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Added more shares good day for it.
I'll be happy with two places to the left followed by two more places to the left..
Can anyone imagine a market maker looking at his screen trading 2Mil shares of PPHM in a range of 1.5 cents??? what a headache!!! Hard to watch trades go off 4 places to the right of the decimal day after day................we NEED NEWS>>>>>>>>
Remove the RS specter off this stock then it would be prudent to buy a lot of cheap shares and hold as an investor because this SP will eventually move up higher. Right now it will through the eventual RS. IMHO
One solid PR would push this whole process up several months to meet compliance coupled with the continued growth of Avid. That solid PR would need to be significant however. Partnership? Of course I am stating the obvious.
Avid is a successful and growing CDMO business generating significant revenue and one of our key goals going forward is to help ensure that its value is appropriately represented in the market cap of our overall business.
Correct investors very tuned in now on PPHM.
Pump and dump is a very artful scheme wouldn't you say CP?
Yes this has been the MOA here for a long time. Hit nail on head.
Got to wise up to them.
Thoughts to ponder....
The actions of this company are not share holder friendly and are guaranteeing a RS unless they have a carrot for the Shareholders. Perhaps a Partner lined up at last. That would be a stretch but you never know.
I am surprised they used 10.3 mil in ATM last quarter. Ugh.
Hypi I Unloaded 80K for profit will reload @.29-.30 and start again. Not much reason to hold a stock like this for now. Just trade it. Perhaps around 2018 they will be more appetizing to buy and hold.
Cheap options awarded, cheap ATM sales for more dilution, RS around the corner plus much more...BOD salaries first, crumbs for shareholders why hold for that?
IMHO
-- Total costs and expenses for the second quarter of FY 2017 were $27,447,000, compared to $23,347,000 for the second quarter of FY 2016. For the second quarter of FY 2017, research and development expenses decreased 51% to $7,022,000, compared to $14,190,000 for the second quarter of FY 2016. Cost of contract manufacturing increased to $15,441,000 in the second quarter of FY 2017 compared to $4,741,000 for the second quarter of FY 2016, primarily due to an increase in the cost of contract manufacturing associated with higher reported revenue. Also contributing to this increase and impacting gross margins for the period is the higher cost of operating the new Myford facility as well as the higher cost associated with performing process validation runs during the quarter. For the second quarter of FY 2017, selling, general and administrative expenses increased to $4,984,000 compared to $4,416,000 for the second quarter of FY 2016 primarily due to the company's growing manufacturing business.
CORRECT
To be compliant for NASDAQ I would say it is inevitable.
Previously NASDAQ Granted Extension To Immune Pharmaceuticals Inc. To Regain Compliance With Requirements Under NASDAQ Listing Rule 5810(c)(3)
Barring any substantial partnerships or news expect anywhere from
1/2 to 1/25 reverse split sometime in December.
Jul 6 16
On July 6, 2016, Immune Pharmaceuticals Inc. received a notification from the Listing Qualifications Department of The NASDAQ Stock Market LLC (NASDAQ) indicating that the company had been granted an additional 180 calendar day extension, or until January 3, 2017, to regain compliance with the requirements under NASDAQ Listing Rule 5810(c)(3). The notification stated that Extension determination was based on the company meeting the continued listing requirement for market value of publicly held shares and all other applicable requirements for initial listing on the Capital Market, with the exception of the bid price requirement. The notification has no immediate effect on the NASDAQ listing or trading of the company’s common stock. As previously reported on a Current Report on Form 8-K dated January 11, 2016, the company had received a prior notification from NASDAQ, dated January 5, 2016, indicating that the company was not in compliance with the Rule because the minimum bid price of the company’s common stock on the NASDAQ Capital Market had closed below $1.00 per share for 30 consecutive business days. In the event the company does not regain compliance with the Rule by January 3, 2017, NASDAQ will notify the company that its common stock will be delisted from the NASDAQ Capital Market, unless the company requests a hearing before a NASDAQ Hearings Panel. This information is being provided solely to comply with NASDAQ Listing Rules requiring public announcement of the company’s receipt of the letter from NASDAQ.
I am a little top heavy on the shares just in case Krakatoa turns into a smolder? 25K AH was me plus another 5K up for grabs.
No more nibbling off of my 30K order in AH placed AON
Your correct-
In connection with the Company’s efforts to regain compliance with the Rule, the Company’s Board of Directors has unanimously adopted resolutions approving a proposal to amend the Company’s certificate of incorporation to effect a reverse stock split of the Company’s outstanding shares of common stock, at a ratio to be determined by the Company’s Board of Directors in its sole discretion, but in all cases within a range of 1-for-2 and 1-for-25 shares.
Note: The tortoise did beat the hare in the end though.
Activation of blood coagulation in cancer: implications for tumor progression
Several studies have suggested a role for blood coagulation proteins in tumor progression. Herein, we discuss (1) the activation of the blood clotting cascade in the tumor microenvironment and its impact on primary tumor growth; (2) the intravascular activation of blood coagulation and its impact on tumor metastasis and cancer-associated thrombosis; and (3) antitumour therapies that target blood-coagulation-associated proteins. Expression levels of the clotting initiator protein TF (tissue factor) have been correlated with tumor cell aggressiveness. Simultaneous TF expression and PS (phosphatidylserine) exposure by tumor cells promote the extravascular activation of blood coagulation. The generation of blood coagulation enzymes in the tumour microenvironment may trigger the activation of PARs (protease-activated receptors). In particular, PAR1 and PAR2 have been associated with many aspects of tumor biology. The procoagulant activity of circulating tumor cells favours metastasis, whereas the release of TF-bearing MVs (microvesicles) into the circulation has been correlated with cancer-associated thrombosis. Given the role of coagulation proteins in tumor progression, it has been proposed that they could be targets for the development of new antitumor therapies.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3763425/
GOV program politics and timing was front and center on this particular budget cut.
BIO My wife worked for the Defense Threat Reduction Agency so I got ahead of that PR. I like to think of it as privileged information.
Too much drama on this one now. Made nice gain unloading will wait and see on side line-will keep the curtains open for 12/6 PR just in case another play is in order?
Reminder
NASDAQ Granted Extension To Immune Pharmaceuticals Inc. To Regain Compliance With Requirements Under NASDAQ Listing Rule 5810(c)(3)
Barring any substantial partnerships or news expect upto 1/55 reverse split sometime in December.
Jul 6 16
On July 6, 2016, Immune Pharmaceuticals Inc. received a notification from the Listing Qualifications Department of The NASDAQ Stock Market LLC (NASDAQ) indicating that the company had been granted an additional 180 calendar day extension, or until January 3, 2017, to regain compliance with the requirements under NASDAQ Listing Rule 5810(c)(3). The notification stated that Extension determination was based on the company meeting the continued listing requirement for market value of publicly held shares and all other applicable requirements for initial listing on the Capital Market, with the exception of the bid price requirement. The notification has no immediate effect on the NASDAQ listing or trading of the company’s common stock. As previously reported on a Current Report on Form 8-K dated January 11, 2016, the company had received a prior notification from NASDAQ, dated January 5, 2016, indicating that the company was not in compliance with the Rule because the minimum bid price of the company’s common stock on the NASDAQ Capital Market had closed below $1.00 per share for 30 consecutive business days. In the event the company does not regain compliance with the Rule by January 3, 2017, NASDAQ will notify the company that its common stock will be delisted from the NASDAQ Capital Market, unless the company requests a hearing before a NASDAQ Hearings Panel. This information is being provided solely to comply with NASDAQ Listing Rules requiring public announcement of the company’s receipt of the letter from NASDAQ.
Thanks CJ EOM
Sorry DIA perhaps next week.
Perhaps BMY approved in the IO space now will reach back and offer up a big partnership deal. Nah guess not?
Your assessment is welcoming with possibilities and in my opinion Bavi is in the mix. Not sure to what extent though at this time.
The MOA of Bavi leads me to believe the combination treatments will be the norm.
Previously NASDAQ Grants Extension To Immune Pharmaceuticals Inc. To Regain Compliance With Requirements Under NASDAQ Listing Rule 5810(c)(3)
Barring any substantial partnerships or news expect upto 1/55 reverse split sometime in December.
Jul 6 16
On July 6, 2016, Immune Pharmaceuticals Inc. received a notification from the Listing Qualifications Department of The NASDAQ Stock Market LLC (NASDAQ) indicating that the company had been granted an additional 180 calendar day extension, or until January 3, 2017, to regain compliance with the requirements under NASDAQ Listing Rule 5810(c)(3). The notification stated that Extension determination was based on the company meeting the continued listing requirement for market value of publicly held shares and all other applicable requirements for initial listing on the Capital Market, with the exception of the bid price requirement. The notification has no immediate effect on the NASDAQ listing or trading of the company’s common stock. As previously reported on a Current Report on Form 8-K dated January 11, 2016, the company had received a prior notification from NASDAQ, dated January 5, 2016, indicating that the company was not in compliance with the Rule because the minimum bid price of the company’s common stock on the NASDAQ Capital Market had closed below $1.00 per share for 30 consecutive business days. In the event the company does not regain compliance with the Rule by January 3, 2017, NASDAQ will notify the company that its common stock will be delisted from the NASDAQ Capital Market, unless the company requests a hearing before a NASDAQ Hearings Panel. This information is being provided solely to comply with NASDAQ Listing Rules requiring public announcement of the company’s receipt of the letter from NASDAQ.
In light of all of the knowledge being complied surrounding PS as a central player I would think the upside should be tremendous for many treatment regimens. Certainly all the potential partnership possibilities are beginning to come in view. If it is noticed by the investors. Then?
This was my immediate conclusion back in February. Ironically this could provide more validation in the trail. In spite of control arm issue Bio markers are relevant.
..and we haven't heard boo about the number of patients in the "control group" that left for newer therapies when the data was presented. Why is that?
I find it almost impossible that the control group just happened to have an incredible outcome without such a variable added to the equation.
They have to know the statistical facts related to that the control group of the phase 3...How many left and how did it positively impact their survival?
One RS was pre SK while TCLN around 1983 I believe.
Need the Partnership to move things along.
GEO the bio marker established with the Sunrise patients along with other possible bio markers is a step in that direction. The case is building for a MOA. MSK and NCNN are part of this process with combo pre-clinical trails. It is clear there is some refining (trial design) required for maximum results on future trials. I visualize Bavi in the mix with several triple combination treatments for future trails.
Bavi will eventually be approved as a SOC in triple combination treatments in several cancers. IMO
The fight against cancer is complex to be sure.
New innovations in treatment evolve over time often with setbacks but that is the essence of any scientific endeavor and there will always be the skeptics preceding the development process until a break through is achieved then they fade away.
The Bavi story has not ended it is still relevant.
Agreed EOM
Facts without conjecture:
Apoptosis is an evolutionarily conserved and tightly regulated cell death modality. It serves important roles in physiology by sculpting complex tissues during embryogenesis and by removing effete cells that have reached advanced age or whose genomes have been irreparably damaged. Apoptosis culminates in the rapid and decisive removal of cell corpses by efferocytosis, a term used to distinguish the engulfment of apoptotic cells from other phagocytic processes. Over the past decades, the molecular and cell biological events associated with efferocytosis have been rigorously studied, and many eat-me signals and receptors have been identified. The externalization of phosphatidylserine (PS) is arguably the most emblematic eat-me signal that is in turn bound by a large number of serum proteins and opsonins that facilitate efferocytosis. Under physiological conditions, externalized PS functions as a dominant and evolutionarily conserved immunosuppressive signal that promotes tolerance and prevents local and systemic immune activation. Pathologically, the innate immunosuppressive effect of externalized PS has been hijacked by numerous viruses, microorganisms, and parasites to facilitate infection, and in many cases, establish infection latency. PS is also profoundly dysregulated in the tumor microenvironment and antagonizes the development of tumor immunity. In this review, we discuss the biology of PS with respect to its role as a global immunosuppressive signal and how PS is exploited to drive diverse pathological processes such as infection and cancer. Finally, we outline the rationale that agents targeting PS could have significant value in cancer and infectious disease therapeutics.
Facts
PS externalization during apoptosis and cell stress are mediated by scramblases Xkr8 and TMEM16, respectively.
Exposed PS is an evolutionarily conserved anti-inflammatory and immunosuppressive signal.
An astonishing number of pathogens causing major infectious diseases utilize PS and apoptotic mimicry to evade host immune responses.
PS signaling is highly dysregulated in the tumor microenvironment and autoimmune diseases.
PS-targeting therapeutics (e.g., AnxA5, bavituximab) can stimulate immune activity.
Open Questions
Is PS dysregulation a universal mechanism of immune evasion for bacteria, viruses and protists?
Should PS targeting be considered a global therapeutic option for infectious diseases?
Should PS be considered a global checkpoint inhibitor for cancer?
Are all PS signaling equally immunosuppressive?
Are cofactors involved?
Many critical biochemical pathways require the presence of specific phospholipid classes in the inner and outer leaflet of the plasma membrane. Virtually all eukaryotic cells have an asymmetric distribution of phospholipids across their bilayer membrane, where the choline-containing phospholipids, phosphatidylcholine (PC) and sphingomyelin are predominately maintained on the outer membrane leaflet, and the amino-phospholipids (phosphatidylserine (PS) and phosphatidylethanolamine (PE)) are predominately localized in the inner membrane leaflet.1 This asymmetry is actively maintained by the regulated activity of ATP-dependent lipid transporters. However, membrane asymmetry collapses under a variety of physiological and pathological conditions resulting in dramatic changes in the biochemical properties of the membrane. For example, the redistribution of PS to the external face of the plasma membrane flags cells for their recognition, phagocytosis,2 and ultimate degradation by phagocytes (efferocytosis). Moreover, the interaction between PS-expressing cells and immune cells elicits profound immunological consequences by triggering immunosuppressive pathways that prevent both local and systemic immune activation. Although these pathways are used by apoptotic cells to quell potential immune sequelae against ‘self’, these same pathways are hijacked by pathogens and tumors to promote their sinister life-threatening expansion. Taken together, these observations suggest that PS functions as an upstream immune checkpoint that suppresses the development of immunity. This raises the possibility that PS blockade by the therapeutic administration of PS-targeting agents can restore pathogen and tumor immunity.
PS Asymmetry in Biological Membranes
PS, the most abundant negatively charged glycerophospholipid in eukaryotic membranes, is comprised of a glycerol backbone esterified at the sn-1 and sn-2 carbons of the glycerol moiety with two fatty acyl chains of variable length and saturation, and a phosphate linkage at the sn-3 position (Figure 1).3 Compared with related phospholipids PC and PE, the distinguishing feature of PS is the covalent attachment of serine to the phosphate, giving PS a net negative charge on the head group. Like other glycerophospholipids, PS is synthesized at specialized intracellular structures called mitochondrial-associated membranes (MAMs), structural and functional domains located between the mitochondria and endoplasmic reticulum (ER) that contain enzymes involved in calcium and innate immune signaling, and phospholipid biosynthesis.4 In higher mammals, PS synthesis occurs by two homologous enzymes, phosphatidylserine synthase 1 (PTDSS1) and PTDSS2, both localized in MAMs that appear to have partially redundant activity. Although knockout of either enzyme in mice have unremarkable phenotypes, double PTDSS1/PTDSS2 knockout mice fail to produce PS and is embryonically lethal.5, 6 In contrast, yeast deficient in PTDSS (encoded by a single CHO1 gene) are able to survive when grown on high concentrations of ethanolamine,7 suggesting that PS is an essential membrane lipid in higher metazoans. Interestingly, genetic linkage analysis suggest that rare sporadic dominant gain-of-function mutations in PTDSS1 occur in patients with Lenz-Majewski syndrome, biochemically characterized by increased PS in their membranes, and phenotypically by multiple congenital abnormalities of generalized craniotubular hyperostosis.8
Link:http://www.nature.com/cdd/journal/v23/n6/full/cdd201611a.html
Apoptosis is an evolutionarily conserved and tightly regulated cell death modality. It serves important roles in physiology by sculpting complex tissues during embryogenesis and by removing effete cells that have reached advanced age or whose genomes have been irreparably damaged. Apoptosis culminates in the rapid and decisive removal of cell corpses by efferocytosis, a term used to distinguish the engulfment of apoptotic cells from other phagocytic processes. Over the past decades, the molecular and cell biological events associated with efferocytosis have been rigorously studied, and many eat-me signals and receptors have been identified. The externalization of phosphatidylserine (PS) is arguably the most emblematic eat-me signal that is in turn bound by a large number of serum proteins and opsonins that facilitate efferocytosis. Under physiological conditions, externalized PS functions as a dominant and evolutionarily conserved immunosuppressive signal that promotes tolerance and prevents local and systemic immune activation. Pathologically, the innate immunosuppressive effect of externalized PS has been hijacked by numerous viruses, microorganisms, and parasites to facilitate infection, and in many cases, establish infection latency. PS is also profoundly dysregulated in the tumor microenvironment and antagonizes the development of tumor immunity. In this review, we discuss the biology of PS with respect to its role as a global immunosuppressive signal and how PS is exploited to drive diverse pathological processes such as infection and cancer. Finally, we outline the rationale that agents targeting PS could have significant value in cancer and infectious disease therapeutics.
Facts
PS externalization during apoptosis and cell stress are mediated by scramblases Xkr8 and TMEM16, respectively.
Exposed PS is an evolutionarily conserved anti-inflammatory and immunosuppressive signal.
An astonishing number of pathogens causing major infectious diseases utilize PS and apoptotic mimicry to evade host immune responses.
PS signaling is highly dysregulated in the tumor microenvironment and autoimmune diseases.
PS-targeting therapeutics (e.g., AnxA5, bavituximab) can stimulate immune activity.
Top of page
Open Questions
Is PS dysregulation a universal mechanism of immune evasion for bacteria, viruses and protists?
Should PS targeting be considered a global therapeutic option for infectious diseases?
Should PS be considered a global checkpoint inhibitor for cancer?
Are all PS signaling equally immunosuppressive?
Are cofactors involved?
Many critical biochemical pathways require the presence of specific phospholipid classes in the inner and outer leaflet of the plasma membrane. Virtually all eukaryotic cells have an asymmetric distribution of phospholipids across their bilayer membrane, where the choline-containing phospholipids, phosphatidylcholine (PC) and sphingomyelin are predominately maintained on the outer membrane leaflet, and the amino-phospholipids (phosphatidylserine (PS) and phosphatidylethanolamine (PE)) are predominately localized in the inner membrane leaflet.1 This asymmetry is actively maintained by the regulated activity of ATP-dependent lipid transporters. However, membrane asymmetry collapses under a variety of physiological and pathological conditions resulting in dramatic changes in the biochemical properties of the membrane. For example, the redistribution of PS to the external face of the plasma membrane flags cells for their recognition, phagocytosis,2 and ultimate degradation by phagocytes (efferocytosis). Moreover, the interaction between PS-expressing cells and immune cells elicits profound immunological consequences by triggering immunosuppressive pathways that prevent both local and systemic immune activation. Although these pathways are used by apoptotic cells to quell potential immune sequelae against ‘self’, these same pathways are hijacked by pathogens and tumors to promote their sinister life-threatening expansion. Taken together, these observations suggest that PS functions as an upstream immune checkpoint that suppresses the development of immunity. This raises the possibility that PS blockade by the therapeutic administration of PS-targeting agents can restore pathogen and tumor immunity.
PS Asymmetry in Biological Membranes
PS, the most abundant negatively charged glycerophospholipid in eukaryotic membranes, is comprised of a glycerol backbone esterified at the sn-1 and sn-2 carbons of the glycerol moiety with two fatty acyl chains of variable length and saturation, and a phosphate linkage at the sn-3 position (Figure 1).3 Compared with related phospholipids PC and PE, the distinguishing feature of PS is the covalent attachment of serine to the phosphate, giving PS a net negative charge on the head group. Like other glycerophospholipids, PS is synthesized at specialized intracellular structures called mitochondrial-associated membranes (MAMs), structural and functional domains located between the mitochondria and endoplasmic reticulum (ER) that contain enzymes involved in calcium and innate immune signaling, and phospholipid biosynthesis.4 In higher mammals, PS synthesis occurs by two homologous enzymes, phosphatidylserine synthase 1 (PTDSS1) and PTDSS2, both localized in MAMs that appear to have partially redundant activity. Although knockout of either enzyme in mice have unremarkable phenotypes, double PTDSS1/PTDSS2 knockout mice fail to produce PS and is embryonically lethal.5, 6 In contrast, yeast deficient in PTDSS (encoded by a single CHO1 gene) are able to survive when grown on high concentrations of ethanolamine,7 suggesting that PS is an essential membrane lipid in higher metazoans. Interestingly, genetic linkage analysis suggest that rare sporadic dominant gain-of-function mutations in PTDSS1 occur in patients with Lenz-Majewski syndrome, biochemically characterized by increased PS in their membranes, and phenotypically by multiple congenital abnormalities of generalized craniotubular hyperostosis.8
Link:http://www.nature.com/cdd/journal/v23/n6/full/cdd201611a.html
HAPPY THANKSGIVING ALL!! ENJOY!
November 23, 2016 Vanessa Weakley
Shares of Peregrine Pharmaceuticals Inc. (PPHM) have recently come under renewed examination. The Relative Strength Index (RSI) is one of multiple popular technical indicators created by J. Welles Wilder. Wilder introduced RSI in his book “New Concepts in Technical Trading Systems” which was published in 1978. RSI measures the magnitude and velocity of directional price movements. The data is represented graphically by fluctuating between a value of 0 and 100. The indicator is computed by using the average losses and gains of a stock over a certain time period. RSI can be used to help spot overbought or oversold conditions. An RSI reading over 70 would be considered overbought, and a reading under 30 would indicate oversold conditions. A level of 50 would indicate neutral market momentum. Checking on the Relative Strength Index, the 14-day RSI is presently standing at 39.59, the 7-day is 38.67, and the 3-day is resting at 24.2.
In terms of Moving Averages, the 7-day is resting at 0.32. Moving averages have the ability to be used as a powerful indicator for technical stock analysis. Following multiple time frames using moving averages can help investors figure out where the stock has been and help determine where it may be possibly going. The simple moving average is a mathematical calculation that takes the average price (mean) for a given amount of time.
Currently, the 14-day ADX for Peregrine Pharmaceuticals Inc. (PPHM) is sitting at 12.07. Generally speaking, an ADX value from 0-25 would indicate an absent or weak trend. A value of 25-50 would support a strong trend. A value of 50-75 would identify a very strong trend, and a value of 75-100 would lead to an extremely strong trend. ADX is used to gauge trend strength but not trend direction. Traders often add the Plus Directional Indicator (+DI) and Minus Directional Indicator (-DI) to identify the direction of a trend.
Investors have the ability to use technical indicators when completing stock research. At the time of writing, Peregrine Pharmaceuticals Inc. (PPHM) has a 14-day Commodity Channel Index (CCI) of -26.66. Developed by Donald Lambert, the CCI is a versatile tool that may be used to help spot an emerging trend or provide warning of extreme conditions. CCI generally measures the current price relative to the average price level over a specific time period. CCI is relatively high when prices are much higher than average, and relatively low when prices are much lower than the average.
During the most recent trading period, the stock has moved $-0.01 from the opening price of $0.32. At the time of writing, shares had topped out with a high of $0.32 and hit a bottom of $0.3. The investing community will most likely continue to follow company share action closely into the close of the calendar year.
Interested traders may be keeping an eye on the Williams Percent Range or Williams %R. Williams %R is a popular technical indicator created by Larry Williams to help identify overbought and oversold situations. Investors will commonly use Williams %R in conjunction with other trend indicators to help spot possible stock turning points. Peregrine Pharmaceuticals Inc. (PPHM)’s Williams Percent Range or 14 day Williams %R currently sits at -75. In general, if the indicator goes above -20, the stock may be considered overbought. Alternately, if the indicator goes below -80, this may point to the stock being oversold.
Stone never say never on PPHM. Owned many a BIO through the years that fit this scenario some break through and when they do it's smiles all around. The key is to cast a wide net on the spec stocks.
Based on my experience this one is moving forward and will eventually break ground. May be some more pain before we get there though.
Cheers when it does.
May be good point to invest as you stated. No POS right now personally traded out earlier. GLTA
But 2017 (& especially 2nd half 2017)? These guys have one heck of a pipeline(bert., cep., etc.), that this could go to 7 or 8 dollars a share on a Run. There's So Much hope, here. So much possibility & potential.