My guess: Either becuase of: (a) A belief that FDA approval for CLL is about to be announced in advance of the 2/28/14 deadline; (b) Fear of missing this imminent announcement; (c) Expectation of a big earnings beat from Ibrutinib's presecriptions. Anyone know?
The ONLY reason why it was up on Friday was in anticipation of JNJ earning on Tuesday morning. This will give a sneak peak into PCYC's earnings in February. PCYC has partnered with JNJ for this potential blockbuster drug.
maxcoatinc answered your question in his post: Call options representing over 1 million shares are expiring in the money. The sellers, if they have covering positions, can let the shares go or buy more shares to replace them. The sellers of naked calls have to buy shares. Just another form of short squeeze.
PCYC management has stated that they expect FDA decision prior to Feb 28th so I'd say its a given. Considering how strong the weekly call options that expire next week have been trading, I think the market is expecting something as early as next week.
"First, we don't know a lot more than we did the day before the presentation about the CLL indication. Pharmacyclics was asked no less than a half-dozen questions involving the potential for CLL approval, how the Food and Drug Administration views the opportunity for any expanded indications, and potential CLL labeling restrictions and treatment pricing. Essentially none of Wall Street's questions received answers, which isn't a big surprise given that the FDA has yet to issue its decision on the CLL indication. About the only thing we know is that Pharmacyclics' management team expects an FDA decision prior to its Feb. 28 PDUFA date."
Read other post...PCYC surging today...this is probably why:
Kathy Boltz, PhD
January 17, 2014 A new study helps confirm that a molecule targeted by the experimental drug ibrutinib is critical for the development of chronic lymphocytic leukemia (CLL), the most common form of adult leukemia.
In clinical trials, ibrutinib has often shown exceptional activity in people with CLL. The agent targets a molecule called Bruton's tyrosine kinase (BTK). It permanently incapacitates the molecule, and this stops the transmission of an important signal that promotes cell growth and proliferation.
But ibrutinib also inhibits other molecules in CLL cells. Like BTK, these molecules are proteins called kinases, and they might be important for CLL-cell survival, the researchers say.
"Ibrutinib's lack of selectivity might mean that BTK is not the critical target in CLL, and that future drugs developed for CLL should focus on other molecules," said Amy Johnson, PhD, principal investigator and associate professor of medicine in the Division of Hematology, and a researcher at The Ohio State University Comprehensive Cancer Center–Arthur G. James Cancer Hospital and Richard J. Solove Research Institute in Columbus (OSUCCC–James). However, the findings, published in Blood (2013; doi:10.1182/blood-2013-07-515361), validated BTK inhibition.
"This study shows that BTK is an important therapeutic target in CLL," said first author Jennifer Woyach, MD, assistant professor in the Division of Hematology and an OSUCCC–James researcher. "Inactivating BTK alone delayed CLL development in a mouse model, confirming that BTK is a clinically important target in CLL. This suggests that development of selective BTK inhibitors—in addition to multikinase inhibitors like ibrutinib—is reasonable in CLL."
To investigate the role of BTK in CLL, Johnson, Woyach, and their colleagues used CLL cells from patients and two CLL mouse models, one of which spontaneously develops a malignancy very similar to human CL