Wed, Jul 30, 2014, 12:33 AM EDT - U.S. Markets open in 8 hrs 57 mins

Recent

% | $
Click the to save as a favorite.

Oramed Pharmaceuticals Inc. Message Board

biotech_invest 145 posts  |  Last Activity: 13 hours ago Member since: Mar 5, 1998
SortNewest  |  Oldest  |  Highest Rated Expand all messages
  • Looks like last battle for Dr. Mann and he wants to be a winner. When he was talking about partnership he never lied to investors. Question why he never supported an idea about selling MNKD? May be it was a strategic move i.e. "red herring". And now when everybody are talking about partner(s) Mann is negotiating another deal: selling MNKD. He can do it easy with 40% of company ownership.
    BP partnered REGN 5 years ago at cap $1.5B and now REGN cap $30B. So now they can't buy REGN so easy. 5 years ago 100% premium ($3B) was = REGN acquisition.
    So, 100% premium for MNKD now is $7B
    After 5 years MNKD cap might be too high for acquisition.

    Sentiment: Strong Buy

  • biotech_invest biotech_invest Jul 28, 2014 2:52 PM Flag

    Mann can sell company practically without board voting (hold 40% of stock now). He invested $1B in MNKD and need at least 300% gain for a satisfaction. With current pps he will get only $1.1B and for 300% gain MNKD cap should be $7B (pps $18).
    $7B is a reasonable price for first FDA approved rapid-acting insulin (really rapid with Tmax = 15 min) and very valuable technology that allow dose practically everything without syringe: basal insulin, GLP-1, anti-migraine drugs and etc.
    BTW, AFREZZA will easy get an approval in Europe, Japan, China and India. Repay for MNKD buyer that spend $7B will be huge.

    Sentiment: Strong Buy

  • AF form TheStreet said that "MannKind must report second-quarter financials before the end of the second week in August." If it's strong rule MNKD management has just a couple weeks and August 15 is within 6-8 weeks estimated for partnership negotiation.
    If they are in process now there is should be only one final partner (just not enough time for several). Mann can't go to Q2 earning without partner - to big shame for him. So, first week of August (4-8) is a key.
    GL

    Sentiment: Strong Buy

  • But RP is very expensive and complicate surgery procedure (even minimal invasive da Vinci prostatectomy).
    Da Vinci surgery, 4 days in the hospital, followups.
    $50,000-60,000 USD per patient

    HIFU treatment costs about US $10,000-$25,000 (depend on country).

    "Although no formal statistical analysis was planned or performed, the comparison is essentially a non-inferiority comparison to RP"

    Sentiment: Strong Buy

  • Reply to

    Why did

    by esoteric687 Jul 28, 2014 11:43 AM
    biotech_invest biotech_invest Jul 28, 2014 12:15 PM Flag

    still don't understand it? PRAN management did one wrong thing: updated Alzheimer disease development program. AD trial is failed and they must switch to HD. If they start phase IIa for AD retail investors and funds will sell PRAN and pps will go below $1. They already killed recent run up with this stupid AD updates.
    So you can persuade investors to "accumulate PRAN at low" and use arguments about $41M cash but everybody sees now that PRAN executives go to wrong direction. They want spent again very big money on AD trial (phase IIa or even phase III).

    Sentiment: Strong Sell

  • The Ablatherm HIFU dataset, referred to as the
    HIFU Long Term Refined Cohort, was obtained from European registries. Although no formal
    statistical analysis was planned or performed, the comparison is essentially a non-inferiority
    comparison to RP. The results show similar cumulative metastasis rates at 8 years of 1.1% and
    1.4% for Ablatherm HIFU and PIVOT RP (low risk subset), respectively.

    The following questions relate to the approvability of the Ablatherm® Integrated Imaging High
    Intensity Focused Ultrasound (HIFU) system. Please answer them based on your expertise, the
    information you reviewed in preparation for this meeting, and the information presented today:
    • Voting Question 1: Is there reasonable assurance that the Ablatherm® Integrated
    Imaging High Intensity Focused Ultrasound (HIFU) system is safe for the proposed
    indications for use (e.g., the device will not expose patients to an unreasonable or
    significant risk of illness or injury)?
    • Voting Question 2: Is there reasonable assurance that the Ablatherm® Integrated
    Imaging High Intensity Focused Ultrasound (HIFU) system is effective for the proposed
    indications for use?
    • Voting Question 3: Do the benefits of the Ablatherm® Integrated Imaging High
    Intensity Focused Ultrasound (HIFU) system for the proposed indications for use
    outweigh the risks of the Ablatherm® Integrated Imaging High Intensity Focused
    Ultrasound (HIFU) system in patients who meet the criteria specified in the proposed
    indication?

    Sentiment: Strong Buy

  • MNKD can easy do such combination: long-acting basal insulin + GLP-1 co-dried with carrier. It will be more convenient than Novo injection pen: heat-resistant, one puff per day.

    LONDON (Reuters) - A Novo Nordisk drug combining its long-acting insulin degludec with its type 2 diabetes treatment Victoza has been recommended for approval in Europe, in an important boost for the Danish company.

    The European Medicines Agency said on Friday it had issued a positive opinion for Xultophy, previously known as IDegLira, implying the medicine is likely to be formally approved by the European Commission within three months.

    Novo said it planned to launch Xultophy in the first European markets in the first half of 2015.

    Jakob Riis, executive vice president of marketing and medical affairs at Novo Nordisk, said Britain, Germany and Denmark were likely to be among the first launch markets for the product.

    Clinical trial results have shown that the once-daily injection lowers blood sugar more than each medicine taken on its own, setting a new standard for sugar control in diabetic patients.

    Sentiment: Strong Buy

  • Reply to

    Options expire tomorrow

    by plm45889092 Jul 24, 2014 3:51 PM
    biotech_invest biotech_invest Jul 24, 2014 4:03 PM Flag

    and next week Monday we will see again MNKD short interest (for 7/15)
    Did covering start or not?

    Sentiment: Strong Buy

  • biotech_invest biotech_invest Jul 24, 2014 3:58 PM Flag

    just open Figure S7 (D) in Supplementary and see what PBT2 treatment did with phospho-tau in Tg2576 mice. Answer: PBT2 increased insoluble p-tau that is most dangerous one (component of tau tangles).

  • biotech_invest biotech_invest Jul 24, 2014 3:46 PM Flag

    don't worry, it's enough high to compete with best world minds and win :-) And you know that it's true.
    Any arguments beside grammar?
    say thanks pivalde for very good reference about PBT2 - I'll include the results in my comments about PRAN-scam. Especially Figure S7 D where PBT2 treatment increases level of insoluble p-tau (component of tau tangles).

  • biotech_invest biotech_invest Jul 24, 2014 3:18 PM Flag

    sure, buy more PRAN right now
    and where I misleaded - everything is only citation. Authors misleaded investors by showing the results that "prove" metal theory. Other results they put in Supprementary. According to Figure S7 (D) PBT2 is toxic: p-tau increased after PBT2 treatment. I.e. more tau tangles formed.
    Of course, it's mice model but nobody knows what PBT2 is doing in human brain. They should include p-tau (change from baseline) measurement in CSF in clinical trial. But PRAN measured only amyloid. Why?

  • Did you read this paper carefully?
    PBT2 decreases tau phosphorylation in one mice model (APP/PS1) and INCREASE tau phosphorylation in Tg2576 model (see Figure S7 C-D). Tanzi just hided these results in Supplemental Data and showed only beneficial ones :-)

    "We assessed both total tau and tau phosphorylated at Ser396, an epitope that is abnormally phosphorylated in AD and which promotes tau polymerization (Abraha et al., 2000), by western blot in the APP/PS1 mice treated for 11 days in this study to gauge the association of changes in these proteins with the observed improvements in cognition. Our data demonstrated a significant
    reduction in phosphorylated tau in the animals treated for 11 days with PBT2 (soluble fraction: 56%, p = 0.005; insoluble fraction: 38%, p = 0.01), which was not recapitulated in the CQ-treated animals (insoluble: 8%, p = 0.6; soluble: +81% increase, p = 0.02) (Figures 6C and 6D). Neither treatment elicited a change in total tau levels (not shown). Longer-term treatment (35 days) with a lower dose of PBT2 (10 mg/kg/d) in the APP/PS1 mice resulted in a sustained decrease in soluble phosphorylated tau ( 26%, p = 0.03), but the decrease in insoluble phosphorylated tau was not significant ( 27%, p = 0.4) (Figures 6E and 6F). There were again no significant changes in levels of total tau (not shown).
    We also examined tau levels in the Tg2576 mice that were treated with PBT2 (30 mg/kg/d) for 11 days. Unlike the effects observed in the APP/PS1 model, significant changes in total tau were observed. Total insoluble tau levels were decreased with PBT2 treatment ( 24%, p = 0.003) while soluble tau was increased (31%, p = 0.0006) (Figure S7C). In contrast, phosphorylated
    tau levels were not significantly different between treatment groups (Figure S7D). Therefore, there was no concordance between changes in tau and Ser396 phosphorylated tau levels in the two treated Tg mouse models and the observed improvements in cognition"

    Sentiment: Strong Sell

  • Biochem Pharmacol. 2014 Apr 15;88(4):529-39. doi: 10.1016/j.bcp.2013.12.008. Epub 2013 Dec 19.
    Tau-aggregation inhibitor therapy for Alzheimer's disease.
    Wischik CM, Harrington CR, Storey JM.

    Abstract

    Many trials of drugs aimed at preventing or clearing β-amyloid pathology have failed to demonstrate efficacy in recent years and further trials continue with drugs aimed at the same targets and mechanisms. The Alzheimer neurofibrillary tangle is composed of tau and the core of its constituent filaments are made of a truncated fragment from the repeat domain of tau. This truncated tau can catalyse the conversion of normal soluble tau into aggregated oligomeric and fibrillar tau which, in turn, can spread to neighbouring neurons. Tau aggregation is not a late-life process and onset of Braak stage 1 peaks in people in their late 40s or early 50s. Tau aggregation pathology at Braak stage 1 or beyond affects 50% of the population over the age of 45. The initiation of tau aggregation requires its binding to a non-specific substrate to expose a high affinity tau-tau binding domain and it is self-propagating thereafter. The initiating substrate complex is most likely formed as a consequence of a progressive loss of endosomal-lysosomal processing of neuronal proteins, particularly of membrane proteins from mitochondria. Mutations in the APP/presenilin membrane complex may simply add to the age-related endosomal-lysosomal processing failure, bringing forward, but not directly causing, the tau aggregation cascade in carriers. Methylthioninium chloride (MTC), the first identified tau aggregation inhibitor (TAI), offers an alternative to the amyloid approach. Phase 3 trials are underway with a novel stabilized reduced form of methylthioninium (LMTX) that has improved tolerability and absorption.
    Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jul 24, 2014 12:02 PM Flag

    don't have any comments for such delusional conclusion :-)
    "golden opportunity to get in and be trapped"

  • biotech_invest biotech_invest Jul 24, 2014 11:39 AM Flag

    in simple words he got a payment from PRAN for data analysis and "right" conclusions.

  • biotech_invest biotech_invest Jul 24, 2014 11:35 AM Flag

    there are no any updates for earnings announcement. Aug 7 - Aug 8, 2014 is only estimated date.
    Definitely Mann will not go to earning press conf without "piece of pie" for MNKD investors. Question is how big this "piece of pie"?
    Partnership is not a simple and short process: partner will dig all trials data, ask about all doctor's comments and etc. When they know everything they will make an offer. 1-2 months minimal time. And now partner representatives on MNKD site.
    So any day morning we can see news. Most likely at the end of August.

    Sentiment: Strong Buy

  • it's not a theory but just hypothesis. And it's very one-side and poor one. Etiology of AD is still a puzzle.
    "The “amyloid hypothesis” is a prevailing pathological model of AD, accepted by most researchers.
    According to this model, the overproduction and accumulation of amyloid-beta (Aβ) peptides in plaques
    represent an early and central event in the pathophysiology of AD leading to the formation of neuritic
    plaques, whereas the cytoskeletal changes that arise from the hyperphosphorylation and intracellular
    aggregation of microtubule-associated protein tau to form neurofibrillary tangles are regarded as
    downstream phenomena."
    But if tau is a key to AD puzzle all drugs that act against amyloid should fail clinical trials. They did failed. All of them including PBT2.
    PRAN scientists want to fool investors with false statement that PBT2 "activates intracellular signalling pathways which promote neuronal health and plasticity and suppress pathobiological processes including the abnormal phosphorylation of tau". But it's lie because they never publish experimental data showing that the application of PBT2 decreases tau phosphorylation. It's very simple model experiment. Any post-doc can do it: Primary Rat Hippocampus Neurons + PBT2 Western of tau and p-tau Controls: 1) +inhibitor of tau hyperphosphorylation; 2) + inhibitor tau kinase
    If PBT2 suppress tau phosphorylation - bingo!

    "Mechanism of action of PBT2 in AD

    PBT2 prevents formation and toxicity of pathological Aβ species (primarily soluble oligomers) and promotes their clearance. In Professor Masters' presentation he proposes the observed effect upon amyloid burden is due to increased clearance by PBT2 of pools of PIB-detectable non-fibrillar soluble and membrane bound Aβ.

    Through its metal chaperone activity, PBT2 activates intracellular signalling pathways which promote neuronal health and plasticity and suppress pathobiological processes including the abnormal phosphorylation of tau.

    Sentiment: Strong Sell

  • Reply to

    rkf302 has 3732 posts for 1 year

    by biotech_invest Jul 23, 2014 5:41 PM
    biotech_invest biotech_invest Jul 23, 2014 6:15 PM Flag

    Cave? that is all you know?
    Old rats like rkf and eso are more funny than you, naive idiot.
    Well, it's already a happy hour so I should go
    Sciencefan, you must educate yourself and produce some clever posts here. Next time post something about AD etiology and PBT2 breakthrough in AD curing.
    Have fun, sciencefan!

  • Reply to

    rkf302 has 3732 posts for 1 year

    by biotech_invest Jul 23, 2014 5:41 PM
    biotech_invest biotech_invest Jul 23, 2014 6:05 PM Flag

    new member of your team? Teach him some manners :-) Look like that he too young and naive (just 9 posts)
    What is his role in your team? An admirer of Dr Shoulson and his huge achievements in HD area?

  • Reply to

    rkf302 has 3732 posts for 1 year

    by biotech_invest Jul 23, 2014 5:41 PM
    biotech_invest biotech_invest Jul 23, 2014 5:54 PM Flag

    just for fun, sciencefan :-) BTW, do you have something to contribute besides a..ki..ng and lickspittle?
    I'm posting what I want to post

ORMP
8.66-0.02(-0.23%)Jul 29 4:00 PMEDT

Trending Tickers

i
Trending Tickers features significant U.S. stocks showing the most dramatic increase in user interest in Yahoo Finance in the previous hour over historic norms. The list is limited to those equities which trade at least 100,000 shares on an average day and have a market cap of more than $300 million.