Q2 2023 Alector Inc Earnings Call
Good afternoon, ladies and gentlemen, and welcome to the outdoor mid year 2023 earnings conference call. At this time all participants are in a listen only mode. After the speaker's presentation, there will be a question and answer session.
That's a question during this session you will need to press star one on your telephone.
I've been here not I mean message advising your hands it's raised.
To withdraw your question. Please press star one one again.
As a reminder, this conference call is being recorded.
Now like to turn the call over to Katie Hogan Senior director of corporate communication and Investor Relations. Please go ahead.
Thank you operator, and good afternoon, everyone earlier. This afternoon, we released our financial results for the second quarter of 2023.
The press release is available on our website at Www Dot <unk> Dot com.
Our 10-Q was filed with the Securities and Exchange Commission. This afternoon.
Joining me on the call today are Doctor Arnon Rosenthal co founder and CEO , Dr. Sarah <unk> Mitra, President and head of research and development, Dr. Gary Romano, Chief Medical Officer, and Dr. Marc Grasso, Chief Financial Officer.
After our formal remarks, well open the call for Q&A I'd like to note that during this call we will be making a number of forward looking statements. Please take a moment to review our slide on the webcast, which contains our forward looking statement disclosure and we also encourage you to review our SEC filings for more information.
I would now like to turn the call over to Arnon, Rosenthal, Chief Executive officer or not.
Thank you Kathy and good afternoon, everyone.
We appreciate you joining our conference call today.
I'll start by highlighting <unk> key initiatives during the first half.
'twenty three.
Next we show the progress we believe we have we have achieved with our immuno neurology research.
Then I'll invite Scott.
The late stage clinical program.
After all Mark will provide an update on our financial results.
Today electric with a late stage clinical biotechnology company with an advanced pipeline that include novel first in class clinical program.
We also have world class partnerships in which we retain significant price as well as innovative research and technology.
Regarding our <unk> two program.
Provide more details about our two phase two clinical trial.
Thank you.
The thrive is approaching full enrollment.
Nearly all eligible participants are rolling over into the long term extension portion of the study.
We are also looking forward to sharing a few highlights from the <unk> program, we presented at the outcome of Association.
Brian .
In July .
As presented.
In a mouse model of Alzheimer's disease.
Your body.
To see was shown to reduce total cost in the future.
No.
Do you have the biomarker for normal repair.
Well as to increase the ratio of AB <unk>, which made victory modeling of amyloid plaque.
Further we are encouraged that <unk> two was well tolerated in a phase one trial.
Okay.
The fact that we are seeing what appears to be incidences of ARIA E bulk to participate associated with both.
Both titles, we believe is interesting and suggest biological activity.
With enrollment.
Invoked to nearly complete we are advancing closer to potential meaningful data readouts.
We will also share with you the outcome of our recent productive agency interaction with the.
EBITDA in EMEA on our Infront III phase III pivotal trial evaluating <unk>.
Improper temporal dementia.
The enrollment in <unk> three is also nearly complete.
We will also provide a brief update on our two open label phase II clinical trial.
Frontal temporal dementia benign off 72 page.
With that I will turn it over to Sarah to highlight the progress we have achieved with our immuno neurology.
Thank you Anna as.
As we look across the state, yes, Im encouraged to see continued advancement in neuro degenerative disease drug development in 2020.
The accelerated approval of a new treatment and the traditional approval often I'm, sorry, amyloid beta therapy for Alzheimers disease highlights the possibility of program for patients families and caregivers affected by these devastating condition.
Moreover, the paved the way for next generation therapeutics that have the potential to work alone or in combination with this novel treatment approaches.
We applaud this progress by the drive to advance transformative first in class therapy.
Enhanced efficacy and improved the quality of life of patients.
Sadly they disorders impact more than 1 billion people worldwide and result in the loss of $6 8 million lives each year.
As we continue to write the urgency to address the public health challenge has never been greater.
That is why we pioneered the field of immuno <unk>.
<unk> and are advancing a broad portfolio of potential first in class treatments for pain disorders guided by our insights into human genetics immunology and neuroscience.
Like immuno oncology immuno neurology seeks to harness the immune system as a broad effective and long lasting therapy within the brain microglia are the primary cells of the innate immune system.
Our immuno neurology therapies drive to ship ineffective or damaged microglia into effective and beneficial agent.
This translated immuno neurology into a bulk portfolio with transformative potential.
We are developing mesothelioma and L 101 in partnership with GSK.
These candidates are intended to block the.
The degradation receptor for programming.
Programming and levels and enhance microbial activity.
In collaboration with Abbvie.
So developing <unk> two.
With <unk>, we seek to increase <unk> signaling with the intention of stimulating the functionality of microglia.
We believe these candidates represent the most advanced immuno neurology therapies in clinical development worldwide.
We also continue to strategically invest in and advance our innovative research portfolio.
Our development pipeline and to set the stage for our long term success.
While our late stage candidates <unk> penetration and target engagement.
<unk> proprietary versatile blood brain barrier technology, which we may selectively deploy next generation program.
And additional novel first in class program. We are excited about is ADP <unk>, seven which is targeting the GP NMD team for the treatment of both familiar and sporadic Parkinson's disease.
Currently we are in the process of selecting a lead candidate and look forward to providing updates on ADP zero to seven as we progress the program.
Our collaboration with GSK and IP combined with our clinical expertise and differentiated approach allow us to advance our broad pipeline.
Potential to transform the treatment landscape for being the target.
With that I'll turn it over to Gerry to highlight recent progress with our late stage clinical programs.
Thank you Sarah I'll begin with our ALC is here to program. The most advanced <unk> program in clinical development for Alzheimer's disease worldwide.
<unk> two is a novel investigational humanized monoclonal antibody.
It binds to and activates the triggering receptor expressed on myeloid cells with <unk> II.
<unk> is a phospholipid receptor on the microbial membrane that census, pathological changes in the brain.
Finding a trump to its biological substrates, which include April E lipids, a beta and other cellular debris triggers microbial signaling pathways that allow the microglia to adopt a defensive response to disease by clearing pathology and protecting neuronal health.
Loss of function variance in <unk> are known to be deleterious.
So I get mutations in the <unk> reduced functionality of my quickly here and increase the risk of Alzheimer's disease. For example, the <unk> 47, H loss of function variant increases Alzheimer's disease risk by threefold.
<unk> two binds to <unk> II receptors, resulting in clustering of <unk> II in the microbial membrane and activation of <unk>, two signaling pathways, which support microbial survival proliferation and function.
Microglia are the primary innate immune cells of the central nervous system and they play a number of important roles in maintaining brain health and function, including clearing of Misfolded proteins, such as amyloid and other cellular degree and also maintenance of healthy synapses astrocytes Ultra Denver site maintenance of the blood brain barrier and vasculature and.
Intolerance.
Our hypothesis is that boosting microbial function may improve the brain defenses against age related neuro degenerative diseases.
We completed our phase one trial of <unk>, two in healthy volunteers, which demonstrated both dose dependent target engagement and activation of microglia.
Haynesville two is electric phase <unk> study of <unk>, which is now ongoing in patients with early Alzheimer's disease.
<unk> two is a randomized double blind placebo controlled common closed designed study of up to 96 weeks of treatment with <unk>, two and approximately 328 participants with early Alzheimer's disease. It includes three doses of <unk> two that were demonstrated in phase one to activate micro cleanup participants risk.
<unk>, two or placebo as monthly infusions.
Invoke two was designed by electron abbvie to be a biomarker rich proof of concept study.
Primary endpoint is the CVR sum of boxes, and we're also collecting other secondary clinical and functional outcome assessments.
Biomarkers, including CSF in plasma biomarkers of microbial activation and of Alzheimer's pathophysiology.
And there are imaging biomarkers include amyloid and Tau pet and volumetric MRI.
To date, we have enrolled more than 300 participants in the trial is nearly fully enrolled we expect to complete enrollment in the third quarter of this year with their study reading out in the fourth quarter of 2024.
At the Alzheimer's Association annual conference or AIC in July we presented an update on invoke to which highlighted that early in the trial three participants had treatment emergent neurological signs and symptoms and associated MRI findings consisting of vocal based agenda Kadima circle of Fusion's micro hemorrhages and superficial.
Yes.
MRI findings resemble the area that has been reported following treatment with anti amyloid antibodies.
Regarding their MRI features incidents timing of onset related as to the number of April before wheels, as well as the frequency and spectrum of clinical manifestations.
We believe Alcs here two has the potential to work alone or in combination with anti amyloid beta therapies by harnessing the broader but beneficial effects of microglia.
We expect to report in both two data in the fourth quarter of 2024.
At AIC in July we also presented a poster on mouse model data demonstrating that <unk> activation improved Alzheimer's disease, biomarkers, including amyloid and Tau.
I'll now turn to <unk>, our novel first in class candidate and the most advanced therapeutic candidate worldwide in clinical development for the treatment of FTE.
Previously, we disclosed that based on emerging data on the variability of FCB progression from the Egencia and all three cohorts, we plan to meet with regulatory authorities to discuss modifications to the statistical analysis approach for our infront three phase III clinical trial of <unk> in participants with FCB granular.
This was driven by both our and the scientific community so evolving understanding of the variability of FCB granular and disease progression.
Additionally, as a part of routine monitoring we in partnership with GSK conducted a blinded sample size re estimation of the infra III trial, which demonstrated that the variability of disease progression is considerably less than our initial estimates.
Which were based on limited data at the start of the trial.
Accordingly, this supports a significant reduction in the number of symptomatic participants required for our primary efficacy analysis in front III.
Our recent interactions with FDA and EMA, we're productive and based on agency feedback we plan to conduct the primary analysis on symptomatic participants in front III.
The agency has also agreed with our proposed sample size re estimation that is anticipated to support a more focused enrollment of approximately 90 to 100 symptomatic F&B granular and participants for a treatment duration of 96 weeks.
As a result, we plan to complete enrollment in infra III in the fourth quarter of 2023.
Regarding the FTC nine or 72 cohort of our Infront two open label Phase II trial.
We confirmed again, a two to three fold elevation in <unk> levels and CSF in plasma.
We have conducted a preliminary analysis of disease progression rates for 14 participants who were treated with <unk> compared with baseline matched controls from the all SPD registry.
A high degree of variability in disease progression rates in both groups rendered the analysis uninformative regarding treatment effects.
Turning to <unk> hundred one our second product candidate in our pre granular portfolio that we are developing in partnership with GSK.
101 is designed to elevate for granular levels in a manner similar to lead us in that.
It's different pharmacokinetic and pharmacodynamic properties potentially enable dosing regimens for use in the treatment of larger indications, including Alzheimers disease.
Our phase one study in healthy volunteers demonstrated that <unk> hundred one was well tolerated and increased programming levels in plasma and CSF in a dose dependent manner.
We in partnership with GSK plans to initiate a global phase II clinical trial.
Alzheimer's disease.
That overview I'll now turn the call over to Mark to provide an update on our financial results and milestones Mark.
Thank you Gary we summarized our second quarter of 2023 financial results and the press release, we made available after the market closed today.
First I'll highlight that we remain well funded to execute our strategic objectives.
We ended the second quarter of 2023, with a strong cash position of $630 million and a runway extends through 2025.
Collaboration revenue for the second quarter of 2023 was $56 2 million compared to $79 9 million for the same period in 2022.
Total research and development expenses for the second quarter of 2023 were $46 2 million compared.
Compared to $54 $5 million for the same period in 2022.
Total general and administrative expenses for the second quarter of 2023 were $13 6 million compared to $15 8 million for the same period in 2022.
For the quarter ended June 32023, we reported a net income of $1 4 million or <unk> <unk> per share compared to a net income of $9 9 million or <unk> 12 per share for the same period in 2022.
Turning now to 2023 financial guidance, we are increasing our collaboration revenue estimate to be between $90 million and $100 million.
Our anticipated total research and development expenses are reduced to now be between $210 million and $220 million.
In total anticipated general and administrative expenses are tightened to now be between $60 million and $65 million.
In May 2023, electron GSK formally decided to have GSK conduct the initial phase II trial for <unk> hundred one in Alzheimer's disease, resulting in a contract modification to the GSK agreement.
Our guidance updates to revenue in research and development expenses are reflective of this change.
Looking ahead, we expect to achieve several important milestones, namely.
Namely we plan to complete enrollment in our two late stage trials. We are on track to complete enrollment in both to our phase II clinical trial for <unk> in <unk> disease in the third quarter of 2023.
We also anticipate we will complete enrollment in <unk>, our pivotal phase III clinical trial for <unk> and <unk> in the fourth quarter of 2023.
We are well capitalized with a robust cash position and remain focused on advancing our late stage clinical programs.
We look forward to providing additional updates as we advance our work.
That concludes our prepared comments for today's call. Operator, you may now open the line for questions.
As a reminder to ask a question. Please press star one one on your telephone and wait for your name to be announced please.
Please standby, while we compile the Q&A roster.
The first question comes from Greg Harrison with Bank of America. Your line is open.
Good afternoon. This is Mary Kate on for Greg. Thank you so much for taking our question.
We were wondering about the research program that you mentioned could you have additional color behind <unk> research program in Parkinson's disease and media as a follow up could this target to use in other neurodegenerative diseases or is it parkinson specific thank you.
Yes, thank you for that question.
Start and then ill turn over to <unk> to add more color to that so of course, we are excited about our program ADT theater to seven which is our product candidate targeting <unk> for the treatment of Parkinson's disease.
<unk> the risk genes for Parkinson's disease, and caused the transmembrane protein <unk>, which is <unk>.
Actively expressed in microglia and oligodendrocyte and regulate lysosomal function. Our hypothesis is that the pathological genetic variant of GT NMB disrupt the function of multiple lysosomal protein like look to and GVA one.
It leads to an inflammatory factors funds and accumulation of new plan and Parkinson's disease.
We are developing adp's zero to seven which is a human monoclonal antibody that modulate GP NMB to mimic the protective genetic made again for both familiar and sporadic forms of Parkinson's.
Parkinson's disease currently we are in early.
As part of our early portfolio, we are looking forward to a lead selection.
Please standby for next question.
The next question comes from Ron <unk> with TV Cowen Your line is open.
Hi, This is George on for <unk>. Thanks, So much for taking our question maybe just one from us on ALJ.
Hey, Al Jos your line.
Just a little checking timing to data readout for that I think previously you said early 'twenty five.
This re estimated primary analysis sample size and enrollment completing in Q4, just wanted to double check if theres any latest update on timing to data. Thank you.
Yes happy to take that this is mark so.
As we have noted in the press release today, we had a good engagement with with the agencies around our pivotal and Gary can give some more color on that I'll just start by acknowledging specifically as it relates to the timelines, we anticipate that we're going to complete enrollment for that pivotal.
In the fourth quarter of this year.
The study is designed it's a 96 week.
Treatment period.
And Gary do you want to add a little bit more et cetera.
Sure Mark So just to add to the very end there. It's a nice it's a.
We're going to finish enrollment in the fourth quarter of this year 96 weeks later or that would be approximately third quarter. A 25, we will have.
Last patient out and data shortly thereafter.
As I mentioned during the recall.
We had a very productive regulatory interaction that provided us with guidance to help move this trial forward.
We've talked a little bit about FDA feedback in the past. We've recently received scientific advice from EMA, which was generally consistent with FDA.
Based on this positive feedback from the regulatory agencies in partnership with GSK, We plan to conduct the primary analysis on the symptomatic participants in <unk>, that's that's a narrowing of the scope.
<unk>.
Agencies also concurred with our proposed sample size re estimation that supports a more focused enrollment on the symptomatic participants' 90 to 100 symptomatic participants for chicken duration of the 96 weeks.
Please standby for the next question.
The next question comes from Greg <unk> with <unk> Securities. Your line is open.
Hey, it's Greg Savannah, that's thanks for taking my questions I had.
One just regards to your <unk>.
Discussions with the FDA and the European regulator.
Lori authorities.
And kind of the changes that you are announcing.
With the phase III trial, and I'm, just curious as to.
Whether the topic of looking at Biomarkers with specifically discussed in the agencies view around whether you could look at Biomarkers, that's perhaps a surrogate endpoint.
Maybe also take a look at efficacy.
Just wanted to see.
At least in this particular disease.
How that discussion.
<unk>.
Yes, so we did discuss it.
Higher trial with FCA and.
Interacted also with EMA.
Yes.
This is a biomarker rich study, we will have a number of biomarkers, but I want to emphasize that our analysis.
Our primary analysis.
As to use for a clinical treatment effect, that's using the CVR <unk> NEK.
Some are boxes, and we have a lot of confidence that we will.
Be able to achieve a full approval or traditional approval.
Based on the clinical outcome measure supported by the biomarker data.
But in the event that we were disappointed in the.
The primary.
Primary clinical outcome measure, we will have a very rich biomarker study and we of course will we will look to that date at that point to decide what the rehab.
Sufficient data for a.
Accelerated approval approach.
Okay. Thank you so much and then.
Maybe just a follow up question. If you could just share more details just on the blood barrier technology blood brain barrier technology that you are advancing.
Maybe with a lens on how your approach might differ versus others.
Including neighbors in your backyard and others on the East Coast, just if you could help us understand that thanks.
Yes.
<unk>.
Thank you Greg.
Have developed there.
Mobile technology that can be specifically.
Also each cargo that can be used with different types of antibodies.
<unk>.
That can be used.
Therefore protein and enzyme replacement.
The uniqueness of our technology.
Pvp.
<unk> two will be lower.
Knowledge into each specific car.
Go.
And we will disclose more about this technology in the near future.
Thank you very much.
Please standby for the next question.
Our next question comes from Paul Matteis with Stifel. Your line is open.
Hi, This is James on for Paul Thanks for taking our question.
So I believe the original study with FTE was powered around a 40%.
Slowing of disease effect size.
What is the effect size of the study is powered around now with with 100 patients curious if theres any color you can provide there and if there's anything in the kind of blended analysis, you did that kind of reinforces your confidence in that power ray. Thanks.
Yes sure. Thanks. This is Gary so our clinical trial design remains unchanged, that's the clinical endpoint biomarkers to duration of treatment et cetera.
This meeting we had with FDA about our statistical analysis approach was whats typical and necessary step before eventually finalizing our system Statistical analysis plan in the next year.
This analysis that we were focusing on is still going to provide.
Sufficient power to detect a 40% treatment effect.
The specifics around that will be finalized of course in our statistical analysis plan later next year.
In terms of your question about <unk>.
Why that is.
<unk>.
The real advantage here are focusing the analysis on the symptomatic subjects is that the variance of their disease progression is considerably less than the at risk subjects that we originally include planned.
Plan to include in the primary analysis, so by focusing on the symptomatic subjects, which by the way we've also.
Somewhat easier time enrolling and are nearly complete.
We can.
We will have still adequate adequate power to detect a 40% treatment effect.
Okay, and maybe just one clarifying so is there anything different about the stats plan or the analysis.
That gives you that it is still powered for a 40% effect size with meaningfully less patients.
On just the variance or is it really just that the variance is lower so.
That's our statistically it still power for 40% with a much smaller.
Sample size.
Yes, that's the estimate the main what's really driving this is the fact that.
I think I mentioned, we mentioned previously.
<unk>.
We had.
Originally disclosed based on emerging data on the variability of disease and this comes from both the <unk> cohort.
We wanted to go to regulatory authorities to discuss the <unk>.
Since fiscal analysis approach. So it was really driven by the fact that.
There is.
The variance was significantly less than we are.
Had concern.
<unk> had considered with our initial estimates which were based on very limited data at the time of the trial nearly three years ago.
So that's the main driver.
Makes sense. Thank you.
Please standby for the next question.
The next question comes from Tom Shrader with <unk>. Your line is open.
Hi, good afternoon, thanks for taking the questions.
You guys seem cautious about calling your effects for trim to ARIA is it somehow different or are you just being cautious because it's new and also are you taking a beta scans. In this trial I think you said you were going to is that something we will see that you take baseline scans.
I have a follow up.
Yes, Thanks, it's a great question.
We're just being cautious.
It's a different mechanism and although the MRI.
Features are.
The.
Both of the MRI features and the clinical aspects of the.
The area that we're seeing is really.
And distinguishable if you will and thats not going to take it for me that's from a number of.
Thought leaders that we've shown that we've discussed the data with.
So because it's a different mechanism, we don't want to presume that this is related necessarily to amyloid clearance.
Of course.
Clearance of Misfolded proteins, including amyloid is one of the functions of microglia and so boosting microbial function.
Maybe maybe meetings that we have it will have a rich data set including.
Plenty of amyloid pet so we will have.
Certainly.
More about that mechanism when we opened the study next year.
And then a beta scanning or you're doing that.
Yes, yes, I'm sorry, so we do have a debate of pet.
At.
This study includes both amyloid and Tau Pet studies sub studies and so we will have that data for certain.
And then housekeeping for the <unk> one trial, how many asymptomatic patients.
Did you get.
Just going to continue to treat those and what do you do with patients that progress while on treatment.
Are they counted in the bucket of symptomatic.
Yes, so we have a.
A relatively smaller much smaller number of at risk subjects.
Then we do symptomatic subjects and those at risk subjects are.
In fact, we could see this with a blinded sample size re estimation.
<unk>.
Are not progressing very much so that hasnt really been an issue.
I think the.
The second part of your question was how many of the symptomatic patients have been enrolled so how many other became symptomatic, but it sounds like it might be done.
Yes.
Yes.
From what we can tell by sample size, we estimate re estimation.
It doesn't look like we're seeing progression in those patients yet.
Okay. Thanks for the detail.
Yes.
As a reminder to ask a question. Please press star one one on your telephone.
Please standby for our next question.
The next question comes from Myles Minter with William Blair. Your line is open.
Hi, Thanks for taking the questions.
Just on the <unk> for analysis.
One is basis.
And you're saying the same variability on a symptomatic patient population as what you saw what they saw in Genesee true.
Specifically looking at the.
<unk> analysis that you did with the <unk>.
Patient population versus the 10 pacing should pick from Gen fighter like is it is it that sort of level of variability that we should be looking at that you are saying on a blinded basis same from Craig. Thanks.
Yes, thanks for the question Myles so.
When we speak about the variance.
And as a basis of the.
Change in the statistical analysis plan for.
The phase III study, we're speaking about variance in that study which is.
As you said as you said, where we're enrolling 90 to 100 patients and we're nearly finished so.
That's we're talking we're talking about sample size re estimation based on that data to.
The datasets for the Phase II study, which I think I heard you referenced.
This is a very small cohorts and turn up.
Up to 2014 and senile.
Nine cohort.
Very very small really too small.
To really draw any conclusions about app out.
Disease progression.
That study was really designed to be a biomarker proof of concept study was not designed or powered as determined treatment effects.
So there is you can't really say much about looking at those very small cohorts.
About about overall barron's.
So you would caution against extrapolating that in saying that in the placebo patients that kind of decline by 12 points on city or on placebo.
I mean, I would say we've looked very carefully at the <unk> data and we sat down with the people who are running those studies.
The variance.
Actually recently, we thought about this in the first place was reading through that in a recent paper that came out in all of last year.
Adam stuff erroneous, we'd author that.
And studying that where he then that paper he suggested that that future trials in FTE could potentially be significantly smaller than our original study design and when we look at the variance they share their data with us and we've looked at that and it was considerably less than our original estimates for our own trial and Thats, where we are.
Went in and looked.
And found with our sample size re estimation that in fact, our variance was.
As I said much less than we originally.
Anticipated.
Conservatively based on the original whatever data was available three years ago.
I'd like to also maybe quantify a little bit I think you are asking about the variability in the in the phase II study, but thats been the C. Nine population and not the brand in that population.
When the viability and the grow annually.
The phase two study.
Terrific.
I mean, if you look just the supermarket.
If you look at.
You seem to be going through the variability is much higher conversion rate.
Much less predictable so.
So the variability.
Phase III, if commodity can be.
So can we become a smaller and if you combine the kind of three <unk>.
So Mike we can phase III female commodity group.
Okay quick one on in factor.
Were there any patients that were positive April .
But potentially positive for cerebral amyloid angiopathy that might imply that those are the signals.
Not that we know of no.
Hello.
Thanks for the question.
I show no further questions in the queue I would now like to turn the call back to Mark for closing remarks.
Thank you operator, and before we end the conference call I, just like to share that electric will be participating in a number of upcoming conferences, including <unk> virtual Biotechnology conference on August seven.
<unk> 18th annual Biopharma Conference on September 7th and Boston Morgan Stanley Morgan Stanley 's Global Healthcare Conference on September 11th in New York and HC Wainwright Global investment Conference on September 12 also in New York.
Thank you again for your time and attention today.
This concludes today's conference call. Thank you for participating you may now disconnect.
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[music].
Yes.
Okay.
[music].
Sure.
Okay.
Okay.
Thank you.
Perfect.
Yes.
Sure.
[music].
Yes.
Thanks.
Okay.
Yes.
Yes.
Sure.
Okay.
Yes.
Okay.
Okay.
Okay.
Yes.
Okay.
[music].
Yes.
[music].