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Geron Corporation (NASDAQ:GERN)

Update on Imetelstat Clinical Development Program Conference Call

September 10, 2012 8:30 am ET

Executives

Anna Krassowska – Investor and Media Relations

John A. Scarlett – President and Chief Executive Officer

Stephen M. Kelsey – Executive Vice President, Head of Research & Development and Chief Medical Officer

Graham K. Cooper – Executive Vice President, Finance and Business Development and Chief Financial Officer

Analysts

Karen E. Jay – JPMorgan Chase & Co.

Brian Klein – Stifel Nicolaus & Company, Inc.

Charles Duncan – JMP Securities

Ryan Martin – Lazard Capital Markets

Operator

Good day, ladies and gentlemen, and welcome to the Geron’s Conference Call to provide update on Imetelstat Clinical Development Program. My name is Ann and I will be your coordinator for today’s call. At this time, all participants are in listen-only mode. (Operator Instructions) We will be facilitating a question-and-answer session following the presentation.

I would now like to turn the presentation over to your host for today’s call, Anna Krassowska, Investor and Media Relations. Please proceed.

Anna Krassowska

Thank you, Ann. Good morning everyone, and thank you for joining us to hear this update on our clinical development program for imetelstat. With me on the call this morning are Dr. John Scarlett, President and Chief Executive Officer; Dr. Steve Kelsey, Executive Vice President, Head of R&D and Chief Medical Officer; and Graham Cooper, Executive Vice President, Finance and Business Development and Chief Financial Officer.

Following our remarks, we will take questions. The press release issued this morning provided an update on the imetelstat program is available on our website at geron.com. Today’s call is being webcast live on Geron’s website and will be available for replay until October 10.

We would like to remind listeners that except for statements of historical facts, the statements in this conference call are forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. These include without limitation, statements regarding the timelines and plans for Geron’s research and product candidates, including anticipated timelines for clinical trial enrollment, results and data, the clinical results and therapeutic potential of Geron’s product candidates and financial or operational projections or requirements, including spending guidance, the sufficiency of Geron’s cash resources and statements regarding the potential divestiture of Geron’s stem cell business.

These statements involve risks and uncertainties that can cause actual statements to differ materially from those in such forward-looking statements. Information concerning factors that could cause actual results to differ materially from those in the forward-looking statements is contained in Geron’s periodic reports filed with the Securities and Exchange Commission under the heading, Risk Factors, including Geron’s quarterly report for the quarter ended June 30, 2012.

Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, and the facts and assumptions underlying the forward-looking statements may change. Except as required by law, Geron disclaims any obligation to update these forward-looking statements to reflect future information, events or circumstances.

I’ll now hand the call over to Chip.

John A. Scarlett

Thanks, Anna. I thank all of you for joining us. The purpose of the call today is to give you an update on the Imetelstat Clinical Development Program. We announced in the press release this morning that we’re discontinuing our trial in metastatic breast cancer. we’d like to give you further information regarding that decision and review for you the rest of the imetelstat development program.

I’d like to start by putting this trial into the context of the overall program. Because of the role of telomerase and extending cancer cell longevity and proliferation, we believe that inhibiting telomerase may be an effective strategy for treating a broad range of malignancies.

We designed imetelstat to inhibit telomerase and in Phase I studies of imetelstat, we established doses and schedules for Phase II that were tolerable and that achieved target exposures that were consistent with those required for efficacy and preclinical cancer models. Of those doses, telomerase inhibition was observed in patient tissue samples.

Based on these and other data, Geron designed a Phase II imetelstat program in both solid and hematologic malignancies. the tumors we chose to study were those for which we had supportive preclinical data, evidence of the disease was driven by a cancer progenitor cell proliferation and in which imetelstat could be tested either as the single-agent treatment or in combination with cytotoxic chemotherapy.

Two solid tumors, metastatic HER2-negative breast cancer and advanced non-small cell lung cancer and to liquid or hematologic tumors, essential thrombocythemia and multiple myeloma were selected for this Phase II program. We designed the Phase II imetelstat program to test multiple, independent hypotheses. therefore the findings in one study would not necessarily impact the conclusions from the others.

We’ll begin by discussing the rationale for studying imetelstat in the two solid tumor indications and at the conclusion of this call; we’ll just touch a rationale and plans for setting imetelstat and hematologic malignancies. The lung cancer solid tumor trial was designed to evaluate whether single-agent maintenance imetelstat could extend the duration of progression-free survival after tumor debulking by conventional chemotherapy had been completed.

By administering imetelstat alone in the treatment arm, we were able to use maximum doses of the imetelstat. In contrast, the metastatic breast cancer trial was designed to evaluate whether using imetelstat in combination with debulking chemotherapy could extend the duration of progression-free survival in patients.

The principal challenges for this study were the overlapping hematologic toxicities of the imetelstat and paclitaxel, the chemotherapeutic agent being used, which necessitated the use of the lower starting dose and less frequent dosing schedule for imetelstat in the metastatic breast cancer trial and in the lung cancer trial. Today, we announced our decision to discontinue the imetelstat Phase II metastatic breast cancer trial.

I’m going to ask Steve Kelsey, our Head of R&D and Chief Medical Officer to walk through the rationale for that decision and to discuss the implications of this decision on the ongoing Phase II trials in lung cancer and hematologic malignancies.

Stephen M. Kelsey

Thank you, Chip. In our Phase II breast cancer study, 166 patients with HER2-negative metastatic breast cancer were randomized one-to-one to receive either paclitaxel or paclitaxel with imetelstat. Patients were stratified by whether they have received concomitant bevacizumab.

Paclitaxel was administered on day one and day eight of the 21-day cycle at initial doses of 90 mg/m2. Imetelstat was administered on day one of the 21-day cycle at a dose of 300 mg/m2 or approximately 7.5 mg/kg.

Modifications to paclitaxel dosing were made as per approved labeling. there were no specific dose adjustment guidelines in the protocol for imetelstat, although dosing delays were committed. 83 patients were randomized to the imetelstat treatment arm and 83, to the control arm.

Overall, 76% of the population were first-line metastatic breast cancer patients and 24%, second-line. 28% of patients received bevacizumab, the distribution of second-line patients, triple-negative disease, and bevacizumab administration was similar in each study arm.

The Phase II HER2-negative metastatic breast cancer trial prospectively included scheduled periodic reviews of patient safety data conducted by Geron’s Internal Safety Monitoring Committee, which makes assessments and recommendations independent to investigators and company management. included in these reviews, were the number of deaths and discontinuations of study therapy, including paclitaxel in both arms of the study.

Late last Wednesday, the Internal Safety Monitoring Committee reported to us that they had identified a greater number of deaths and number of patients permanently stopping paclitaxel in the imetelstat arm compared to the control arm. They also informed us that based on these observations, they had directed an unplanned interim analysis of efficacy to be performed and they reported the results to us.

At the time of that analysis, 85 progression events have occurred, representing 91% of the pre-specified, 93 events required for the primary analysis. The analysis showed that median progression-free survival for imetelstat treated patients was 6.2 months compared to 8 months for patients treated with paclitaxel alone.

The hazard ratio was 1.62, which was statistically significant with the p-value of 0.028. although the absolute number of deaths was higher in the imetelstat arm, 16 versus 10, there was no statistically significant difference in overall survival. There were two complete responses in each study arm.

overall response rate was 48% for imetelstat treated patients and 41% for paclitaxel alone treated patients. Primarily, because the PFS for imetelstat treated patients was significantly shorter than the patients in the control arm, we stopped the trial. The series of sensitivity analyses of the data suggested the reductions in the dose intensity of paclitaxel administered to subjects in the treated and the imetelstat arm were likely responsible for the difference in progression-free survival.

Despite the sensitivity analyses, it remained unclear to us whether imetelstat was contributing to the increased risk of progression, independent of reduced paclitaxel dosing. In addition, we needed to ensure that imetelstat was not accelerating disease progression in the advanced non-small cell lung cancer trial.

We’ve as well made the decision to perform an unplanned interim safety and efficacy analysis of our lung cancer trial. Patients in this trial were randomized 2:1 to receive either imetelstat a single-agent maintenance therapy or observation alone in the control arm. Patients were stratified by whether they also received concomitant bevacizumab.

At the time of the lung cancer analysis, all of the pre-specified progression events have occurred, but the dataset has not been fully cleaned. The analysis suggests a modest trend in PFS in favor of the imetelstat arm. The hazard ratio was 0.78.

The Kaplan-Meier curve separated just before the median, resulting in no meaningful difference in median progression-free survival between the two arms. median progression-free survival for the imetelstat treated arm was 2.8 months compared to 2.6 months for the observation-only arm. Thus, no evidence was found that imetelstat was accelerating disease progression in this study.

In addition, these data suggest that imetelstat was not contributing to the increased risk of progression independently or reduced paclitaxel dosing in the metastatic breast cancer study. Therefore, at this time, we are not aware of any factors responsible for the shorter PFS in the imetelstat arm of the breast cancer study other than the reduced paclitaxel dose intensity.

We find there are reasons to stop the lung cancer study and therefore it is continuing as planned. We will perform additional analyses as called for in the protocol and we will expect to publish the results of those analyses in the scientific forum at some later date.

Nevertheless, it is unlikely with our pre-specified success criteria, a hazard ratio of 0.5 or a difference in median PFS of at least two months, imetelstat treated subjects compared to the control arm will be met. Therefore, unless subsequent analyses result in substantially different conclusions, we believe it is unlikely that Geron will take imetelstat force into a Phase III study in advanced non-small cell lung cancer.

We do not plan to provide further investor updates on the results of this study. Let me now talk about the implications of this new information for the imelstat program in hematologic tumors. Despite the data from the two solid tumor studies that we’ve shared with you today, our plans for further development of imetelstat and hematologic malignancies have not been adversely impacted.

We still believe that telomerase is a relevant target in hematologic tumors and the imetelstat is an active inhibitor of that target. The hypotheses that we are testing in our hematologic malignancies studies remain valid, because they’re largely independent to those tested in the solid tumor program.

In our essential thrombocythemia and multiple myeloma studies, we are evaluating the hypothesis that inhibiting telomerase will selectively inhibit the proliferation of malignant progenitor cells responsible for these diseases as well as the hypothesis that imetelstat is active against malignant cells with short [p-limits]. These studies leverage nonclinical observations that imetelstat distributes well to bone marrow and selectively inhibits the clonal proliferation of leukemic progenitors.

In both the ET and myeloma trials, we have selected biomarkers that allow us to measure the effect of imetelstat on leukemic progenitors. In the ET trial, we are also evaluating clinical and hematologic responses. We are not providing specific details on these results at this time, and we continue to expect to release results from these studies in the fourth quarter.

John A. Scarlett

Thank you very much, Steve. That concludes our prepared remarks. We’d now be very pleased to take questions.

Question-and-Answer Session

Operator

Thank you. (Operator Instructions) And our first question comes from the line of Karen Jay with JPMorgan. Please proceed.

Stephen M. Kelsey

Hi, KJ.

Karen E. Jay – JPMorgan Chase & Co.

Hi, good morning, thanks for taking the questions. This is KJ in for Cory Kasimov. Given I’m new today; I think we would assume a bit of a shift of focus perhaps on 1005. So I know the call was meant to discuss imetelstat, but wondering if you could update us on those two trials enrolling and how of course, you’re too heading enrollment target and whether or not there has been a safety review for those two trials yet?

Stephen M. Kelsey

Yes, KJ. The GRN1005 breast cancer trial (inaudible) GRABM-B is enrolling well on schedule. and I think we have reported that we will be presenting interim data from that study at the San Antonio Breast Cancer Symposium in December. We have performed interim analyses of safety and the study is currently ongoing under an amendment, which allowed us to reduce the starting dose from 650 mg to 550 mg/m2. The lung cancer study is behind our projected enrollment schedule and we’re currently actively engaging our lung cancer investigators to see what we can do about that.

Karen E. Jay – JPMorgan Chase & Co.

Okay, thank you.

Stephen M. Kelsey

And an interim analysis of the safety from that study, which is the regular safety updates are performed and the first one is to, I believe at the end of this month.

Karen E. Jay – JPMorgan Chase & Co.

Okay. And then for the other [hema-t] malignancy programs, the initial data that you’ll be getting in the coming months for them, are you expecting that that will be enough to prompt the decision on more randomized trials or what I guess, what is your vision there going forward for those two programs?

Stephen M. Kelsey

Well, this was certainly, we’ll be using that information to determine the scope of the hematologic malignancies program, but we haven’t completely finalized the details of what that program will be at this stage. so we’ll probably have more information for you once that data is fully analyzed and reported, will be, I’m sure will be able to share our times with you at that stage.

Karen E. Jay – JPMorgan Chase & Co.

Okay, thank you.

Operator

And our next question comes from the line of Brian Klein with Stifel Nicolaus. Please proceed.

Brian Klein – Stifel Nicolaus & Company, Inc.

Hi guys, thanks for taking the questions.

Stephen M. Kelsey

Yeah, good morning.

Brian Klein – Stifel Nicolaus & Company, Inc.

Good morning. So going back to imetelstat in breast. can you tell us if there was any impact of Avastin at all, specifically in terms of the deaths in the dose reduction that you saw any relationship with Avastin dosing?

Stephen M. Kelsey

Brian, firstly let me preface my remarks by saying that there are a large number of subgroup analyses that were both pre-specified in the protocol and the number of exploratory analyses that weren’t and some of those still need to be performed. At this stage, all I can tell you, there was no, no one knows statistically significant differences in the outcome of the study when we corrected the bevacizumab use versus no use. there was a difference in the hazard ratio; it actually was closer to one. so that it’s very difficult to say that that was a meaningful difference.

Brian Klein – Stifel Nicolaus & Company, Inc.

Okay. And can you give us a sense of the degree of dose reductions that occurred in the trial?

Stephen M. Kelsey

I can, the totality is the dose intensity for paclitaxel has not yet been calculated, but we estimate that patients in the imetelstat arm received approximately 85% of the amount of paclitaxel of the patients in the control arm received.

Brian Klein – Stifel Nicolaus & Company, Inc.

Got it.

Stephen M. Kelsey

And that is an amalgamation of dose reductions, dose delays, and our premature terminations of paclitaxel therapy.

Brian Klein – Stifel Nicolaus & Company, Inc.

Okay. and at this time, are you concluding that the dose reductions are related to the combination of the side effects profile? Was it specifically the neutropenia, thrombocytopenia? Was there something else that led to the dose reductions?

Stephen M. Kelsey

At this stage, we are working on the assumption that it was predominantly hematologic toxicity induced by the combination of imetelstat and paclitaxel that was responsible for the dose reductions, but we have not had a chance to fully analyze the data and the one of the things that we will also need to look at is whether or not imetelstat increased the instance of neurotoxicity from paclitaxel. We don’t have any evidence at this stage to suggest one way or the other.

Brian Klein – Stifel Nicolaus & Company, Inc.

Got it, when you look back on some of the earlier stage trials that were conducted, did you every see any synergy between paclitaxel and imetelstat in terms of efficacy or was it only additive?

Stephen M. Kelsey

There were synergies seen in nonclinical models. and as you know, we did a Phase Ib study, which was presented at ASCO two years ago, which suggested that the combination of paclitaxel that we could schedule and that doses schedule with imetelstat was reasonably well tolerated and the response rate was at least as high as that reported for paclitaxel alone and that study was performed in combination with bevacizumab.

Brian Klein – Stifel Nicolaus & Company, Inc.

Right.

Stephen M. Kelsey

But the implications of that study were what led to the design of the Phase II study that we’ve just reported.

Brian Klein – Stifel Nicolaus & Company, Inc.

Okay, great. And then maybe just a question for Graham, can you tell us the percent of R&D spend currently on imetelstat and also the number of employees at Geron that are related to the imetelstat program?

Graham K. Cooper

Let me come back to you on that.

Brian Klein – Stifel Nicolaus & Company, Inc.

Sure.

Graham K. Cooper

I don’t know what at the top off my head.

Brian Klein – Stifel Nicolaus & Company, Inc.

Sure, okay. Thanks a lot for taking my questions.

Operator

And our next question comes from the line of Charles Duncan with JMP Securities. Please proceed.

Stephen M. Kelsey

Hi, Charlie.

Charles Duncan – JMP Securities

Hi guys, good morning. Thanks for taking the call. I wanted to talk more about the hem program. I guess I’m kind of wondering if you could further expand on the mechanistic rationale for the drug, it seems pretty clear, but if you could expand on that and why you think this is different in terms of combination. The other thing is what can you share with us in terms of the blinded information that you’re seeing in the hem studies that are ongoing?

Stephen M. Kelsey

Let me address your first question first, Charles. I think there has been and is today considerable evidence that hematologic malignancy is, particularly myeloid leukemia is whether acute or chronic are driven from a cancer stem cell or cancer progenitor cell and early progenitor cells, early hematologic progenitor cells have very high levels of telomerase.

So it’s reasonable to believe that inhibiting telomerase would inhibit the external proliferation, we have evidenced from nonclinical studies that that is in fact, the case and we also have data to suggest that the leukemic genesis are relatively more dependence on telomerase than the normal hematopoietic progenitors, that’s the primary rationale for doing the clinical trials.

There are two other things, I think that are noteworthy. One is, we have evidenced from our Phase I program that imetelstat has a direct effect on the hematopoietic lineage actually, we saw thrombocytopenia and neutropenia, which we appreciate could be due to a range of different mechanisms, but I think we believe that it’s predominantly an integration of telomerase.

So the two other things are that imetelstat does distribute preferentially to bone marrow was one of the, is a highly lipophilic molecule and we get very high concentrations in human bone marrow and of course, the last thing is certainly the myeloproliferative neoplasms of chronic diseases and if we believe economical theory that imetelstat needs to be on board for sometime before the effect on telomere-shortening can be observed, then the [prolisity] of these diseases may make them more amenable to treatment with telomerase than the some of the more aggressive tumors. But one of the problems, if we track back to the lung cancer study, it’s quite possible that one of the reasons why there was a modest effect, but not a big effect was that the progression of that disease just may have been too rapid for the disease that we have to cope with.

And your second question if I understand was about the data from those two studies. all I can say is that we’re currently in the middle of evaluating those trials, so that we can maintain our commitment to report the (inaudible) in Q4 and we remain committed to doing that.

Charles Duncan – JMP Securities

Okay. And then it seems that we can pretty much forget about imetelstat in terms of solid tumor cancer development?

Stephen M. Kelsey

I don’t think that’s necessarily true. we have a number of studies still ongoing in solid tumors and we will – these being run by cooperative groups, and also by individual investigators and we will see how they go, again these are – I don’t think that we are at this stage likely to pursue any further development in metastatic HER2-negative breast cancer or advanced non-small cell lung cancer, but there are tumors with very different biologies and tumors where imetelstat is not being combined with conventional cytotoxic chemotherapy and those studies are still ongoing.

Charles Duncan – JMP Securities

(Inaudible) going to ask you, Steve that it seems like this is not so much imetelstat, but it’s the combination and can you imagine some indications in which in solid tumor cancers where the approach might make sense?

Stephen M. Kelsey

Well, I think there are one or two that they – again based largely on preclinical and biologic rationale. the two obvious groups are the primary brain tumors and the pediatric tumors. As I said, we do have the study that the children’s oncology group are currently running a study in pediatric tumors and we have an IST with ongoing in glioblastoma. so I think there are a few niche indications, I think but you’re right it does seem difficult to combine imetelstat approved doses in combination with conventional cytotoxic chemotherapy and that’s an issue in a liability that we will be working around.

Charles Duncan – JMP Securities

And then my final question is getting back to GRABM kind of the follow-on to the previous analyst and that is present R&D spend not on imetelstat, but on this particular set of programs, any implications for the burn rate at least in 2012?

John A. Scarlett

Thanks, Charles. and I can address Brian’s comment as well. so the effect on burn rate in 2012 is likely to be small, because these trials were winding down, we’re nearing completion of these trials. and so what we haven’t had a chance or have not adjusted guidance for 2012; if the implications are likely to be pretty de minimis for overall spend for this year. With regard to Brian’s question about the allocation of spend between imetelstat and 1005, I think reasonable estimate is sort of half-and-half between imetelstat in 1005 year-to-date. as the imetelstat trials have been winding down that may be more heavily weighted toward 1005 in the second half of the year, but as an estimate for 2012, 50-50 is a reasonable estimate.

Charles Duncan – JMP Securities

And then my final question is on 1005 program, you mentioned possibly [presentation] at San Antonio, is that just a target or have you actually submitted an abstract and if so, can you provide any color on the content of that?

Stephen M. Kelsey

We submitted an abstract, which is accepted, and I believe will be presented on December 7. The content of the abstract was somewhat light on data, but we do expect to be presenting both efficacy and safety data at the meeting.

Charles Duncan – JMP Securities

Steve, you said December 7?

Stephen M. Kelsey

I believe it’s December 7.

Charles Duncan – JMP Securities

Okay. Thank you for taking the questions.

Stephen M. Kelsey

I’ll have to check Charles, but I believe that is December 7.

Operator

And our next question comes from the line of Ryan Martin with Lazard Capital Markets. Please proceed.

Ryan Martin – Lazard Capital Markets

Hi, thanks for taking the call. Just want to follow up, Steve, you mentioned 1005, it was a dose reduction, just want to find out at what point after enrollment was an amendment made and what was the rationale for doing that?

Stephen M. Kelsey

Okay. So the amendment was, the change was made after we had enrolled 13 patients, and all subsequent patients being enrolled in the starting dose of 550 mg/m2. The main reason for the change was that specifically in the patients with metastatic breast cancer and brain metastases, these patients develop that brain mets relatively late in their treatment course, and they have had multiple prior cytotoxic regimens for their breast cancer.

So they’re less able to tolerate the 650 mg/m2 dose of GRN1005. And what we were noticing was a high incidence of paclitaxel related toxicities and (inaudible) from GRN1005. So that’s why we’ve reduced the dose. The interim analysis of safety after the reduction of the dose does suggest that the tolerability profile is significantly improved with the dose reduction.

Ryan Martin – Lazard Capital Markets

Thanks and can you remind us what the efficacy data was in prior studies from those two doses?

Stephen M. Kelsey

Well, there was no efficacy data presented in the Phase 1 program at the 550 mg/m2, dose because it was part of the dose escalation only three patients were in fact treated at that dose level. Most of the data that we’ve presented previously has been of the 650 mg/m2 dose where only six patients with breast cancer were treated. And my recollection from, is that two of these six patients had an intracranial response.

Ryan Martin – Lazard Capital Markets

Okay. Thanks, Steve.

Operator

Ladies and gentlemen, this concludes today’s question-and-answer session. I would now like to turn the call over to Dr. John Scarlett for closing remarks.

John A. Scarlett

Great, I’d just like to also reiterate that the planned presentation of 1005 data at San Antonio Breast Cancer Meetings is based on interim data and that the full data set is still anticipated to be released or at the top line from that, is still anticipated to be released in the second quarter of next year.

So everyone, thank you very much for joining us today, as you can imagine, these are not the kind of clinical results we enjoyed sharing with you. We all undertake the development of new therapies in order to help patients and we do want to express our sincere appreciation to all the investigators and patients who participate again, and continue to participate in our clinical trials.

We’re obviously disappointed that imetelstat didn’t appear to be providing the benefit that we hope to where the metastatic HER2-negative breast cancer or in advanced non-small cell lung cancer. However, we do believe the remained, these diseases with significant unmet medical need were treatment with imetelstat could confirm, clinically meaningful benefit and I think the question-and-answer period really brought that out and we thank all the participants for those questions.

We also continue to pursue development of our peptide-drug conjugate 1005, GRN1005 in brain metastases, and I think that also was covered in the question-and-answer period. So thank all of you for your continued interest and support and we look forward to further communications in the future.

Operator

Ladies and gentlemen, we thank you for your participation in today’s conference. This concludes the presentation and you may now disconnect. Have a good day.

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