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Xinyuan Real Estate Co., Ltd. Message Board

staccani 176 posts  |  Last Activity: Apr 6, 2015 3:34 AM Member since: Sep 24, 2011
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  • staccani staccani Feb 22, 2015 3:19 AM Flag

    Akanz, whilst I know that the Primary endpoint is 'Composite endpoint of CV death, MI, stroke, coronary revascularization, and hospitalization for unstable angina', what is the % of improvement the treated group need to achieve vs the control group to meet the primary endpoint? And to get an early halt for efficacy? You mention 20%, is it the minimum threshold for early halt for efficacy?

  • Reply to

    They got their free shares and dumped

    by invest83838 Feb 20, 2015 3:18 PM
    staccani staccani Feb 22, 2015 3:04 AM Flag

    you still have no clue, have you? A warrant is the right to purchase a (newly) issues share at a predefined price (ie $1.5). However you put it, and regardless how many involved subject you involve, you still make a loss exercising a warrant at $1.5 and selling it below $1.5.

  • Reply to

    They got their free shares and dumped

    by invest83838 Feb 20, 2015 3:18 PM
    staccani staccani Feb 21, 2015 4:14 PM Flag

    You are really clueless. Whoever got the warrants , (even assuming they got them for free, which is not true as they got them as part of capital raise), to exercise a warrant they need to pay $1.5 for each share bought. And then what do they do? They sell the share they have just spent $1.5 on and they sell it below $1.5 , at loss (w/o even considering the price they have paid to purchase the warrant) ?

  • staccani staccani Feb 21, 2015 4:02 PM Flag

    Well, from somebody who writes the below nonsense about the expiring $1.5 warrants, it sounds as complimet to me. Evidently you have no ideas what you write about , and I do not even need to comment, as anybody who has some basic finance knowledge will understand.
    And since you would not understand it I will not give you the link to the SunTrust report and their revenue and earning projections for Marine indication only, which are the same as I have
    QUOTE
    They got their free shares and dumped
    by invest83838 • Feb 20, 2015 3:18 PM Flag
    just had to get to $1.50 for their free shares and they did that.
    UNQUOTE

  • staccani staccani Feb 21, 2015 2:27 PM Flag

    Akanz, have a look at SunTrust projections based on Marine indication only. AMRN is projected to be break even and be cash flow positive in 2016. No need of further dilution to complete REDUCE IT, even if it is not stopped earlier. Basically the same model I put together almost one year ago and that both you and HDGabor commented as not realistic . I still remember your words: 'Sorry, staccani, HDGabor rules' :-)

    Sentiment: Strong Buy

  • Reply to

    They got their free shares and dumped

    by invest83838 Feb 20, 2015 3:18 PM
    staccani staccani Feb 20, 2015 4:03 PM Flag

    LOL, I agree. That must be the most clueless post I have read in 2015.

  • staccani staccani Feb 20, 2015 3:44 PM Flag

    I think some analysts and some investors are starting to realize that this company could be worth Billions USD, without even considering the High Trigs segment.

    Sentiment: Strong Buy

  • Reply to

    By the end of 2016, this company will:

    by staccani Feb 20, 2015 2:13 PM
    staccani staccani Feb 20, 2015 2:29 PM Flag

    you are right. I think you just need to short more and more as scripts keep growing week over week. You will make a fortune eventually

  • 1) have $70-$80M revenue per quarter
    2) be profitable
    3) be able to finish REDUCE IT w/o capital infusion, unless the trial is stopped earlier for efficacy

    With $100M + projected revenue in 2015 , and 100% yoy growth, I think AMRN should be already $1B market cap now or $6 PPS (P/S of 10)

    Sentiment: Strong Buy

  • Unfortunately all trials expansions, enlargments, government recognition, endorsement, single case studies, private investors capital infusions, high insider's ownerships, vaccine safety, shorts bashing, company responses, smooth Ph 1 /2 transition, DCVax L trial built in safety nets, pre.clinical results, information arm results etc etc DO NOT MATTER. All it counts is EFFICACY. Is DCVAX efficacy high enough to compete with or improve CI ? Until we know that price will not move.... unless, as usually happens, somebody gets to know that before the others

    Sentiment: Hold

  • staccani staccani Feb 20, 2015 1:51 AM Flag

    Akanz, I think we see it differently... I remember discussing this over one year ago. My take is the same as one year ago:
    1) that AMRN will not need further dilution to complete REDUCE IT, as sales and margins will continue to grow, reaching break even point before the end of 2016
    2) that AMRN could be a profitable company selling around $1B even w/o being approved for high trigs (remember only US market for this segment is ca $4B annually)
    3) that AMRN will be selling in the billions/tens of billions USD (multiply by 5-10 to get market cap) if it gets approved also for High Trigs worldwide. Only 10% penetration in a 150M peple / $200B potential global market could warrant that

    Sentiment: Strong Buy

  • Lovaza will disappear , $1B annual sale market just in US will be just Vascepa.
    If we then consider non US countries just for Hyper trigs then $5B annual sales is achievable.
    If we then add High Trigs segment then we need to multiply $5B annual sales by ca 10 times.
    So depending on which scenario we look at we may have annual revenue between $1B and $50B annual revenue, market cap between $5B and $250B, PPS between $30-$1,500

    Sentiment: Strong Buy

  • staccani by staccani Feb 19, 2015 2:52 PM Flag

    Can anybody give us an update on weekly scripts 02/13?

    Sentiment: Strong Buy

  • Fibrotic diseases occur in a variety of organs that lead to continuous organ injury, function decline, even failure. Nevertheless, there are currently limited effective treatment options. Galectin-3 (Gal-3) is a pleiotropic lectin which plays an important role in cell proliferation, adhesion, differentiation, angiogenesis and apoptosis. Accumulating evidence indicates that Gal-3 activates a variety of pro-fibrotic factors, promotes fibroblasts proliferation and transformation, and mediates collagens production. Recent studies have defined key roles for Gal-3 in fibrogenesis in diverse organ systems including liver, kidney, lung, and myocardial. To help set the stage for future research, we review recent advances about the role played by Gal-3 in fibrotic diseases. Herein we discuss the potential pro-fibrotic role of Gal-3 and inhibition of which may represent a promising therapeutic strategy against tissue fibrosis.

    Sentiment: Strong Buy

  • © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
    Human Galectin-3 (Gal-3), a β-galactoside-binding protein expressed by tumor cells, has been reported to act as an immune regulator in antitumor T cells. However, its effect on natural killer (NK) cells is elusive.
    Using a recombinant human NK cell-activating receptor, NKp30 fusion protein (NKp30-Fc), we found that soluble NKp30-Fc could immunoprecipitate Galectin-3. The direct interaction between NKp30 and Galectin-3 was further confirmed using surface plasmon resonance experiments. Because Galectin-3 was mainly released from tumor cells in a soluble form in our study, the binding assay was performed to show that soluble Galectin-3 specifically bound to NK cells and NKp30 on the surface of the NK cells. Functionally, when soluble Galectin-3 was added to the NK-tumor cell coculture system, the NKp30-mediated, but not NKG2D-mediated, cytolysis and CD107a expression in the NK cells were inhibited, and these phenotypes could be restored by preincubation of soluble Galectin-3 with NKp30-Fc fusion protein or the addition of anti-Gal-3 antibody alone. Moreover, genetic down-regulation of Galectin-3 (shGal-3) resulted in tumor cells being more sensitive to NK cell lysis, and, reversely, Galectin-3-overexpressing HeLa cells (exGal-3) became less sensitive to NK cell killing. The results of these in vitro experiments were supported by studies in shGal-3-HeLa or exGal-3-HeLa xenograft non-obese diabetic/severe combined immunodeficiency mice after NK cell adoptive immunotherapy, indicating that Galectin-3 strongly antagonizes human NK cell attack against tumors in vivo. These findings indicate that Galectin-3 may function as an immune regulator to inhibit NK cell function against tumors, therefore providing a new therapeutic target for tumor treatment.

    Sentiment: Strong Buy

  • Published Online: February 10, 2015
    International Journal of Cardiology
    Methods and Results
    One-hundred-fifty patients were enrolled (males 73%; age 58, SD 14 years), with a NICM diagnosis according to the World Health Organization criteria. All patients underwent a comprehensive clinical assessment and biohumoral characterization, including galectin-3 assay, and cardiac MRI, with LGE assessment of fibrosis. Median galectin-3 value was 14.4 ng/mL(IQR 11.7-19.0 ng/mL), and LGE was detected in 106 (71%) patients. Patients with LGE had higher galectin-3 than those without (15.4, 11.8-21.0, vs 13.1,11.7-16.4 ng/mL, p = 0.006). Among univariate predictors of LGE presence (galectin-3, male sex, disease duration, arterial hypertension, left and right ventricular ejection fraction, left ventricular stroke volume), galectin-3 maintained its predictive value at multivariate analysis, together with sex, hypertension, disease duration and right ventricular ejection fraction. At receiver operating characteristic analysis the optimal galectin-3 cut-off for LGE prediction was 14.6 ng/mL (AUC 0.651, sensitivity 57%, specificity 73%).
    Conclusions
    Galectin-3 is associated with LGE-assessed myocardial replacement fibrosis in patients with NICM. These results support the hypothesis that galectin-3 is involved in cardiac fibrosis and remodeling in NICM, and that its assay may help to select subgroups at higher risk.

    Sentiment: Strong Buy

  • Reply to

    Short Interest Climbs by 22.7%

    by jimmyco2008 Feb 15, 2015 7:00 PM
    staccani staccani Feb 16, 2015 2:14 PM Flag

    1 year ago BGMD was off my radar and anyway the company is in much better position now with the FDA clearance of automated Gal 3 test and a lot of scientific evidence produced in the last year or so about the utililty of Gal 3 biomarker for many conditions. Shorts my succeed to keep it down for a while, but eventually fundamentals will re-align market cap to economic value

    Sentiment: Strong Buy

  • Reply to

    Short Interest Climbs by 22.7%

    by jimmyco2008 Feb 15, 2015 7:00 PM
    staccani staccani Feb 16, 2015 1:55 AM Flag

    Shorting a company that will probably have Billions USD in sales per year and has $30M market cap, is like dancing on a minefield. GL

  • staccani staccani Feb 15, 2015 2:50 PM Flag

    I agree. 45% of all deaths in developed world are linked by fibrosis (heart, lung, liver, kidney etc etc); Gal 3 is proven to cause fibrogenesis and to be all cause death predictor. I think Gal 3 test will become standard blood test for all conditions similarly to LDL/HDL. The more I look into it to more I believe BGMD is going to multiply PPS by 1,000+ times in the next few years

    Sentiment: Strong Buy

  • Do you see a link between the two? If Gal 3 cause fibrosis, fibrosis is behind 45% of all deaths in the developed world, might Gal 3 testing and downregulation the 'Holy Grail'??

    November 20, 2014
    Harvard team identifies rare stem cells that give rise to chronic tissue scarring
    Fibrosis has a number of consequences, including inflammation, and reduced blood and oxygen delivery to the organ. In the long term, the scar tissue can lead to organ failure and eventually death. It is estimated that fibrosis contributes to 45 percent of all deaths in the developed world

    Galectin-3: A Central Regulator of Chronic Inflammation and Tissue Fibrosis
    Fibrosis is a major cause of morbidity and mortality worldwide. Tissue injury, with chronic inflammation and fibrogenesis, results in disruption of tissue architecture and eventually organ failure. Currently, the therapeutic options for tissue fibrosis are severely limited and organ transplantation is often the only effective treatment for end-stage fibrotic diseases. However, demand for donor organs greatly outstrips supply, and so effective anti-fibrotic treatments are urgently required. In recent years, Galectin-3 has gained prominence as a central regulator of chronic inflammation and fibrogenesis. Tissue fibrosis models in multiple organs have demonstrated that galectin-3 has profound effects on organ fibrogenesis and scarring

    Sentiment: Strong Buy

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