Mabio, I've positions in some other bios- ONXX, AMRN, NLNK, PATH,- and everyone of them seems to be much better candidate (from the "risk/reward" standpoint) for shorting than CLDX! There is absolutely nothing wrong from fundamental point of view with CLDX! No single trial has even half failed! The management does not do "data phishing" and rather takes super conservative (IMHO) view to everything,- starting with trial design and ending expected dates! So, from the technical standpoint the stock could go down with the market for some time, but from all my 30+ years experience (and I've been day trader for couple years too) I know - it is extremely hard to pick the right point where to unload the position. So, I just wonder, why do you insist on shorting CLDX? I'd understand if you were playing devil's advocate (like Boar or me sometimes) and pointed to obvious flaws of management, PR, trial design, corporate strategy, etc (and for the record, I think AM could do things differently- why there is no world about getting "breakthrough designation" for example?),
but shorting it??? So far only good (scientifically speaking) things came from EVERY announcement they've made and my advice to you: just move to greener pastures in some other stocks. (My suggestion- start with ONXX, - you probably lose less, or AMRN,- you'll be in better company than here...)
Good morning Mab. I believe everything into falling into place for Celldex. We are talking about having one drug approved within 2 1/2 yrs and a second drug approved in about 3 1/2 yrs. The stock will run up a lot more long before approval.
Amgen – In March 2009, Celldex entered into an agreement with Amgen in which Celldex acquired exclusive rights to develop and commercialize two immune-stimulatory molecules known as FMS-like tyrosine kinase 3 ligand or Flt3L (now referred to as CDX-301) and CD40 ligand (CD40L). Background Fms-like tyrosine kinase 3 ligand (Flt3L) is a potent endogenous growth factor for myeloid dendritic cells (mDC) and plasmacytoid dendritic cells (pDC). Its administration to mice and humans leads to dramatic increases of various DC subsets while Flt3L−/− mice show reduced DC numbers. Flt3L and its receptor (CD135) have been poorly studied in the setting of autoimmune diseases in general. Typically, CD135 is expressed on early myeloid and lymphoid progenitors and is activated by its soluble ligand, Flt3L. The highly differentiated cellular pattern in rheumatoid arthritis (RA) synovium made the authors hypothesise that Flt3L, with its ability to induce proliferation and differentiation, could be of importance in induction and/or progression of arthritis.
Conclusion The data presented in this study point to inflammatory role for Flt3L/CD135 system. Moreover, as the Flt3L/CD135 system is implicated in the generation of DC and B cells, inflammatory cells important in RA pathogenesis, this system might be of importance in RA. Achieving a detailed understanding of Flt3L function(s) in arthritis may lead to the development of novel immunotherapies for RA and other immune-mediated inflammatory diseases.
Have you ever heard of a small biotech selling for around $11 that has numerous potential cancer blockbusters, a HIV vaccine in phase 1 and a compound that might be useful for rheumatoid arthritis? Be careful Mab.
Weight, please, I'm begging you, don't spooke one of the last shorts we still have! How many times do I've to remind you that we need them!! We all know that fair valuation of CLDX one day will be about 4B (i.e. $50), but we need people that disagree with that valuation...