The Most (Only) Interesting Comment on Geron's Call

The Most (Only) Interesting Comment on Geron's Call

After Geron spiked 45% yesterday because of an abstract released before the American Society of Hematology, or ASH, meeting next month, I figured we'd get a little more details about the positive but perplexing data.

Instead, investors got stonewalled by President and CEO John Scarlett's assertions that ASH prevents the company from discussing the data before the meeting.

"We're not able to make any commentary on the subject of the abstract which this question -- your question -- implies."

"I think you're going to have to read the abstract again for yourself ... because I'm just not going to able to comment on the abstract as we've said a couple of times on the call, sorry."

"Unfortunately that is covered within the 4 corners of the abstract, and that's a part of the embargo."

And on and on it went.

I understand why ASH doesn't want companies and researchers talking about data not in the abstract -- why would anyone come to the meeting if the data has already been presented?

It's a little less clear why they can't discuss the data in the abstract that's already public knowledge. But alas, Geron has to play by the rules. Getting banned from the conference would be detrimental if imetelstat is eventually approved to treat myelofibrosis or some other blood cancer. ASH is important for investors because it's a place to see clinical data, but it's important for companies because it allows them to promote their approved drugs to doctors.

There was one interesting comment on the call. The analyst had to ask it as a hypothetical, but it helps to answer the perplexing part of the data where imetelstat is causing positive changes in cells morphology in some patients, but no improved clinical outcomes were reported. Changes in cell morphology are important because they're a sign of the underlying disease; in patients with myelofibrosis, cells look like they're growing out of control. But ultimately reducing symptoms, such as an enlarged spleen, is what's important to the patient.

Here's the full answer from Scarlett from the Capital IQ transcript of the call:

Well, from a theoretical perspective, as you quite rightly pointed out, not commenting on any data contained within the abstract. The -- I think that if you see -- look, the goal is obviously having meaningful disease modification, and as far as we know, the symptoms are associated with cytokines that come from, presumably, from the underlying malignant progenitor cell neoplasm. So theoretically, one should expect, I would think, to see changes in all of these different criteria that make up the response criteria, the IWG response criteria, at some point. The exact nature of how long it takes and so forth may be both individualized, and also, I don't think that we can make any further comments about that without breaking the embargo. But I would just simply say that, theoretically, one should expect to see things. If you get the underlying neoplasm headed in the right direction, I would expect most of these criteria to head in the right direction.

There aren't any drug cures for myelofibrosis, so it's a little hard to know exactly what would happen if the mutated cells are all killed. As Scarlett says, we'd expect the clinical symptoms that are part of the IWG response criteria to begin improving as well, but it might take awhile and it might be individualized and it might be something else that we'll find out about at ASH.

If you want to read between the lines in Scarlett's response -- and that's dangerous with money on the line -- it's possible he already knows that clinical symptoms are improving and that's why he caught himself mid sentence. The ASH abstracts were due in mid-August , so he likely has a lot more information than was available when the abstract was submitted.

Pop-worthy data?
Most certainly. How much remains to be seen.

Incyte's Jakafi is the only drug approved to treat myelofibrosis, although there are a couple of other drugs -- Cell Therapeutics and Gilead Sciences' momelotinib and simtuzumab -- that work by attacking the same JAK2 pathway. The drugs from Incyte, Cell Therapeutics, and Gilead help reduce spleen size, but don't attack the underlying disease. They're certainly not a cure. Any drug that could cure the disease would certainly be able to take a lion's share of the market.

Imetelstat could be a cure, but investors haven't factored that in yet. Incyte is a $5 billion company; Geron is a $0.6 billion company. We're years away from imetelstat being on the market -- Geron has to run one, possibly two, trials first -- but it's clear Geron has room to run if the presentation at ASH next month shows a clinical benefit.

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Originally published