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Inovio Pharmaceuticals, Inc. Message Board

alwayslong337 43 posts  |  Last Activity: Apr 29, 2016 2:55 PM Member since: Sep 28, 2011
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  • alwayslong337 alwayslong337 Apr 29, 2016 2:55 PM Flag

    "Perhaps Inovio loaned him the money". If you had a clue or did any DD you would know that MC was their money connection in the beginning. Not the other way around.

  • alwayslong337 alwayslong337 Apr 29, 2016 2:50 PM Flag

    Close. Morton Collins has been with them from the beginning. It's not that he thinks there is fabulous news coming. It's that he thinks there is a fabulous future ahead. That's why the majority of those shares went into his children and grandchildren's trust accounts.

  • Reply to

    lolololololololl is a paid pumper!

    by alwayslong337 Apr 29, 2016 2:32 PM
    alwayslong337 alwayslong337 Apr 29, 2016 2:45 PM Flag

    His kind is worse than the basher guy wisker. He just wants to flip for a few bucks and is detrimental to the long time holders

  • You are his herd. there is only one thought process here and that is his. Now shut up and do as he says

  • Paid pumper

  • Can not bump his own posts because he is too stupid to make a legitimate post

  • Reply to

    Somebody loves us

    by catchinem Apr 28, 2016 10:05 AM
    alwayslong337 alwayslong337 Apr 28, 2016 1:28 PM Flag

    catch, thanks for the reminder. Could be some new names starting to see the path Inovio is on.

    I was hoping to cross paths with you tomorrow in Mobile but I'm stuck in P'cola thru Saturday. Enjoy the Music Fest. Things are looking good at the moment. GL

  • Reply to

    legit question...

    by rotorsurfer Apr 27, 2016 1:00 PM
    alwayslong337 alwayslong337 Apr 27, 2016 1:32 PM Flag

    Look up this abtsract from Journal of Global Infectious Disease

    "Association Between Hepatitis C and Hepatocellular Carcinoma"

    Hepatocellular carcinoma (HCC) is the fifth most common cancer, the third most common cause for cancer death in the world, the major cause of death in patients with chronic hepatitis C virus infection,

  • Reply to

    legit question...

    by rotorsurfer Apr 27, 2016 1:00 PM
    alwayslong337 alwayslong337 Apr 27, 2016 1:26 PM Flag

    From the CDC;

    To lower your risk for liver cancer, get vaccinated against Hepatitis B, get tested for Hepatitis C, and don’t drink too much alcohol.

  • Reply to

    legit question...

    by rotorsurfer Apr 27, 2016 1:00 PM
    alwayslong337 alwayslong337 Apr 27, 2016 1:06 PM Flag

    NCI is trying to get one step ahead of Cancer. Treat it before it turns to Cancer. Explore their website. It's a very interesting approach and, imo, well conceived.

    The Division of Cancer Prevention (DCP) is the primary unit of the National Cancer Institute devoted to cancer prevention research. DCP provides funding and administrative support to clinical and laboratory researchers, community and multidisciplinary teams, and collaborative scientific networks.

  • alwayslong337 alwayslong337 Apr 27, 2016 12:58 PM Flag

    I would suggest google search ; VGX-3100 "intent to treat" data

    I tried to post some but YH deletes it

  • alwayslong337 alwayslong337 Apr 27, 2016 12:37 PM Flag

    VGX-3100 is a vaccine designed to treat cancer and pre-cancers of the cervix (known as cervical dysplasia) caused by human papillomavirus, or HPV, types 16 and 18. In a phase 2 study, VGX-3100 met its primary and secondary endpoints. The vaccine led to a regression in higher-grade cervical dysplasia (CIN grade 2 or 3) to CIN 1 or no disease in 49.5% of all trial patients compared to just 30.6% of the placebo group. Secondarily, 40.2% of the 107 patients in the intent-to-treat group experienced HPV clearance and CIN 2/3 regression to CIN 1 or no disease compared to only 14.3% of the placebo group.

  • alwayslong337 alwayslong337 Apr 27, 2016 12:26 PM Flag

    This has been out since the results in 2014. It has been explained by J. Kim multiple times

    Intent to treat results were also statistically significant.

    "In the per protocol analysis of this three-immunization regimen, CIN2/3 resolved to CIN1 or no disease in 53 of 107 (49.5%) women treated with VGX-3100 compared to 11 of 36 (30.6%) who received placebo. This difference was statistically significant (p

  • alwayslong337 alwayslong337 Apr 22, 2016 11:24 AM Flag

    A blackout period is a duration of time when access to something usually available is prohibited.

    In a financial context, a blackout period is a duration of time when a company's executives and/or employees who are privy to inside information are restricted from buying or selling any corporate securities. The purpose of blackout periods is to prevent insider trading based on information that is not available to the general public.

    Many companies have regular blackout periods in conjunction with fiscal quarter and fiscal year earnings reporting because corporate insiders are in possession of information prior to its public disclosure. A company may also enforce a blackout period when news of some event or potential event will not immediately be made public. Examples of such events are mergers and acquisitions (M&A), technological advances and corporate reorganization, among a great number of other possibilities.

    Trading blackout periods are mandated by the company in question, rather than the Securities and Exchange Commission (SEC) or some other organization that regulates trading-related activities. However, the SEC does prohibit insider trading during blackout periods.

    A related term, quiet period, refers to similar periods of time, related to similar events, that prohibit corporate insiders from selectively divulging information to some investors before that information has been made public.

  • Reply to

    Presentation Abstract

    by alwayslong337 Apr 16, 2016 3:04 PM
    alwayslong337 alwayslong337 Apr 18, 2016 8:45 AM Flag

    Title;
    Trial of pIL-12/MK-3475 in Metastatic Melanoma

    Clinical Trials identifier NCT02493361

    This is a multi-center, Phase II, open label, single-arm trial of intratumoral pIL-12 EP in combination with pembrolizumab in patients with low TIL melanoma. Patients will initiate treatment of pembrolizumab concurrently with the first cycle of intratumoral pIL-12 EP. Pembrolizumab will be administered at 200 mg flat dose every 3 weeks. Cycles of intratumoral pIL-12 EP (each cycle consisting of treatment on days 1, 5 and 8) will occur every 6 weeks as long as patients have accessible lesions for EP. Patients will be evaluated for response every 12 weeks by RECIST v1.1. Patients will continue on therapy if they have stable disease or better, defined under investigator evaluation at the time of disease evaluations. Therapy will be given until disease progression or unacceptable toxicity. The only exception will be those patients who experience a confirmed CR and who have been on treatment for at least 6 months; these patients may discontinue treatment at the investigator's discretion. Patients may reinitiate either therapy post-complete remission relapse if the study remains open and the patient meets the conditions outlined in the protocol. Patients will be followed continually for safety and tolerability by assessment of adverse events.

  • Reply to

    Oncosec Presentation at AACR tomorrow

    by alwayslong337 Apr 17, 2016 12:01 AM
    alwayslong337 alwayslong337 Apr 17, 2016 12:05 AM Flag

    Author Block;
    Suresh de Silva1, George Fromm1, Jamil Haque2, Jean S. Campbell2, Robert H. Pierce2, Taylor H. Schreiber1. 1Heat Biologics, Durham, NC; 2Oncosec Medical Inc., San Diego, CA

  • Reply to

    Oncosec Presentation at AACR tomorrow

    by alwayslong337 Apr 17, 2016 12:01 AM
    alwayslong337 alwayslong337 Apr 17, 2016 12:03 AM Flag

    The last two sentences are interesting;

    "Our findings demonstrate that in situ manipulation of intratumoral cells to express Gp96-Ig/Fc-OX40L stimulates potent antigen-specific cross priming to tumor specific neoantigens that culminates in robust systemic anti-tumor response. These findings provide exciting proof-of-principal and warrant further investigation into the direct delivery of molecular chaperones such as Gp96-Ig/Fc-OX40L and/or pro-inflammatory molecules for elevating the immunogenicity of tumors for a potent anti-tumor CD8+ T cell response."

  • Presentation Title;
    In vivo intra-tumoral electroporation of Gp96-Ig/Fc-OX40L stimulates CD8+ T cell cross-priming to tumor specific neoantigens
    Time; Sunday, Apr 17, 2016, 1:00 PM - 5:00 PM
    Abstract;
    Cancer immunotherapy relies on presentation of shared- and neo- antigens from a patient’s tumor cells for recognition and clearance by the immune system. However, the tumor microenvironment deploys multiple strategies to evade immune recognition and often remains non-immunogenic, which is one of the challenges that need to be addressed when designing new therapies. Among the strategies to increase a tumor’s immunogenicity is their genetic manipulation in situ via expression of molecular chaperones, T cell costimulators and/or pro-inflammatory genes using DNA/RNA vectors packaged in oncolytic viruses, lipid based components or through electroporation. In vivo electroporation-mediated gene transfer of IL-12 triggers tumor regression and systemic anti-tumor immune responses in experimental mouse models and in patients, demonstrating the feasibility of this intratumoral (IT) gene-transfer technology. We set out to test whether intratumoral electroporation of Gp96-Ig/Fc-OX40L, a re-engineered molecular chaperone, designed to export and deliver MHC I-associated antigens to APCs in context of OX40L expression, would generate a robust anti-neoantigen CD8+ T cell response. Gp96-Ig/Fc-OX40L is a re-engineered molecular chaperone, designed to export and deliver MHC I-associated antigens to APCs in context of OX40L expression. To assess antigen-specific CD8+ expansion, mice were adoptively transferred with OT-I cells after B16.F10-ovalbumin cells were injected to generate primary and contralateral melanotic tumors. Contralateral tumors were monitored to assess whether a systemic CD8+ T cell response could be elicited following primary tumor electroporation. IT electroporation of DNA expressing Gp96-Ig/Fc-OX40L in the primary tumor triggered a significant expansion of antigen-specific OT-I cells, which was absent in control mice. Remarkably, increases in antigen-specific OT-I cells correlated with regression of both the treated primary and untreated contralateral tumors. We further validated our findings in a CT26 mouse colorectal cancer tumor model, in which the expression of Gp96-Ig/Fc-OX40L from electroporated DNA stimulated an expansion of antigen-specific CD8+ T cells and again led to regression of both the treated primary and untreated contralateral tumor. Our findings demonstrate that in situ manipulation of intratumoral cells to express Gp96-Ig/Fc-OX40L stimulates potent antigen-specific cross priming to tumor specific neoantigens that culminates in robust systemic anti-tumor response. These findings provide exciting proof-of-principal and warrant further investigation into the direct delivery of molecular chaperones such as Gp96-Ig/Fc-OX40L and/or pro-inflammatory molecules for elevating the immunogenicity of tumors for a potent anti-tumor CD8+ T cell response

  • Reply to

    Presentation Abstract

    by alwayslong337 Apr 16, 2016 3:04 PM
    alwayslong337 alwayslong337 Apr 16, 2016 11:44 PM Flag

    Not sure if you are talking about Heat Biologics HTBX. If you are here is some info on that;
    Presentation Time;
    Monday, Apr 18, 2016, 1:00 PM - 5:00 PM
    Abstract;
    Combination cancer immunotherapy incorporating T cell costimulation, vaccination, and checkpoint inhibition is anticipated to broaden clinical response compared to any single agent. Because T cell costimulation occurs at the site of immunization, we asked whether the delivery of a costimulator by a gp96-Ig secreting allogeneic vaccine would provide comparable costimulation to systemically administered agonist antibodies. As proof of concept, we engineered gp96-Ig vaccines that locally secrete Fc-OX40L and demonstrate that the priming of antigen-specific CD8+ T cells (peak of 13.3% of total CD8+) is significantly higher when compared to combinations with OX40 antibodies (8.4%) or vaccine alone (5.6%). Vaccine-expressed Fc-OX40L was associated with increased CD127+KLRG-1- memory precursor cells and antigen-specific CD4+ proliferation, with reduced off-target inflammation. Importantly, vaccine-expressed Fc-OX40L stimulated IFNγ+, TNFα+, granzyme-b+ and IL-2+ by antigen-specific CD8+ T cells, which enhanced rejection of established CT26 and B16.F10 tumors. We have subsequently expanded our repertoire of combination vaccines to secrete gp96-Ig along with either Fc-tagged TL1A, 4-1BBL or ICOSL.Each costimulator secreting vaccine cell line has a unique functionality, without the negative consequences of off-target inflammation associated with systemic administration of its agonist antibody counterpart. For example, costimulation with a TNFRSF25 (receptor for TL1A) agonist antibody synergized with gp96-Ig vaccination and generated a robust antigen-specific CD8+ T cell response. However, TNFRSF25 treatment also lead to a significant accumulation of FOXP3+ regulatory T cells (Treg). A gp96-Ig vaccine co-secreting Fc-TL1A resulted in similar antigen-specific CD8+ T cell production with no activation of the Treg compartment. Additionally, combining two separate gp96-Ig vaccines (one secreting Fc-OX40L and the other Fc-TL1A) leads to an additive increase in memory precursor production (CD127+KLRG1-), which may play a vital role in maintaining effective anti-tumor immunity. Together, we demonstrate that the magnitude and specificity of vaccination can be enhanced by locally secreted costimulatory molecules when delivered within a single product. This may simplify clinical translation and importantly, provide significant patient benefit by improving safety and lowering costs.

  • Reply to

    Presentation Abstract

    by alwayslong337 Apr 16, 2016 3:04 PM
    alwayslong337 alwayslong337 Apr 16, 2016 4:46 PM Flag

    Background: Intratumoral electroporation of plasmid IL-12 (IT-pIL12-EP) induces tumor infiltrating lymphocytes (TILs) and anti-tumor immunity in melanoma as described in previous Phase 1 and 2 clinical trials. PD-1 and PD-L1 antibodies induce durable tumor responses in advanced melanoma, however responses to these agents are far less common in tumors lacking significant numbers of TILs. Therefore, in this retrospective study, patients were evaluated for response to anti-PD-1/PD-L1 therapies post IT-pIL12-EP.
    Methods: A multi-center, Phase 2 trial of IT-pIL12-EP was conducted in patients with stage III/IV melanoma. Upon disease progression or treatment discontinuation with IT-pIL12-EP, many patients received subsequent PD-1/PD-L1 inhibitors. Patients with documented follow up history and evaluable for anti-PD-1/PD-L1 response were included in this analysis.

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