's businesses will not be
integrated successfully, the termination of existing Aurora pharmaceutical
and biotechnology collaborations, the combined company's inability to further
identify, develop and achieve commercial success for new products and
technologies, and risks associated with Aurora's new and uncertain
technology, dependence upon pharmaceutical and biotechnology collaborations.

                              *********************



THE FOLLOWING IS THE SCRIPT OF A PRESENTATION PRESENTED TO ANALYSTS, INVESTORS
AND OTHERS ON MAY 31, 2001 AND POSTED ON VERTEX'S WEBSITE ON JUNE 1, 2001.


                               VERTEX INVESTOR DAY

                    "MEDICAL POTENTIAL OF KINASE INHIBITORS"
                               ROBERT MASHAL, M.D.

MASHAL: Hi. We'd ask you all to take your seats and I'll get started. My name's
Robert Mashal. I'm not a familiar face to most of you. I'm a Program Executive
for the MDR Program at Vertex. But one of the other things I do is serve on the
Joint Reseach Committee for the Vertex/Novartis collaboration. And it's that hat
that I'm wearing today.

And, what I'd like to do is to tell you all a little bit about the medical
potential of kinase inhibitors. And show you some of the progress that we're
making in bringing kinase inhibitors through the discovery process and into the
clinic. And talk about, I think, how Vertex and Novartis are positioned to hold
a very significant position. We think it is going to be a very fruitful field
for drug discovery over the next 10 to 15 years.

So, I'm going to talk about kinases. What they do in terms of their role in
cellular signaling and human disease. I'll give you some historical and new
perspectives on kinase drug development. And then talk to you about the
advantages that the Vertex/Novartis collaboration will have going forward. And I
think that our partnership is going to lead to a very significant position in
the field.

So, I'll talk a little bit about Why Kinases, Why Now, and Why Us? And I
think, that there are several good reasons for this. It's been known for
quite some time that kinases are important in many pathways that are relevant
to human disease. That evidence first started coming out in the late '70's
and early '80's. And people have always thought that these might be
interesting drug targets. But, historically, there were lots of concerns
about drug development efforts. So, as recently as the late '80's and early
'90's -- drug companies had these small sort of nice efforts, aimed at
targeting kinases. But they were viewed with sort of cautious skepticism --
in the sense that people thought it was very, very difficult to make in
inhibitors that were specific to individual kinases. And, because kinases
played a lot of roles -- and you were going to wind up making drugs that had
a lot of different kinases, you are going to have a lot of toxicity problems.
And those notions about drug specificity and toxicity have largely been
dispelled, I think, over the last few years. And it's something that I'm sure
that you've been reading about -- with the recent approval of Gleevec and
CML. And, finally, why us? I think that Vertex and Novartis are uniquely
positioned in the field. Our chemogenomics and structure-based platforms, I
think, really do give us a significant, competitive advantage in bringing
drugs into the clinic. And working with a partner who has proven expertise in
kinase inhibitor development -- and now, sales and marketing. I think it's
going to give a very, very significant competitive advantage -- all the way
through commercialization to the Vertex/Novartis partnership.

So, let me just start by telling you what is a kinase? A kinase is an enzyme.
And what that enzyme does is put a phosphate group on another biological
molecule. And that other biological molecule is usually a protein. The phosphate
group comes from ATP. So, what I've got here on the left is a protein. I've got
here a picture of ATP. These three pink things are phosphate groups. And ATP
gets converted into ADP. And one of the phosphate groups from ATP gets stuck on
this biological molecule. And what a kinase does is catalyze that reaction of
transferring the phosphate group from ATP to the other biological molecule. Now,
when a phosphate group gets stuck on another biological molecule -- it usually
modifies the activity of that target molecule. Usually, that modification is an
activation of function -- although not always. Sometimes it is an inactivation
of function. But, generally what this is -- is when a kinase sticks a phosphate
group in another biologic molecule, that biological molecule





has an altered function -- usually becoming activated. And what inhibitors do is
block that function in 99.99% of the time. And the way they do that is by
occupying the ATP binding side of the kinase.

So that's pictured here. Here's ATP out here. This big, purple glob is a kinase
enzyme. That deep pocket that you see in there is the ATP pocket, where normally
ATP would go. Most of the kinase inhibitors that people are looking at, actually
occupy that kinase binding side. They sit in there so that ATP can't get in
there -- and the kinase enzyme can't perform its function.

So, Kinase Cascades -- they operate in cascades -- are important in lots and
lots of signalling processes. So, what Kinases do is that they help cells
mediate signals. Those signals generated usually on the outside of the cell
- --and transmitted into the nucleus -- telling the signal what to do. And,
kinases are generally the intermediary, messenger model. So they're involved
in signallings for growth factors. For blood vessel growth. For telling the
cell to divide -- which all provide targets for cancer. There are kinases in
T Cells which are important to transplantation and autoimmune disease. Kinase
is the insulin receptor. In fact, a kinase of the signal downstream -- most
of the signals downstream are the insulin receptor are mediated through
kinases. So, there are multiple points of attachment for that pathway. For
Diabetes. Adrenaline signals through kinases. That's important in heart
failure and so on, and so forth. What I really want to make a point is --
these are all big diseases.

So if you look at the sort of world-wide drug market -- you know, some of the
diseases I've mentioned -- cardiovascular diseases, anti-infectives, cancer
agents -- these are all multi-billion dollar type markets. And the real point to
take away from this is that kinases are going to be important in many major
pharmaceutical markets over the next few years, I think.

Now, kinases are a particularly rich family for drug discovery. There are about
500 kinases in the human genome. And if you just go historically looking at
families like this one - -something around 10% of these are going to turn out to
be viable drug targets. We know that many of these kinases, play a central role
in major diseases. And a common feature of all of these enzymes is the kinase
domain which includes that ATP binding pocket. And what that means is that this
entire family is amenable to the sort of parallel chemogenomic discovery
approach that we use here at Vertex. And I'm going to show you some ways in
which the structural insights that we gain from using that approach allow us to
develop very specific kinase inhibitors.

So, this is a rather a complicated slide. And what I want to do is to make a
couple of points. All of these things in purple are kinases. And I'll use
that color scheme throughout the talk. The things in orange are what are
called "transcription factors". These are the things that receive signals
from kinases. And then bind from DNA -- telling the cell to make certain
genes which result in changes in cellular function. And, these other
molecules marked in blue are molecules that are involved in kinase function
- -- sorry, in cell signaling --but are not necessarily themselves kinases. The
take-aways from this slide are: 1) there's a lot of cross talk between these
pathways. Most of what I'm about to show you, going forward, is a little bit
of an over-simplification. And, in fact, kinase biology is rather complex.
The second is, that most of these kinases operate in Cascade. So, here it's a
receptor kinase, will activate another kinase, which will activate another
kinase, which will activate another kinase. If it's not sort of linear
process as shown on this slide -- but it is really more of a chain reaction.
And, if you remember -- sort of from your early Physics classes -- where
you're modeling a nuclear chain reaction. And one marble hits two marbles
which hit four marbles, which hit eight marbles -- and that kind of
amplification. That's exactly what happens when kinases are involved. So, a
single molecule like insulin might bind to its insulin receptor. And that
single insulin molecule -- that signal from the single insulin molecule, gets
amplified many




times before it actually gets down here to the nucleus and tells itself to
start making genes that are involved in glucous metabolism. So, I'm going to
show you a little bit of a movie now in terms of the way that kinases work.
Again the things in purple are the kinases. I have here a growth factor. This
is the epidermal growth factor. This is the epidermal growth factor receptor.
And I'm going to turn on the movie and show you what happens. So the
epidermal growth factor -- will bind to its cognate receptor. That will
activate the receptor, which will in fact phosphoralate itself. That
phosphoralation process activates another molecule called Ras. And when Ras
gets activated through a complex pattern -- it recruits Raf, the nucleous,
and Raf gets phosphoralated. Phosphoralated Raf is now active. It goes and
activates MEK. When MEK gets activated, it activates ERK. When ERK gets
activated, it goes and activates ELK by sticking phosphate groups on it. And
when ELK -- this transcription factor --gets activated -- it binds to the DNA
- -- activating the genes. So, normally all of these molecules are sitting in
the cell -- inactive. And they only become activated when this growth factor
binds to its receptor. And that kinase Cascade is the way the EGR tells the
cell to start growing and dividing.

So, most of what you've heard about kinase and kinase inhibitors are in Cancer.
And I think that's going to be true for the next few years. Most of the kinase
inhibitors that you see -- going into the clinic will be developed in cancer.
And that's because kinases play key role in processes central to tumor growth. I
showed you a little bit about a growth factor signalling cascade. And, as you
know, there are a number of drugs out there now which target the EGF receptor
kinase. Kinases, as I'll show you, are involved in cell cycle regulation, or the
process of cell division -- where cells double their DNA -- and split to two
daughter cells. Kinases are also key to the process of Angiogenesis. And in
cancer, we are already noticing a number of successful drugs -- which go after
kinases. Herceptin goes after a growth factor receptor called Her-2. That's, in
fact, a kinase. Gleevec targets the ABL -- ABL kinase and CML and the C-KIT
receptors amd GI stromal tumors was developed by our partner, Novartis. And is,
in fact, the first small molecule kinase inhibitor. Now, there are a number of
other ones following -- Iressa and OSI-774. Small molecules Im-clone,C25, an
antibody. All of which target another kinase -- the one that I showed you
earlier -- the epidermal growth factor receptor.

This brings up the concept of molecularly targeted therapy in cancer. I think
that this is really a new way to think about the treatment of cancer.
Historically, cancer therapy has been relatively non-specific. It's aimed at
any sort of any cells that are dividing or are around. It's comprised mostly
of surgery, radiation, and chemotherapy. Or, if you're a patient -- slash,
burn and poison. Thse are just non-specific ways to kill cells and to kill
any cell that's sitting there dividing. In terms of molecularly targeted
therapy -- we know that many proteins are subject to genetic alteration in
cancer. And so by targeting these proteins that we know cancers alter to
confer a growth advantage -- we know -- we think that we can target tumors
more successfully in terms of being specific for tumor cells, and having
fewer side effects on normal cells. So now with the examples of Herceptin,
Gleevec, IRessa/OSI-774 -- we know that hitting these targets will shrink
tumors, in many cases, more effectively than we can do with radiation and
chemotherapy. And we can do that with fewer side effects than we see with
conventional chemotherapy or radiation therapy. And I think that these drugs
are really just the tip of the iceberg. You know, we're talking about
targeting just a few kinases. There are lots and lots of kinases that fit
this profile of being subject to genetic alteration in cancer. And I think,
over the next few years, you are going to see lots and lots of kinase
inhibitors, aimed at kinases other than these ones here -- enter the clinic,
and start working in cancer patients. And so, I think most people have been
really quite impressed with the effects of Gleevec.

And I think that most people are starting to think like Richard Klausner does --
that this is the way that we're going to target cancer in the future -- not with
non-specific methods of killing




cancer cells. But but by using drugs which are more specific for alterations
that we find in the cancer cells themselves.

So, let me show a little bit about how this works. And what's going on in CML.
CML involves sort of a gene re-arrangement. So a piece of Chromosome 9, gets
moves to Chromosome 22 -- and a piece of Chromosome 22 gets moved to Chromosome
9. So you have this unusual Chromosome called "the Philadelphia Chromosome".
Because that's a city in which it was discovered. Now, it turns out that the
breakpoint on Chromosome 9 -- or the place where Chromosome 9 always brings --
is in the middle of the gene that includes the ABL gene -- which-- abl is a
tryosine kinase. Now, normally this tyrosine kinase is off. And it needs to be
activated by other kinases. But, when it is translaticated to Chromosome 9 --
you make an infusion protein -- this BCR abl protein. And the BCR abl protein is
an activated form of the gene. So, sticking that piece of BCR gene in front of
the abl gene - -makes it an activated kinase. So, it has natural kinase
activity, and no longer needs to be activated. , And, when cell-- get this. When
blood cells get that molecular event happening, they turn from what you see here
- -- a picture of normal blood into what is, in fact CML. And the major difference
between these two slides is that there is only a couple of cells with purple
centers here. And what's abnormal in the CML patients -- is that you get lots
and lots more of these normal cells. So white counts, normally in the range of
about 10,000 -- will go to the range of 100,000 or 150,000. So, what's happening
to CML is that Novartis developed Gleevec or STI571 -- which is a specific
inhibitor of the abl tyrosine kinase. And they gave it to patients with CML. And
I think they really saw the most dramatic results we've seen in cancer
chemotherapy for a really long time. 98% of the patients treated with this drug
- -- in their initial Phase II study, had their blood picture go from something
like this -- to something completely normal. In something like half of the
patients had most, if not all of the cells-- with this abnormal chromosome
completely disappear from the blood and the bone marrow - suggesting that you're
killing all of the cancer cells -- by specifically targeting the abl kinase.

Now, in many ways, CML is a unique disease. 100% of people with CML have this
molecular alternation. That's not going to be quite as true in many of the solid
tumors. There is not a singular molecular alteration. But it does, I think,
point out the potential of targeting specific genetic abnormalities in cancer.
And I think that for breast cancer, which is a much more molecularly
heterogeneous disease -- there may be three or four or five kinase inhibitors
that are going to be required, in order to fully combat the full spectrum of
patients with breast cancer -- or lung cancer, or any of the more major solid
tumors with heterogeneous disease. Now, there are multiple kinase pathways that
represent potential points of attack. We've talked a little bit about growth
factor pathways, in terms of the Ras pathway. There's another one called the PI3
Kinase pathway. As I mentioned before, there are kinases that are involved in
cell cycle regulation. Or the process of cell division. And I'll talk to you a
little bit more about that. There are also kinases involved in the ability --
the metastatic capability of cancer cells. Or the ability of cancer cells to
grow and move from their original point, and spread to other points of the body.
And, then, another thing that I'll spend a little more time on is -- the process
of Angiogenesis, which kinases play a critical role in the development of new
blood vessels required for tumor growth.

So this is just the picture of the Cell Cycle. Cells are sitting here, normally
in a resting stage. They will then go through this S-phase, where the DNA
divides. They will then go into G2-M where the broader cells will pull apart. As
you can see here, all of these things in purple are kinases that are critical to
this process of cell division. Many of these kinases are involved with the same
sort of either gene amplification as one sees for EGFR. Or rearrangement like
one might see with BCR-abl. And all of these things in purple, represent
potential points of attack for targeting cancer cells.




And so, just to show you some of the progress we've made -- we've developed
inhibitors of one of those cell cycle kinases. What you see here on the left is
the normal process of cell division. Normally the two daughters that you'll form
- -- these tubulin sort of strings that hold onto the DNA. And those strings will
pull apart as you form two daughter cells. And when you target one of the
kinases involved in that process -- with one of our kinase inhibitors -- at
least in the cell, you see that you completely disrupt that normal process of
cell division. And if you treat cells for 24 to 48 hours -- at least in a test
tube of one of those types of compounds - -you completely kill the cells. And
so, we think that's a very exciting results. And are moving those sorts of
compounds now into animal studies.

As I mentioned before, I'll talk a little bit to you about the process of
Angiogenesis, or new blood vessel formation. This is a hot topic out there. And
lots of people are looking for ways to target Angiogenesis. What I'm top point
out to you is how that process works. So, normally, there's these cells that are
called Endothelial cells, which form the inner lining of blood vessels.. Those
will come together to form a tube. But that tube, in itself, it not enough to
function as a blood vessel. And it has to be the recruitment of all of these
other additional cells -- smooth muscle cells. Some Stromo cells and other
things around that endothelial tube, which allow the formulation of a
fully-formed blood vessel. And these blood vessels are required to deliver blood
to the tumor as it grows. So, what tumors do is they send out signals, telling
blood vessel cells to go through this process - -and make no blood vessels to
feed the tumor growth.

Now there are multiple kinases that are involved in this process. One that you
might have heard about are the VEGF receptors. There's a couple of VEGF
receptors out there in the clinic. But what you may not know is that there are
least five or six other kinases that are involved in the process of Angiogensis
- -- at least as shown from multiple kinase knockouts. And in building on that
biology capability that Dr. Boger mentioned in his talk - John Thomson will tell
you a little bit about some additional biology work that we've done here at
Vertex. But to validate additional, proprietary kinase targets that are involved
in this process of Angiogenesis. And we think that by targeting some of these
kinases as well as the kinase that we've identified through our own biology
efforts -- we are going to have a number of drugs that will be effective
Anti-angiogenic agents in the treatment of cancer.

So, moving now from Cancer to some of the other indications where one might be
able to use a kinase inhibitor -- I'll talk to you a little bit about
Restenosis. As you know, coronary artery disease is probably the most common
cause of morbidity and mortality -- at least in developed countries. And in the
United States there are some 700,000 procedures each year, to try and improve
blood flow from blocked coronoary vessels. Now, even after those procedures,
what will happen is that you get Restenosis. So, normally, the edge of this
blood vessel is out here. And after that vessel has been re-opened with a ballon
catheter -- using angioplasty, those vessels will clog up again. And so, instead
of having this big huge looming for blood flow, or this large tube through which
blood can flow -- what happens is, is that it narrows and constricts -- so that
you only get that tiny little hole there. And if you take a look at what's all
this stuff that's clogging up the blood vessel -- it's these things. It's smooth
muscle cells. So, what causes Restenosis is migration of smooth muscles into the
blood vessel, where they then divide and grow and clog up the blood vessel. Now,
in about 20% to 40% of patients, this Restenosis will be significant enough,
that the patients have to be re-vascularized. And, each year in the United
States alone, we spend about $2 billion dollars trying to fix this problem of
re-opening blood vessels that got clogged, even after the first time they were
angioplastied. So what people are trying to do is --is there a way to prevent
the migration and growth of these smooth muscle cells? And one way to do that is
using kinases.

So, one of the factors that causes growth and proliferation of these smooth
muscle cells is PDGF. There are a couple of others. And PDGF signals in a very
similar way that EGF




signals, as I showed you on that first slide -- so that you can target any one
of these receptors here, or any one of these purple things here -- these kinases
- -- to try and prevent smooth muscle growth and proliferation. And, if you do
that, you sort of get the results that we see here. So, here are some smooth
muscle cells. And when you treat them with PDGF you find they start to migrate
in this assay. And when you treat those smooth muscle cells with increasing
doses of a Vertex Kinase Inhibitor -- that migrration is blocked. Similarly, if
you treat those cells with PDGF, not only will they start to move, they'll also
start to divide. And, again, by treating these cells with a Vertex kinase
inhibitor -- you can completely block the growth and proliferation of smooth
muscle cells. And so now we're starting to advance compounds like this one in
animal models of Restenosis.

Now, here's another example of types of kinase signaling. This is sort of death
signalling. So the process of cell death, also known as apoptosis - and there
are a number of signals that came come from outside of the cell-- which are then
transmitted through a kinase pathway, which tell the cells -- now, will you
please start making genes that tell the cell to die. So, sometimes these death
signals are not necessarily ones that you want to have. So, in the case of
stroke -- which is depicted by this MRI scan -- Or in the case of Myocardial
infarction or heart attack -- which is depicted by this EKG scan -- the death
signal is lack of oxygen. And that lack of oxygen signal gets transmitted
through kinases, and the cells wind up dying. So, if you could block some of
these death pathway kinases, you might be able to block the process of cell
death.

And so, we have some inhibitors of those cell death kinases. Whereas you can see
from this slide, when the cells were given a death -- increasing amounts of a
death signal -- you get increasing amounts of cell death. And that process is
almost completely blocked when a Vertex kinase inhibitor is present in those
cells. And so, these are the types of compounds we're advancing into animal
models of myocardial infarction or heart attack -- and to animal models stroke.
So, that's just a few examples. John Thomson is going to show you some examples
of kinase inhibitors in diabetes. But I think we're making lots of progress
across lots of therapeutic areas with our kinase inhibitors. And, as has been
mentioned before -- we're really on track to name two development candidates by
the end of this year for the treatment of a couple of diseases.

Now, I want to talk to you a little bit about the way in which the specificity
problem can be addressed using Vertex's technology platform. As I mentioned to
you earlier, the field of Kinase inhibitor development was really held up -- as
recently as a decade ago. Because people didn't think it was possible to make a
specific inhibitor. And if you couldn't make a specific inhibitor, you were
going to get too much toxicity.

So, I want to show you the way in which we, at Vertex, use some of the tools
that you heard about on the lab tour, in order to help us design a drug. And
this is just some data that relates to VX-745, which is a compound that you
heard about from John Alam. Now, what we'll do is we'll go to these proprietary
databases. And some of you probably saw in the lab tour this morning. And you'll
say -- gee there are three kinases that look like p38 -- but they're also
members of the MAP kinase family. They are the JNK kinase and the erk kinase.
So, ifwe want to make a specific inhibitor, how do we do that? So, the guys at
Vertex who make these tools recognize that one day, doctors might be looking at
this. So we need to make it so they understand it. So we make the important
amino acids. We'll color them in green. So that the doctors will know which ones
to go after. And if you take a look at say, Amino Acid 110 - -that's different
across all three of those kinases. So, if you can make a drug which targets
Amino Acid 110 or targets this GMp38 -- it's probably going to be specific for
p38 -- relative to some of these other kinases -- because that gene is not
present in these other twos. But if you made it, say for a -- if a targeted
amino acid went away to 109




that wouldn't help you because those amino acids are identical, across all three
kinases. So, we'll run some screens, and we little get some lead compounds, and
then, we'll create structures od those lead compounds bound to the enzyme.

And this is a picture of that. So, this is the enzyme back here. And this is one
of our early leads depicted here. There are some important pieces of information
that we can get from that. One is -- it's this back half of the molecule
depicted here, which is really stuck deep in that ATP pocket. So, if what we
want to do is to make the drug more specific, and more potent -- that's the part
of the molecule that we need to change. And we can get information from pictures
like this one, telling us exactly what kind of changes we need to make. The
second thing we need to do is -- or we can learn is -- this part of the molecule
is really out here in the open air. So if we need to do things like alter the
metabolism of the drug, or add groups which make it more bio-available, for
example, we can put some of those chemical groups on this part of the molecule,
and add those qualities -- without really affecting the potentcy or specificity
of the drug. And what you'll notice here as we'd mentioned earlier - this early
lead didn't really target amino acid 110. It did attack Number 109. But that
wasn't one of the ones that really got us to specificity. So what we did was
play with that molecule a bit, and made it so that it formed a hydrogen bond --
not only with amino acid 109,but also with 110. And, if what we thought about --
if what our database tools were telling us was correct -- that kind of a
molecule should be relatively specific for p38 MAP kinase, relative to some of
the other MAP kinases. And that was exactly what we foundwhen we tested VX-745,
and compared and showed it is a very, very specific sort of about a ten-amino
over p38 alpha. But, really doesn't touch R-2, or JNK 1 or JNK 2. Despite the
fact that these are very, very highly related kinases. So that's some matter of
fact the way in which we use our tools to make kinase inhibitors that are
specific for individual kinases.

So,what is it that the discovery part brings? And how will Vertex and Novartis
be successful in the Kinase world? You know, what Vertex brings to the table is
a leading edge discovery technology found in structure-based design in the
chemogenomic approach. So the people who, I think, to a large extent, had been
leaders in kinase drug discovery -- took a look at the way we go out kinase drug
discovery. Took a look at the way we go about discovering drugs as kinase
inhibitors, and said -- you know, that's really a pretty good way to do this.
And we're going to have you guys start working on all the kinase inhibitors that
we're going to be developing over the next decade. Both companies, I think,
bring to the table a strong record in kinase drug discovery. And, what we're
very excited about is working with a committed partner, with proven expertise in
assets, which are going to compliment our discovery technology. They were the
team that brought the first small kinase inhibitor to market. They know how to
develop these drugs. They're learning how to market them. They had critical
development and marketing insfrastructure for the development of these drugs.
And, in addition to all of that -- they can help us on the biology side, as they
have made large investments in proteomics and target validation. And where that
is applicable to kinases, that's information that they're sharing with us, so
that we can apply these tools to the development of kinase inhibitors.

One final point that I'd like to make is that there's still a lot of opportunity
out there. So, if this pie were to represent the 50 kinases that are potential,
viable drug targets -- over the next decade or so -- people are really playing
in a very small space right now. There's really only five or six kinases that
are targeted by all of the drugs out there. One of them is our p38 MAP kinase
inhibitor. You know, there are other companies with kinase inhibitors in the
clinics -- some of which I mentioned. But really, most of this pie -- most of
this space is up for grabs. And, it's this part of the space, that the
Vertex/Novartis collaboration is aimed at capturing. And I think that when I
show you this slide again -- hopefully in 2010 -- you'll




see the Vertex/Novartis chunk of this pie. And we'll have captured a fairly
significant portion of that space.

So what I hope I've shared with you today is that kinases are excellent targets.
They're involved in many human diseases. And those are large human diseases, and
large pharmaceutical markets. But the next decade I think we'll see the
introduction of multiple compounds that are kinase inhibitors. And many of these
compounds are going to have blockbuster potential. And the Vertex/Novartis
collaboration is really positioned to become a dominant player in this space.
And what we hope that means, is that new drugs for patients. And
revenues,profits, and shareholder value -- for all of you who are attending here
today. Thanks so much for your time. And I'll be happy to take any questions.


                               END OF PRESENTATION


                              *********************




Investors and security holders are advised to read the joint proxy
statement/prospectus regarding the proposed merger when it becomes available,
because it will contain important information. Such joint proxy
statement/prospectus will be filed with the Securities and Exchange Commission
by Vertex and Aurora. Investors and security holders may obtain a free copy of
the joint proxy statement/prospectus (when available) and other documents filed
by Vertex and Aurora at the Securities and Exchange Commission's web site at
www.sec.gov. The joint proxy statement/prospectus and such other documents may
also be obtained from Vertex by directing such request to Vertex
Pharmaceuticals, 130 Waverly Street, Cambridge, MA 02139, Attn: Investor
Relations, tel: (617) 577-6000; e-mail: InvestorInfo@vpharm.com. The joint proxy
statement/prospectus and such other documents may also be obtained from Aurora
by directing such request to Aurora Biosciences, 11010 Torreyana Road, San
Diego, CA 92121, Attn: Investor Relations, tel: 858-404-6600; e-mail:
ir@aurorabio.com.

Vertex and Aurora and their respective directors, executive officers and certain
members of management and employees may be soliciting proxies from Vertex and
Aurora stockholders in favor of the adoption of the merger agreement and the
transactions associated with the merger. A description of any interests that
Vertex and Aurora directors and executive officers have in the merger will be
available in the Joint Proxy Statement/Prospectus.

                              *********************




THE FOLLOWING IS THE SCRIPT OF A PRESENTATION PRESENTED TO ANALYSTS, INVESTORS
AND OTHERS ON MAY 31, 2001 AND POSTED ON VERTEX'S WEBSITE ON JUNE 1, 2001.

                               VERTEX INVESTOR DAY

            "CHEMOGENMICS: ACCELERATING VERTEX RESEARCH PRODUCTIVITY"

                                  JOHN THOMSON

     I'm John Thomson. I've just celebrated my 12th anniversary at Vertex. And
     that makes me (laughter) the longest serving member, except for Joshua.
     And, for that whole time, I get enormous pride and a feeling of privilege
     when I talk about the research engine at Vertex. I see other people laugh,
     talking about technologies and strategies for failing fast. Yet, we have a
     research organization that is more pre-occupied with succeeding fast. And
     what I want to do today is discuss with you some brief sampling of science.
     And some of the energy from Vertex. When I get into this, I get a bit
     energetic myself, so I've got to try to corral my thinking by way of a
     structure of this talk. Three basic areas.

     I'd like to talk about the pipeline, and, as Lynne pointed out earlier -
     -we are hoping to announce five new drug candidates this year. A little bit
     on the Kinase Family as a prototype for gene families. Because it has
     important information regarding how we're on track to deliver to Novartis.
     But, as well, we're learning important lessons along the way, that will
     bode as well for the next gene families. And then, new directions. Adding
     new tools, and how we're going to move into new gene families.

     So, to being with the Pipeline. It's impossible to guarantee any specific
     drug candidate in a particular year for many of the programs. So this is a
     list, if you like, of the current crop that we think is most likely to
     generate the five or more new drug candidates that we feel are likely to
     emerge in 2001. As you can see, there are multiple possibilities from our
     Novartis collaboration -- after only one year. They're in major
     indications. We also have a second family-oriented collaboration on
     Caspases that might yield one or two Visit candidates or drug development
     candidates during the course of this year. And then our crop, or class of
     individual targets. Mostly coming from Vertex 1.0 in the first decade. But,
     not all of them. Bacterial Gyrase are a very new program. Doing
     particularly well in terms of progress. And, currently unpartnered. All of
     the other programs are being partnered. So, this is where we expect those
     five or so to come from.





     I'd like to now quickly sort of hop over some of the most likely
     candidates, and not go through that laundry list rigorously. And as we just
     heard from Rob Mashal -- Kinases are important in cell communication
     everywhere. They permeate all sorts of biological processes, and they offer
     opportunities for medical intervention and innumerable important disease
     areas and medical markets. This is just a cover story from one of the
     countless reviews on Kinases in Cellular Communication.

     And to summarize the progress in the first year of our Kinase
     Family-oriented, or chemogenomic approach to kinase. We're doing very well
     on the drug discovery side of things. Developing component, drug-like
     compounds, in multiple models that, as you can see here, are major market
     potential, and major indications. So we feel that we're doing well towards
     delivering to Novartis. And we're also doing very well on the biology.
     Stuff that is driving the target validation to make sure that we're using
     all of this sort of drug design stuff on targets. As Joshua alluded to
     earlier -- we although we haven't touted this in the past, we are also
     proud of our biology at Vertex.

     Now, to go into some of the specific examples. And, this elaborates a
     little more a set of data that Rob Mashal started to discuss. We have a
     Kinase target here that we believe is going to be important to cancer. And,
     we are investigating the Vertex Kinase Inhibitors in various cancer cell
     lines in vitro. And then, we're looking at a couple of biological markers.
     Histone phosphorylation, which really indicates condensation of chromosomes
     prior to cell separation. And then, tubulin assembly. The infrastructure of
     the cell that then separates to pull the two daughter cells apart. And we
     believe that these are two good representatives of cell division. And, as
     we know, in cancer cells -- cell division is what we want to stop. It's
     uncontrolled cell growth and division. So, here we see, uncontrolled cells
     in vitro. Here we see effective Vertex Kinase inhibitor in vitro. And you
     can see that it is almost completely inhibiting the chromosome
     condensation. And it is really perturbing the tubulin assembly. An effect
     that is very reminiscent of what's seen in Taxol. So, we see here, a
     Taxol-like effect. Its similar potency, and a non-Taxol-like affect. But,
     both effects-- being very relevant to halting the untethered proliferation
     of these cancer cells. So, in effect, these block mitosis - -they lead to
     cell death. And we've shown that basically the same pattern emerges in
     multiple cell cancer cell lines. The extra panel down here is just a
     different sort of photograph which shows that these cells are actually
     dying at last.





     This is an example of coming about the science in a slightly different
     manner. Working with multiple kinases at the same times -- sometimes you
     find that you have a drug. And the target that you think is pretty
     interesting, and you'd really like to explore the drug opportunity, but
     you're not too sure of the target. So, we set out with our biology
     infrastructure -- to investigate this kinase with a knock-out experiment.
     Now, in a normal mouse, during early embryogenesis, the yolk sac of the
     mass embryo -- you can see regular vascularization down here in a different
     sort of staining. And this is reminiscent of angiogenesis. In Rob's talk.
     And prior to that you have all heard of the importance of angiogenesis. So,
     we thought that this particular target that we were going to develop a drug
     for, could be important to angiogenesis. So, we knocked it out. And well,
     the mice were early stage embryonic lethal. Now, some people would walk
     away and say, OK, that's a bad target to go and inhibit. But no, careful
     analysis of this shows that probably the reason that these mice weren't
     surviving, was because they're lacking this mechanism for angiogenesis. And
     it's not surprising that building blood vessels in an early-stage embryo is
     an important thing. But, in some indications, angiogenesis, or blood vessel
     formation is not such a good thing. Cancer, of course -- where want to
     limit the blood supply to the cancerous tissue. Or diabetic retinopathy
     --two of the examples where we might want to control angiogenesis. So, we
     think that this series of experiments, starting from a chemical interest
     and starting point, led to an exploration of an interesting knock-out, and
     established a novel kinase target in a validated kinase pathway associated
     with angiogenesis. You can see that there is patent protection being sought
     for this.

     And, I'm sorry, I can't share with you the identity of that particular
     kinase.

     This is another example. This is one that I can tell you what the target
     is. It's a Diabetic Kinase. We believe it is one of the best, most favored
     diabetes targets in any class. And we recently solved its crystal
     structure. Now, traditionally, we've been very good at solving crystal
     structures.





     ...this whole process of -- really this picture describes structure-based
     drug design. Made crystals. Self-structured. Take that information to build
     molecules - do it again, and then make the molecules better. So, we've
     always done the central part well, and given us a strategic advantage - but
     it's always been a tool to us. Other companies have been founded on the
     principle that this is the whole company. We're miniaturizing, automating
     and industrializing this process. That's why the companies are doing these
     pure-plays. But that's not where all the magic is in this process. The
     magic is over here where we're making drugs. That's where the value
     creation occurs. So, all of this -- it's complicated stuff to get right.
     And these are very sophisticated tools to develop. But they are tools. As I
     said, this is where the drugs emerge, and the valuation creation occurs.
     So, we are constantly refining good tools on this occasion. We accelerated
     the right to determine the process. The crystal deflection quality
     crystals, solve the structure quickly -- and then went on to multiple
     inhibitor structures that guided our drug design. And what are these
     magical part of the process? Well, here's some biological experiment from
     some of the inhibitors from that.

     And this is in a knock-out of a knock-out mouse that is a well-respected
     diabetic mouse model. And what we do here -- it's an acute model. We
     introduced a slug of glucose to the mouse. Then, looked at the effect of
     Vertex compound dosed orally. And if we look at the heterogenous mouse,
     which really behaves normally, after the glucose does, it really handles
     the disposal very well. But the knock-out mouse, where the phenotype is
     expressed, doesn't dispose of the glucose well. It rises rapidly, and then
     maintains. When that mouse is treated only with the Vertex compound - -it
     disposes of the glucose in a much more healthy fashion. So, these results
     -- or these effects showed those responsiveness. So, we believed that
     they're following the right mechanism relating to our drugs. And the
     magnitude of this effect is quite significant. This can be compared to a
     horrible model -- not an exact replica of this model -- but a comparable
     model in which traglitazone was tested. And in that model, the effects were
     very similar. In fact, if you tried to normalize between comparison of
     apples and oranges, one would argue that this is, in fact, a bigger effect
     -- because it is the acute model. So, we believe this is the reflection of
     the magic in a drug-designed part of the process.

     So, to change gears a little bit, and move to Caspases. Caspases have been
     implicated in two fundamentally important cellular pathways. Inflammation,
     and cell death. Programmed cell death or apoptosis. Both of these are
     extraordinarily complicated. But they can be roughly divided into
     inflammation - dominated if you will by Caspase I or Interlukin I
     converting enzyme, and a few others. But mostly Caspase I. And then, some
     other Caspases. But, generally programmed caspases contribute in sort of an
     integrated fashion, a cascade fashion to this process of programmed
     intended cell death. And it is this intended or programmed cell death
     avenue that we are now focusing on with our research team in the U.K.





     And we've identified many human diseases - -important human diseases that
     have apoptosis underlying their mechanisms. Now, that is not to say that
     all of these are equally reliant on Caspases for this programmed cell
     death. Probably those that are most reliant on caspases, are those
     indications in here that are triggered by some sort of obvious stress
     scenario. The ones that we think are probably most relevant to caspase
     inhibition are here in red. And the starting points for our therapeutic
     interest. To summarize we have major market opportunities in myocardial and
     neurological conditions -- both big markets. We've done the regular Vertex
     style chemistry. Lots of scaffolds. Lots of patents around chemistry. And
     lots of crystal structures, and the structure-based drug design process
     behind it. And now, this has given us multiple chemical processes that
     we're exploring in many disease models. Therapeutic models to show the full
     potential of these processes of molecules. There's where we're up to in the
     Caspase program. And we believe that we have some possibilities coming to
     fruition. Now, this is the analysis of one of the Caspase program. And we
     believe that we have possibilities coming to fruition.

     Now, this is the analysis of one of the Caspase inhibitors in a model in
     which what we do is to try to trigger an avalanche of the Caspase cascade
     in mice. We put an antibody signal here. This is a very heavy-handed sort
     of a model. But it really says, systemically -- OK, Caspase, go crazy and
     just avalanche. And what happens is that most of these mice die within 7
     days, unless protected. And you can see by the start's response curve, that
     in an IV bolus, our Vertex Caspase inhibitor protects in that same period
     of time - -almost to 90 percent. Now, this shows a number of things.
     Firstly, our compounds not only protect cells. We're way beyond that. We
     can show you other data showing that these compounds protect cells. But
     they protect animals in a profoundly important way in a heavy-handed model
     of organ failure that has relevance to some very serious human situations.
     Sepsis. Liver distress, and other things.

     Off the Caspases -- and onto the Bacterial Gyrases. As I said, one of our
     newer programs. And the underpinnings of this are that antibiotics is a
     huge market. But we're all concerned that the medical profession and
     industry is going to be experiencing worsening anti-biotic resistance.
     There is great potential here for new classes of antibiotics. The gyrase
     enzyme is a complicated enzyme. And it's a well-validated enzyme; but
     targeting in a different way than we are doing. Roughly $4 billion dollars
     annually is made by Gyrase inhibitors. But they're targeting the A-sub
     unit. For complicated technical reasons, we believe that targeting the
     B-sub units shown here is a better way to avoid resistance, and definitely
     a better way to get into new classes of antibiotics. So, that's our general
     strategy. It's a new program, but already we're experiencing very promising
     results.

     This is just a token result showing a typical anti-proliferation,
     antibacterial, I would say -- using E.Coli. When, e.coli are allowed to
     divide and grow they stay well-separated and the division process goes on.
     When that is inhibited, by a mechanism that interferes with DNA replication
     they stay - -they fail to stay free-swimming and happy. But they form these
     long filaments and stop dividing. Eventually, those filaments degrade and
     die. We see that with a non-potent inhibitor of Gyrase B -- we see the sort
     of filamentation and cell death. We see the same sort of effect with one of
     our Vertex compounds, or a number of our Vertex compounds. We're doing well
     on the structural biology of this particular program with, I think, upwards
     of 20 structures solved already. And this is driving novel, patentable
     scaffolds. We have multiple compounds already. Equivalent potency to
     Novobiocin. And positive results in E.Coli, and some clinical S. Aureau.
     Now the challenge is to make it evenly broad across all clinically-relevant
     strains. Cell permeant and cell active -- in all clinical strains. So - we
     believe that we're making remarkable progress in that program.





     I think this one takes it to another level yet again. HCV is a medical
     problem of enormous importance. It causes debilitating liver disease in
     three to four million Americans. And huge numbers world-wide. Current
     therapies are improving all the time. But they still are not as effective
     as they might be. Not clearly virus permanently in more than 50 percent or
     60 percent of the population. And, having significant toxic side effects.
     And these reasons are partially related to the fact that both of the
     therapies -- the Ribaviron and the Interferon, target us -- the host of the
     viral infection. Not the virus itself. So they give rise to side effects,
     and uncertainty. Undesirable effects, and lack of efficacy. We believe that
     there is a major opportunity by targeting the virus directly. The world is
     acknowledging this. We've seen the power of this approach.

     What happened when we started targeting the HIV Protease. It revolutionized
     the care in therapy for HIV sufferers. And we believe the same profound
     effect in medical treatment would be experienced by targeting this virus
     directly. But it is a very great challenge. Because unlike HIV Protease, it
     has a very flat surface area in the active side, where we have to do the
     business of our design. As our head of crystallography likened this to --
     it's like trying to climb a rock-face. If there are footholds, fine. But if
     there are no footholds,you have a tough time. That's sort of what this
     problem is like. But we believe, and many of the competitors are
     experiencing a tough time, and announcing the departure from this
     particular approach. We feel very good about our program. And again, we've
     solved many, many structures. We have multiple proprietary lead compound
     classes, and they look like drugs at this point in time. Good cellular
     potency, followed by oral bioavailability. And favorable liver and plasma
     PK. Now, this is important because it's an infection that is centralized in
     the liver. But it's distributed also in compartments throughout the body.
     So, it's a unique PK targeting kind of requirement that we need here. Our
     compounds show very favorable PK profiles. Preclinical toxicology has
     begun. And, thus far, they look very promising.

     Along the way we did some pretty clever biology here as well. This was a
     program that we got into, knowing that there was no in vitro, viral
     replication assay. And along the way, we built a surrogate for that. This
     shows a surrogate viral replication assay developed at Vertex - -where
     we're measuring a titration of a Vertex compound, showing that it
     dose-responsive. And that it is potent in these cells. That it is
     mechanism-based on the protease target. Now, taking this sort of cellular
     potency, and putting it together with the promising PK data - we could have
     multiple chemical classes. We can actually design several options going
     into the clinic. We're intending to do that so that we may not only achieve
     one drug development candidate in the near future -- but two, or even more
     -- to enable us to adapt in the clinic. To walk the real requirement that
     -- PK requirements -- that drug delivery are going to represent. So,that's
     the pipeline. Now moving onto back to the sort of general technology. The
     concept of Vertex 1.0 and 2.0.





     This was essentially the first decade of history at Vertex. Vertex 1.0. We
     focused on one target at a time. We took a little while to get started ---
     from an inception of 1989. Only because this is a clinical analysis -- you
     know, entry into the clinic. But, thereafter, we had a nice ramp-up of
     targets at about the rate of one per year in our first decade. We're very
     proud of this track record. All of these compounds still have real
     potential as important drugs. We're very proud of this record. And we
     believe it is already unprecedented in the pharmaceutical industry. But,
     with the discovery of the -- the unearthing of the genomic information, we
     have enormous new opportunities. Roughly, all of the drugs in all of the
     time, by all of the pharmaceutical companies - -came from about 500
     targets. The new genomic information is unearthing thousands of perhaps
     attractive targets. We have to have a way to mine that effectively. We
     believe we've already developed it with our efficiency of our research
     discovery engine. It relates to certain proprietary tools. Certain trade
     secrets -- just the way we do things. And relating to the structural
     biology. Computational chemistry and bioinformatics, and then an integrated
     platform of science. And it's already resulted in better -- we think,
     better drug candidates faster. And we believe that it is particularly
     suitable for looking at large numbers of related proteins in parallel. And
     that's concept 2.0. And we define it as our key genomic strategy. I believe
     we were the first to use the term. It's the first place that I've heard the
     term.

     In concept, it is all possible drugs against all possible drug targets. And
     that's to some degree -- is an impossible, hypothetical goal. It's a
     concept. But, in practice, it's a highly efficient, highly parallel,
     ambitious drug design on hundreds of targets on one set or family of gene
     targets at once. Now, you can understand that analyzing targets when
     they're related, gives you a certain degree of scientific efficiency. I
     think that can be understood by everyone. Even without knowing what the
     efficiencies are. But it also relates in a certain synergies related to the
     establishment of intellectual property regarding products. And I don't mean
     protein products. Target products. I mean drug products.

     The real value creation stuff in this enterprise. And you've seen that in
     our Version 1.0 -- we had a very healthy rate of new drug candidate
     production. Right now, we're in this phase. Last year, five new drug
     candidates. This year, hoping for -- expecting five or more. And we're
     looking very soon towards 8 to 12. So, I want to walk through with you now
     what we've learned from the Novartis collaboration.

     It's a different model for a collaboration. And one of the things that's
     different is that it is focusing on eight NCE's-- this is why it's
     attracted to Novartis in my opinion. They get eight drug candidates. Pretty
     good stuff. Vertex certainly gets some financial security and a lot of
     attractive stuff on the financial side -- but what's really made me pleased
     about this deal -- is all these other drug targets -- and they belong to
     us. Once we're doing with the eight that are going to be developed by
     Novartis and Vertex - -then, we're into the Vertex only drug targets and
     drug possibilities.





     So, in the first year of that Novartis collaboration, there are a few
     things happening. We're transforming the research organization. We're
     mapping the kinase universe-- learning all that kinases and developing new
     tools. And I believe that we're establishing strong chemistry, and
     intellectual property foundations. And I'd like to quickly touch on each of
     those areas.

     We have hired aggressively. People have said from the beginning that it was
     going to be one of our biggest challenges. No problem. We have done very
     well in this regard. We're on target to meet the 160+ or so scientists
     needed in 2001. But, of course, this requires new organizational models as
     well. Not just sort of bringing in lots of people. And we've introduced
     successful new organizational models. And all, without an interruption of
     the process. And without any dilution of the flavor or the culture of
     innovation at Vertex.

     We're very proud of Vertex 1.0. And how much we work on the balance of
     these different core competencies or basic technologies. And this has been
     evolving platform for Vertex in that first decade. It still remains at the
     heart of what we're doing in Vertex 2.0. But at this scale, working on many
     targets at once -- and at this scale -- there are the synergies that can be
     captured by arranging around teams. Teams that are supposed to be focusing
     on a specific part of the overall process to use the knowledge-base of the
     integrated platform -- what works well for one target. But to do things in
     a way that organizationally are more specific to many targets at once. So
     it is this team of different parts of the overall process -- around our
     core technology that is sort of different organizational model that we are
     finding more appropriate for chemogenomics. Also on the science side. We
     knew very early that we need to think about the problem of kinase inhibitor
     designed a little differently. You've got to define kinase chemical space.
     Normally people think about kinase's pathways, file the genetic trees, or
     sequence analysis. These are all important. But they are also important to
     introduce concepts of structure, and what's going on with what you're
     trying to do -- the drug design path. And it's knitting that altogether
     with sometimes quantitative analyses of the active sites of kinases that's
     important. And when you do that, you use various informatics tools to build
     rigorous scientific representations of kinase space. Multidimensional
     matrices as a various physical parameters of the kinase active sites.

     And when we do this, we build up a kinase universe. And what happens with
     this is that you find related kinases culture, generally -- often. And, the
     kinases shown in red here, in this complete universe- the medically
     important ones --sometimes end up in different clusters and roll away from
     one another. And sometimes not the way you've worked before in the green --
     these green targets are where we've worked previously. Perhaps medically
     important, perhaps not. And what we need is a way to sort of get to these
     red zones -- the therapeutically validated targets. This is easy to
     represent by something of a cartoon. Sort of a galaxy cartoon. And sort of
     two-dimensional cartoon that you can see -- if we're starting here, and we
     want to get, however, here to this kinase of interest - -there are
     connectivities between this clusters in this kinase universe that might be
     difficult to traverse if you don't know anything about these kinases
     in-between. But if you've got stepping stones to carry you across there,
     you are making short jumps to get across the kinase universe. And this
     enables you to reuse scaffolds and chemical classes to navigate the Kinase
     universe.





     This is a static picture what we have here -- a cartoon. But, in reality
     this picture is constantly evolving. When every new piece of information
     that we put into it, it evolves. And we've built complicated tools --
     sophisticated tools in our bioinformatics group to sort of describe this
     and keep track of it. And I think this will start on its own. This is one
     of those tools that's showing sort of a representation of Kinase space. The
     Vertex logo in this case is really hung by its - or it's ap-crop. Where
     we've worked on Kinase. And one, we've invested time, and it's just a
     period. And, as we learn about all that kinase, and learn more about the
     other kinases, we build the knowledge base. We expand the Kinase -- the
     non-Kinase universe. And it keeps expanding by our own information, and by
     information being gained externally and being pumped into our
     bioinformatics tool and database. And, eventually, we have outposts through
     that kinase space. And whenever a new kinase becomes implicated it is
     medically relevant. We're only a short distance to hop over and take a
     chemical class to be a relevant -- we believe biologically relevant kinase
     inhibitor to that target. So that's some of the technical lessons that
     we're learning in the kinase exploration.

     One of the things that we're learning is that there are some pretty
     innovative things that you can do on the biology side, and on the
     intellectual property side. Now, the question just came up about what do we
     do about other people's target of intellectual property? This is one of the
     things that you can do, by understanding all kinds of kinases together. We
     genetically engineered a particular kinase that we liked using. But we used
     that as a template to build in the characteristics of the active site of
     other kinases that we wanted to target. We're never using the intellectual
     property,or the clone of that other kinase.

     We're using our own clone that is protected by our patent. This approach is
     applicable, we believe to all kinase space - -and it will be one of the
     innovative things that comes out of this broad family-oriented exploration.
     But, of course, it's the drugs that come from it that is the most important
     thing. True to form. And we've already determined over 200 kinase inhibitor
     structures filed. Patent filings covering more than 100 distinct scaffold
     classes. And the structures and chemical classes explored in greater than
     80 percent of its kinase universe. So, we believe that we're in the process
     of conquering kinase space.

     What about new universes? What's next? Well Protease is a parallel universe
     that we feel very interested in. Already with non-drug sales of about $9
     billion -- it's to some degree -- a market validated family -- but, this is
     only in two classes of targets. HIV Protease inhibitors dominate completely
     the protease drug market. So, with 400 other human protease genes-- many of
     which we believe to be essential and crucial biological events, and
     important to different therapeutic areas - -we believe that this is a very
     rich family.





     And this is supported by what's going on in pharmaceutical research across
     the board. With more than 300 research programs under way in the industry.
     Just a sample of what's going on. These are some of the more interesting or
     favored protease targets. And you can see a number of things. They cover
     many important indications, and medical needs. Big markets. Big numbers in
     terms of prevalence. And the targets are -- importantly -- they're
     scattered across different sub-classes of proteases -- of different part
     clusters of protease universe. We believe we have an extremely impressive
     track record in protease research. We have studied proteases individually,
     or in families. In every case, we've been well-respected by collaborators
     with action with their checkbooks -- to the tune of these numbers.

     We've also produced a drug. We've produced advanced clinical candidates.
     We've got middle stage clinical candidates, and early stage drug
     candidates. We feel very good about the productivity gone in the past in
     this area. And we've also covered much of protease space - covering
     Cysteine proteases. Aspartyl proteases, and Serine proteases. We've already
     invested three of the four most important protease classes. So, we're
     starting to develop the tools.

     Mapping the Protease space. And we intend to put posts throughout the
     Protease universe -- in a fashion reminiscent of what I just showed was
     going on in kinases. Re-use the scaffolds to design from one end of the
     universe to the other. The global picture here is the same with proteases
     and with many gene families. The tools that we require will actually be
     different. This is not something that you can clone what we did with
     kinase, and make it work for proteases. No. This scale of enterprise
     requires hands-on care for each gene family. And we're going to have to add
     new tools.

     But so far, we've also made a good start in terms of other targets here.
     One exciting program that we're making fast progress in now -- Alzheimer's
     disease is a complicated process. And there are multiple mechanisms going
     there. But, basically, in the gumming up of the brain, and the lack of
     performance that follows, Beta Secretase, and its processing of the Beta
     Amaloyd Protein, is regarded as perhaps the most compelling target,overall,
     -- causative of Alzheimer's disease. We've solved this structure. We have
     launched a chemistry effort. We feel very good about the status of this
     chemistry effort. I can't tell you too much about the status of this
     program. But this is one of the flagships emerging from that protease
     universe quest. So, we're underway with kinase, Caspases, spreading out to
     proteases. The broad family of proteases.

     What's next? There are many other drug-rich target families. Some of them
     are not enzymes though. So those classes, in particular, we are going to
     have to add new tools.





Or, as Joshua pointed out earlier -- we are going to get, we believe some of
those tools by a collaboration -- or the acquisition of Aurora Biosciences.
Aurora also, had been from the beginning a visionary bio-tech company. They had
been technologically advanced and sophisticated. They don't have undue overlap
with Vertex. The offer great synergies. They're going to strengthen our ability
to produce through-put in enzyme targets. More or less along the lines of what
we've done in the past - and to expand our ability there. But they're going to
offer us abilities in other non-enzyme areas. Because they're already world
leaders in some of these targets that we've only been amateurs in. So, together
this forms a very exciting amalgamation of what Aurora brings to Vertex. You've
already heard a little bit about the vision. We think that the Novartis deal was
a good example here.

We're in the process there of rejuvenating a big pharma companies own product
pipeline. And at the end of it, we get to co-promote those drugs with the big
pharmas rejuvenated pipeline. And if we really do it well, we're also going
to finish up adding to our own independent drug pipeline. I took out the next
step of this vision that I was going to ask you to imagine for yourselves --
but Joshua's already shown it. That is -- the next gene family. And the next
and the next -- each establishing its own new class of drug targets. We
believe the vision is exciting, and I think I'm going to leave it there for
the moment, and leave it for Vicki Sato, shortly to try to come and help us
out understand this overall vision a little more. And savor it a little more.
So, with that I'd again like to point out that we've got a great scientific
team at Vertex who deserve all the credit to enable me to go on the road to
show -- on the road with a show that focuses on success like this. Thanks a
lot. Any questions?

                              *********************





Investors and security holders are advised to read the joint proxy
statement/prospectus regarding the proposed merger when it becomes available,
because it will contain important information. Such joint proxy
statement/prospectus will be filed with the Securities and Exchange Commission
by Vertex and Aurora. Investors and security holders may obtain a free copy of
the joint proxy statement/prospectus (when available) and other documents filed
by Vertex and Aurora at the Securities and Exchange Commission's web site at
www.sec.gov. The joint proxy statement/prospectus and such other documents may
also be obtained from Vertex by directing such request to Vertex
Pharmaceuticals, 130 Waverly Street, Cambridge, MA 02139, Attn: Investor
Relations, tel: (617) 577-6000; e-mail: InvestorInfo@vpharm.com. The joint proxy
statement/prospectus and such other documents may also be obtained from Aurora
by directing such request to Aurora Biosciences, 11010 Torreyana Road, San
Diego, CA 92121, Attn: Investor Relations, tel: 858-404-6600; e-mail:
ir@aurorabio.com.

Vertex and Aurora and their respective directors, executive officers and certain
members of management and employees may be soliciting proxies from Vertex and
Aurora stockholders in favor of the adoption of the merger agreement and the
transactions associated with the merger. A description of any interests that
Vertex and Aurora directors and executive officers have in the merger will be
available in the Joint Proxy Statement/Prospectus.

                              *********************