輝瑞 (PFE) 2011 Q1 法說會逐字稿

Good morning, ladies and gentlemen and welcome to the Icagen First Quarter 2011 Earnings Conference Call.

(Operator Instructions) I would now like to turn the conference over to Dr.

Richard Katz, Executive Vice President and Chief Financial Officer.

Please proceed.

Thank you, operator.

Good morning, everyone and thank you for joining us today to discuss our corporate research and clinical progress, as well as our financial results for the first quarter.

With me here today is Kay Wagoner, our CEO, as well as Greg Rigdon, our Head of New Product Development.

Kay will begin the call today with a general overview, I will then provide a financial update and all of us will be available for to take your questions following our prepared remarks.

Before we begin, I would just like to read the following regarding any forward-looking statements that we may make today.

Various remarks that we may make about the Company's future expectations, plans and prospects constitute forward-looking statements for purposes of the Safe Harbor Provisions of the Private Securities Litigation Reform Act of 1995.

Actual results may differ materially from these forward-looking statements as a result of various important factors, including those discussed in our most recent quarterly and annual reports on Forms 10-Q and 10-K, as filed with the SEC.

In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date.

While we may elect to update forward-looking statements at some point in the future, we specifically disclaim any obligation to do so, even if our estimates change, and therefore you should not rely on these forward-looking statements as representing our views as of any date subsequent to today.

So let me now turn the call over to Kay.

Thanks, Rich.

We are off to an excellent start for 2011, with both of our clinical programs proceeding as we have planned.

Our research programs are also going well and as they mature, I'll ask our new CSO, Doug Krafte, to join us in updating you on those programs.

First I'd like to say a few words about our pain program with Pfizer and then our KCNQ epilepsy program.

Following my summary, Greg Rigdon, our VP of New Product Development, will summarize the clinical trial results for ICA-105665.

He had an opportunity to present those at the 11th Antiepileptic Drug Trials Conference last week.

And then Rich will complete the conference call presentation with an update on our financials and finally, we will be take your questions.

So first, turning to the Pfizer update, as you will remember, in our collaboration with Pfizer we're focusing on discovering and developing potent and selective antagonists of certain subtypes of sodium channels for new and better pain treatments.

We have a lead compound, which is in Phase I clinical trials.

It is a very selective antagonist for the sodium channel called Nav1.7 or SCN9A.

This is a target which has been genetically linked to pain and we believe its one of the most exciting pain targets in the industry today.

As you may recall, Nav1.7 has been genetically linked to a variety of pain disorders, including congenital indifference to pain, that is no experience of pain or CIP, and as well to inherited erythromelalgia, or IEM.

Our lead compound with Pfizer is in its first Phase I study and provided that that study continues to go well, we would expect that Pfizer would advance its compound into a second Phase I study later this year, following which a Phase II study would be the next logical step.

As you may remember, in 2010 we received $4.0 million in milestone payments when this compound was selected and advanced into clinical studies.

If the Phase II study is initiated, we would be eligible to receive an additional and larger milestone payment, so we are extremely pleased with the progress that's being made in this important clinical program.

We do believe that selective study in channel blockers represent a very unique and highly promising approach to the treatment of pain.

There are, of course, marketed sodium channel blockers which are used for a variety of conditions, including the blocking of pain transmission and sensation, but none of those are truly selective for this particular ion channel target.

We believe that our compounds discovered in the collaboration with Pfizer are among the most selective Nav1.7 compounds being developed today.

In addition to this lead compound, we're continuing to make progress indentifying the other compounds that target the sodium channels in our collaboration for potential utility in the treatment of various types of serious and chronic pain, so the program is going really well.

You may have seen, actually, a press release earlier this week announcing a three-party collaboration among ourselves and Pfizer and Yale University.

This joint effort with the laboratories of Dr.

Steve Waxman and his colleagues at Yale School of Medicine will study the effect of selectively blocking Nav1.7 sodium channels with the compounds that Icagen and Pfizer have indentified in our collaboration.

The Waxman team has previously shown that mutations of Nav1.7 channels occur in patients suffering from IEM, the condition that I mentioned earlier, inherited erythromelalgia.

These genetic mutations increase the activity in these neurons leading to the pain associated with the disease.

Working together, we will determine whether the Icagen-Pfizer compounds block the Nav1.7 channels that have been mutated in this disease and if they do, that would provide the rationale for clinical studies in IEM patients.

Of course, any information that we gather from this work will also useful in advantage our compounds into other, more common pain disorders.

So we're very excited about our partnership with Pfizer and our new partners at Yale in this important project.

We have been and continue to combine the scientific and clinical expertise.

Pfizer and Icagen are now with the Waxman's lab.

We look forward to finding new medicine to treat pain.

So let me turn now to our KCNQ program.

You will remember that we have a compound called ICA-105665, which is in clinical development Phase II and we are in the final preparations for a Phase II study that will start later this year.

This study will be in the target population, that is partial onset seizure patients, and that's an important point.

This is the first time that we will do a long-term, four-week study in the target populations.

This study will be a double-blind, placebo-controlled study.

As I mentioned, it will last for four weeks.

As is standard in the development of novel antiepileptic drugs, which I'll generally call AEDs, the patients this study will have not only partial onset seizures, they will continue to take their current AED treatments during the trial and despite those current treatments, these individuals still have seizures, at least four seizures each month.

So this is the largest segment of the epilepsy market and they really need better treatments today.

We anticipate enrolling about 60 patients and approximate 10 to 15 sites in the US.

The dose that we've selected is 200 milligrams BID.

This is a dose that we have shown, in earlier trials, to be extremely well tolerated in both healthy volunteers and patients and to record seizure-like EEG activity in patients who are prone to have this seizure EEG response when they are subjected to flashes of light.

In addition to establishing safety and tolerability, this upcoming trial will give us the first indication for the patient for efficacy and based on our promising preclinical and clinical results to date, we are very excited about entering into this safety and efficacy trial.

Our primary end point is safety over the four weeks and that's important, because the longest study that we've done to date is a one week study, so it's important to establish that safety during this longer period.

Additionally, as designed, this placebo-controlled trial will give us an evaluation of efficacy in terms of reduction in seizure frequency in this intended target population.

For a long time now and continuing into the future, a leading industry epileptologist, Dr.

John Messenheimer, will be helping us with this study, both the planning and the execution.

Dr.

Messenheimer is a leader in his field.

He's been in both academics and industry and his primary focus has been, and continues to be, new treatments for epilepsy.

He has been really involved with the development of many antiepileptic drugs, most notably GSK's Lamictal.

The timeline for starting this study is this summer and we're really working hard to meet that timeline.

The last thing I would say before I turn this over to Greg to give us some update on our clinical results is that ezogabine, which used to be called retigabine and is now called Trobalt in Europe, has just recently been approved in Europe by EMEA.

So we're happy that that has occurred, because it further validates the mechanism of action of our compound, because ICA-105665 works like retigabine to open KCNQ potassium channels.

We believe our compound has a number of potential advantages over ezogabine and we could address that, if you're interested, in the Q and A.

So let me turn this over to Dr.

Greg Rigdon to give us some of the clinical result updates that he presented last week at the AED trials meeting and then, after that, he will turn the call over to Rich.

Thanks, Kay.

As you may remember, ICA-105665 is a compound that was discovered and patented by Icagen and as Kay mentioned, it opens neuronal KCNQ potassium channels.

Compounds that have this mechanism of action are efficacious in animal models of seizures and also have a genetic link to epilepsy.

And also, as Kay noted earlier, ezogabine, which is another compound that opens these channels, has been shown to have efficacy in patients with partial epilepsy in Phase II clinical trials.

Thus, we think we have a validated a new approach as a treatment for patients with partial seizures.

In four Phase I studies, ICA-105665 demonstrated a very favorable safety and tolerability profile.

So far, 27 patients and 126 healthy volunteers have received single or multiple doses of ICA-105665.

Single doses up to 400 milligrams, as well as twice daily doses up to 300 milligrams or 600 milligrams per day, have been well tolerated for seven days.

In healthy volunteers, there have been no serious adverse events or dropouts and importantly, no evidence of urinary retention or QT prolongation, both of which have been associated with ezogabine.

Moreover, the drug has been well tolerated without the need for dose titration.

Recently, in a Phase II proof of mechanism study, ICA-105665 was investigated at single doses of 100 milligrams to 600 milligrams in patients with photosensitive epilepsy.

These are rare patients but a well defined subset of patients with epilepsy.

They have seizure-like activity on their EEG when they are exposed short bursts of flashing light.

ICA-105665 suppressed EEG responses to the flashes on light IND doses ranging from 100 milligrams, where one of four subjects responded, to 500 milligrams where four of six subjects responded.

This confirms that although the drug is tolerated at these doses with no SAEs and few side effects, that there are adequate amounts getting into the brain and getting to the target ion channel, the KCNQ channel.

At the highest dose study, 600 milligrams, the first subject experienced a brief approximately 30-second tonic-clonic seizure that occurred an hour after dosing.

Consequently, as per pre-designated in the protocol, we stopped the study and submitted our data and future plans to the FDA.

After reviewing the materials, the FDA approved our protocol and our plan to move to Phase II in the target population, that is patients with partial onset seizures.

Kay described the planned study earlier in this call and we're currently working diligently to initiate the study this summer.

We look forward to reporting progress on the development of ICA-105665 on future calls.

Now I'd like to turn the call over to Rich for a review our financials.

Thank you, Greg.

I'll be brief, just to highlight a few points.

Revenues for the first quarter of 2011 were $1.0 million; this compared to $1.5 million during the same period in 2010.

The decrease was reflective of decreased reimbursed R&D funding and funding from our collaboration with Pfizer as a result of just normal, slight decreases in FT funding from year-to-year.

Operating expenses for the first quarter of 2011 were $3.2 million; this compared to $4.7 million during the same period in last year.

There was a significant decrease, largely as a result of the cost cutting efforts that we've pursued over the past year or so.

In addition, we had reduced clinical development expenses this quarter because of the timing of studies and so forth, by about $0.5 million.

The balance was due to the reduction in G&A and research.

So our net loss for the first quarter was $2.2 million.

This compared to $3.2 million during the same period in 2010, so again, a significant improvement as a result of the factors that I've just mentioned.

On an ongoing basis, our cash burn rate is down.

It was about $1.7 million at a steady state level this quarter and that's for the internal operations of the Company.

Clinical development expenses, of course, would be in addition to that figure and we would expect those to start later this year.

I should also note that during the first quarter we raised approximately $1.7 million of net proceeds pursuant to the first ATM sales agreement that we had filed with McNicoll, Lewis and Vlak.

That was completed in January and that cash is reflected in our cash balance as of the end of the first quarter.

In addition, we filed a second ATM to raise up to $4.6 million and the substantial majority of the capacity of that has not yet been tapped, so we have access to that going forward.

We ended the quarter with approximately $11 million of cash and cash equivalents.

I'll pause there and we'll all be happy to answer any questions that you may have.

(Operator Instructions) Christopher James, McNicoll, Lewis & Vlak

Hi, good morning and thanks for taking my questions.

Can you hear me?

Absolutely.

Yes.

Hi Chris.

Okay, great.

Hi, congrats on the progress made, particularly with the Pfizer collaboration and with Yale.

My first question is with 665.

Thanks for all the clarity for a little bit about the trial details, but can you help us understand the cost of the study and when we could potentially see some data coming from that study?

Sure.

The cost of the study is projected to be about $4.0 million, maybe a little bit more than that, but certainly close to $4.0 million and we have been successful in terms revenue from our collaborations and raising capital on the ATM and that's helped our cash balance, as you know.

So we believe that we have adequate funding for this trial.

The study is going to start in the summer.

Right now we're looking at early third quarter.

It's important to say how long it will take to get to the top line data and we start enrolling, so I'd like to defer a little bit on that timing of the top line data until we start enrolling the study.

Generally, these things take eight-to-twelve months to actually complete because of the enrollment.

But that may be shorter or longer than that, so let me talk about the (inaudible, background noise) to the top line data once we start enrollment.

Sure.

That's helpful and you mentioned some of the differences between 665 and retigabine.

Can you talk a little bit about hepatic excretion, urinary excretions; are there any major defenses that we should sort of infer from that?

Sure.

This is Greg Rigdon again.

One of the problems with ezogabine is that they have rare events of urinary retention, but it can be very serious and we believe this is because it's renally excreted and there's a high concentration in the urine.

105665 is metabolized by the liver and almost no compound is found in urine and we certainly haven't see any evidence of urinary retention either in the animals or in the clinical studies thus far.

So that's one difference.

Retigabine is also dosed TID.

Our plan is to dose BID.

They have a fairly long titration schedule.

As I mentioned earlier, there's no need for titration so far at the doses that we've used with 105665 and they also some effects on QT interval in there thorough QT study and we don't believe that there will be any of those effects with 665 based on our animal studies and the clinical data so far.

Great and then just moving on to the Pfizer collaboration, when do you think you can start a Phase II program and remind us what milestone could that potentially trigger?

It typically takes about a year to do a Phase I program and they started in December of last year, so typically we would expect a Phase II to start in about a year from that day, so that would put it late this year.

I don't have any more information on the specifics of the timing of that, but I would certainly hope that that time schedule is a reasonable one.

As I noted, we have received $4.0 million in milestones so far for the selection and the initiation of clinical studies and the milestone that we received upon initiation of Phase II is larger than that.

I don't believe that we have given specific information about the size of that milestone, but it is significantly larger than $4.0 million.

And then on the patient that you -- thanks for some clarity on the AE, I'm assuming that the patient that had the 30-second tonic-clonic seizure.

Did this patient return back to baseline?

Were there any focal deficits?

Were there any electrolyte abnormalities that we should know about?

No.

No, so this was not a new seizure type for this patient.

They've had tonic-clonic seizures in the past.

It had just been a few years since their last one and they were still that in clonic seizures.

So there were a lot of mitigating circumstances around that.

So the patient had juvenile myoclonic epilepsy, which is a type of generalized epilepsy, so our target population going forward is actually going to be in partial seizures, not generalized.

But the patient recovered very quickly from the seizure.

There was no effects that lasted beyond a few hours with that.

Okay and then finally, Kay, you didn't mention any progress with the ICRAC program.

Can you help us understand sort of what's going on with that program, anything that we could hear about it in 2011?

So I think the program that you may be referring to is our TRP-A1 program.

Oh, I'm sorry, the TRP-A1, right.

Right.

So the TRP-A1 program is going really well.

We have really good compounds and some very nice animal results, it is progressing well and we continue to have interest from major pharmaceutical companies in that program and so it is making progress.

I hope that on the next quarterly call we'll have Doug Krafte, our new CSO, give you a little bit more color on that.

Great.

Thanks for taking my questions.

I'll jump back in the queue.

Thank you.

There are no further questions.

I'll turn the call over to Dr.

Richard Katz for closing remarks.

Okay.

Well, thank you all for joining us today and we certainly appreciate it.

We'll look forward to keeping you updates on our next try call.

Thank you.

Pardon the interruption.

There is a question.

Oh.

Sure.

There is a question from the line of Chris Richard, with Merlin.

Please proceed.

Yes, I'm sorry.

I believe Dominique, who was also on the call, had a question.

No.

I did, but -- good morning, everyone.

Hi.

Hi.

Hi.

Sorry, no I did.

I wanted also to ask about a quick update on the TRP program and the question has been answered with two other questions.

Oh, sure.

No, that's --.

Do you have anything, Chris?

No, no, no.

Okay, sorry about that.

Sorry about that.

No problem, of course.

There are no further questions.

Very good.

Super.

Thank you all again.

Ladies and gentlemen, that concludes today's presentation.

All parties may now disconnect.

Great day.

1