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Check out the black buy volume bars on this 1 minute chart.
http://bigcharts.marketwatch.com/advchart/frames/frames.asp?show=&insttype=Stock&symb=ziop&time=1&startdate=1%2F4%2F1999&enddate=12%2F31%2F2015&freq=9&compidx=aaaaa%3A0&comptemptext=&comp=none&ma=4&maval=3%2C6%2C9&uf=16&lf=268435456&lf2=2&lf3=1024&type=4&style=320&size=2&x=39&y=3&timeFrameToggle=false&compareToToggle=false&indicatorsToggle=false&chartStyleToggle=false&state=11
Very patient waiting for a bottom. Then boom.
Patience while it decided the 6.90-7 area. Then buy, buy, buy.
Very nice view of the ST action lines to watch on Monday as possible support/resistance. Big buyers were in the 6.80 7.00 range. See where they are on Monday.
Have a great weekend.
Green in sixteen.
PS: Late market swoon dragging it down below 7.00.
I hope this gap closes Monday or Tuesday. I also hope if it does touch low 6 that many shorts would cover their positions.
It's been a rough few months here since hitting all time high. I believe this will all day be meaningless. I have high hopes for the company for the next 3 to 5 years.
Just hope I can continue to stomach the volitlity and have the patience to reap the potential rewards.
Thanks for your opinion C.
Best wishes!
Stay Green pal!
Tp
tp24, the fact that we are this close to the gap gives it high odds to close, though not if the story is strong enough. The gap and how it resolves is what is keeping me from jumping all over it right now. If it is going to close, in the ST, then 7.07 aug low is the likely resistance/ceiling area.
The LT weekly 200day is at 5.72 with the bottom of the gap 6.09. For the price to fall below 5.72 would require some significant bad news IMO.
Talking about 3's now is nonsense. It's possible to find gold in my back yard, as it is possible to get to the three area, but what are the odds?
Absolutely nothing to talk about until 5.72 if that occurs and I find some quartz or black sand in my yard.
That's my story and I'm sticky to the opinion. You know enough not to trade my silly opinions.
Trade Green in Sixteen
Going back to 3's.
I think the 6 gap will get filled.
Hope it doesn't go to 3.
explain what? the 6-7 gap or going back to 3's!
Yes it is heavily shorted like ZIOP. ADXS institutional holdings have gone way up over the last year, really can't be a lot of stock available to cover those shorts if and when news hits.
SRNE chart looks interesting, I'll look into them
I like AKBA alot anywhere under 10$, BLCM under 20$, ADAP is too high now anywhere under 10$
I like ADXS as well. Also heavily shorted like ZIOP. Once shorts start to cover down here 2016 should turn out pretty good for the two of them.
Not too good for large caps either.
What a terrible quarter this has been.
Let's hope not only ZIOP but the entire market turns around soon.
Yes I agree. I like SRNE and ADXS as well as ZIOP to rebound. Science speaks
The time to buy bio tech is on bad days like this, ziop was 13$ a month ago and gonna run back at some point
Yes certainly not a good day if invested in small bio techs
I guess nobody that trades NASDAQ uses message boards lol. Looking forward to a run back over 10$ after the JP Morgan Conference brings new money.
this qtr compared to this qtr last year is really bad and thus going foreward.maybe back to 3's?
gap fills when there is bad news but so far, it's doing fine. Look at BLUE, it filled the gap after the expectation of their drug is lowered. Another reason a gap can fill is when the market tanks hard which put pressure on ZIOP but so far, a lot of buyers come in when it went below $8 these last several days.
The gap was the results of partnership with Anderson last year so it gapped up with good news.
As long as they continue to post good data, I don't think the gap will fill.
The JP Morgan conference is going to bring some buying volume, added more shares today.
just go to 2 yr chart daily and you will see it 6-7 gap
may happen this week or next
Gotham City Capital tweet of ZIOP chart FYI
Gotham City Capital ?@TravisMKnight Jan 1
$ZIOP Beautiful Rounded Bottom Forming, #MACD Cross, Bullish Options Chain. In #ZIOP 1/3 POS And Likely Adding. pic.twitter.com/xoDHWeiuNJ
Been trying to find the gap but I'm having trouble can you post chart?
$ZIOP recent bottom base consolidation indicates a possible upside move of 8% from yesterday's close.
Could this be used by XON ECC Sun Pharmaceutical with their macula degeneration treatment?
Sleeping Beauty (SB100X) clinical study for Macular Degeneration
Antiangiogenic and Neurogenic Activities of Sleeping Beauty-Mediated PEDF-Transfected RPE Cells In Vitro and In Vivo
Sandra Johnen, 1 Yassin Djalali-Talab, 1 Olga Kazanskaya, 1 Theresa Möller, 1 Nina Harmening, 2 Martina Kropp, 2 Zsuzsanna Izsvák, 3 Peter Walter, 1 and Gabriele Thumann 1 , 2
Abstract
Pigment epithelium-derived factor (PEDF) is a potent multifunctional protein that inhibits angiogenesis and has neurogenic and neuroprotective properties. Since the wet form of age-related macular degeneration is characterized by choroidal neovascularization (CNV), PEDF would be an ideal candidate to inhibit CNV and support retinal pigment epithelial (RPE) cells. However, its short half-life has precluded its clinical use. To deliver PEDF to the subretinal space, we transfected RPE cells with the PEDF gene using the Sleeping Beauty transposon system. Transfected cells expressed and secreted biologically active recombinant PEDF (rPEDF). In cultures of human umbilical vein endothelial cells, rPEDF reduced VEGF-induced cumulative sprouting by ≥47%, decreased migration by 77%, and increased rate of apoptosis at least 3.4 times. rPEDF induced neurite outgrowth in neuroblastoma cells and protected ganglion and photoreceptor cells in organotypic retinal cultures. In a rat model of CNV, subretinal transplantation of PEDF-transfected cells led to a reduction of the CNV area by 48% 14 days after transplantation and decreased clinical significant lesions by 55% and 40% after 7 and 14 days, respectively. We showed that transplantation of pigment epithelial cells overexpressing PEDF can restore a permissive subretinal environment for RPE and photoreceptor maintenance, while inhibiting choroidal blood vessel growth.
To avoid the side effects associated with virally mediated gene delivery, we have used the hyperactive Sleeping Beauty (SB100X) transposon system to transfect pigment epithelial cells with the PEDF gene [41]. SB100X has a number of advantages over virally mediated gene delivery: it integrates transgenes exclusively into TA dinucleotides with specific predilection for dinucleotides that have distinct structural features, integrates transgenes with high efficiency, results in stable integration, integrates large inserts, and does not primarily integrate into transcriptional sequences [42–45].
This study was designed to investigate whether the SB100X transposon system can efficiently transfect primary pigment epithelial cells with the human PEDF gene and whether the secreted rPEDF is functional as an inhibitor of VEGF-mediated endothelial cell function and as a neuroprotective agent in vitro and whether PEDF-transfected pigment epithelial cells have the potential to inhibit neovascularization in vivo in a model of CNV.
Discussion
The retinal pigment epithelium maintains the avascularity of the retina and a healthy choroidal vasculature by expressing and maintaining a balance between angiogenic and antiangiogenic factors, in particular VEGF and PEDF. The evidence that in neovascular AMD the equilibrium is shifted in favor of the angiogenic VEGF [51, 52] led to the development of inhibitors of VEGF, for example, the humanized monoclonal antibody bevacizumab (Avastin), its Fab fragment ranibizumab (Lucentis), and aflibercept (Eylea), which engendered a new era for the treatment of neovascular AMD and other ocular neovascular diseases [53–55]. We theorized that the side effects, resulting from frequent intravitreal injections of anti-VEGF antibodies to prevent CNV, could be alleviated by subretinal transplantation of genetically modified pigment epithelial cells that continuously secrete antiangiogenic PEDF. Autologous pigment epithelial cells transplanted to the subretinal space in neovascular AMD patients [28, 29] were well tolerated over a long period of time. However, no significant beneficial effects have been shown on vision. We postulate that vision improvement requires the inhibition of neovascularization by higher levels of PEDF. To insure that the transplanted cells secrete continuously a sufficient quantity of recombinant PEDF, we have developed an efficient nonviral transfection protocol, based on the Sleeping Beauty (SB100X) transposon system, and have shown that recombinant PEDF secretion in culture by PEDF-transfected cells was stable and constant for more than 1 year [41].
PEDF is a multifunctional protein that exhibits varied cellular actions, indicating that there are distinctive receptors that elicit diverse events. In fact, the two functional epitopes identified, a 34-mer peptide (residues 24–57) and a 44-mer peptide (residues 58–101) [50], appear to bind to two different receptors: the 44-mer peptide binds to a 80?kDa protein found in retinoblastoma Y-79 cells, neuronal cells, and retinal cells [56, 57] and induces neuroblastoma cell differentiation but does not prevent vascular leakage, whereas the 34-mer peptide binds to a 60?kDa receptor on endothelial cells [58] and prevents vascular leakage, suppresses new but not established blood vessels, and has no effect on retinoblastoma cells. Since the ultimate goal of transplanting PEDF-transfected pigment epithelial cells subretinally is for the cells to secrete active PEDF to inhibit CNV, it is critical that the recombinant PEDF secreted by the transfected cells is fully functional. In this study, we analyzed the functionality of purified recombinant human PEDF secreted by ARPE-19 and rat RPE cells transfected with the PEDF gene using the SB100X transposon system. Affinity-purified recombinant PEDF showed neurotrophic activity, as evidenced by the differentiation of human neuroblastoma cells in culture and protection of photoreceptor cells from degeneration in organ cultures of neural retinas. In vitro, the antiangiogenic properties of recombinant PEDF were confirmed by the inhibition of VEGF-stimulated sprouting and chemotaxis: rPEDF, secreted by RPE cells transfected using the SB100X transposon, is a potent inhibitor of HUVEC sprouting, the inhibition is concentration dependent, and the inhibitory activity is approximately 2000 times more potent than the activity of bevacizumab.
Conclusions
The results demonstrate that SB100X-transfected pigment epithelial cells secrete constant levels of rPEDF. Homologous PEDF-transfected rat RPE cells transplanted to the subretinal space prevent development of severe CNV lesions and limit the area of neovascularization in a rat model of CNV. Since SB100X-mediated transfection integrates the transgene and since RPE cells survive in the subretinal space, autologous SB100X-mediated PEDF-transfected cells transplanted to the subretinal space of neovascular AMD patients should secrete recombinant PEDF and inhibit CNV for the life of the patients.
Nice to see green for a change
ZIOP/XON CEO's in Scientific American Jan 12016 edition What Gene Therapy Needs Now: A Good Off Switch
Scientific America Jan 1 2016 edition What Gene Therapy Needs Now: A Good Off Switch
Below is from Scientific Americian
Researchers are developing molecular switches that can inactivate transplanted genes, paving the way for safer gene therapies. First up—better treatments for cancer
• By Jim Kozubek on January 1, 2016
o Early experiments in gene therapy ran into problems, in part because researchers could not control how active newly inserted genes would become.
o Researchers are addressing the issue by developing molecular switches that can reliably adjust the function of a transplanted gene by remote control.
o Some of these gene switches are already being combined in human trials with experimental immunotherapies to treat cancer.
o Humans don't molt,” R.J. Kirk tells me. Kirk is a billionaire geek who runs his offices out of West Palm Beach, Fla., a balmy land of pelicans and tangled mangroves. He built his fortune on conventional medications that can be taken as a pill, and I had phoned to talk about his newest endeavors in biotech. I wasn't expecting to hear about bugs. But the molting process, in which a growing insect builds a new exoskeleton to replace an old one that no longer fits, turns out to have some very important properties that can be adapted to make gene therapy, still a largely experimental procedure, safer.
o Doctors would like to deliver copies of working genes to people to treat a variety of hereditary ills. Genes provide cells with the instructions for manufacturing proteins, among other things, and so inserting a functional gene into the body can, in theory, provide a lasting supply of whatever missing proteins a patient might need. But gene therapy has had a troubled history, in part because scientists cannot precisely control where a new gene inserts into a cell's DNA and how active it is once there (which determines how much protein is produced). These problems can lead to unwanted side effects—including the development of malignant tumors.
o A logical solution to the problem of having proteins made in undesirable places and amounts would be to combine a therapeutic gene with a switch that could reliably turn it on or off as needed. As it happens, says Kirk—who is chairman and chief executive officer of Intrexon, a company that is developing new genetic engineering techniques—insects routinely use just such a switch to control molting.
Here's the thing. Insects do not just sort of molt, starting and then stopping partway; they either do it, or they don't. The genetic pathway that drives the process must remain completely turned off until the time is right. The gene that interests Kirk serves as the master switch for all this activity. It codes for a hormone called ecdysone. As ecdysone surges through the insect, it turns on a raft of other genes to start building the new exoskeleton. After the new exoskeleton is ready, the insect discards the old one. Once molting is nearing completion, the levels of ecdysone fall to zero—at which point the genetic pathway turns off. More important, from Intrexon's point of view, the switch is airtight when turned off—molting does not happen in the absence of ecdysone. The switch does not allow this group of genes to act together again until molting is set to begin.
The scientists at the company decided to take advantage of this foolproof characteristic to tightly control any genes transplanted into people. Imagine equipping each replacement gene with a biological switch that turns on—and thus activates the therapeutic gene—only in the presence of ecdysone molecules that have been adapted to work with human physiology. Patients given low doses of this activating drug (technically known as a ligand) could turn on only a few copies of the new gene, thus producing low amounts of whatever compounds were encoded. Patients given high doses of this activating drug could turn on many copies of the gene and thus manufacture large quantities of the related compound. In an unexpected emergency, however, withdrawing the ligand would shut the entire process down. No ecdysone, no activity by the introduced gene. As an added bonus, the ecdysone would not interfere with any other genes, which biologists call “cross talk,” because the human body does not otherwise use, or need, the hormone to regulate genetic activity. Or, as Kirk puts it, “Humans don't molt.”
Over the past eight years Intrexon has “wired” its ecdysone switches to thousands of human genes, demonstrating in laboratory tests that virtually any gene in the body can be put under the hormone's control. In addition, Kirk's group has added a second layer of checks by stitching in so-called cell-specific promoters to their switches. Cell-specific promoters are swatches of genetic material that cause genes to turn on (be “expressed”) only in specific tissues, such as neurons or blood or liver cells, or only in certain conditions, such as the low-oxygen environment of a tumor. The addition of these molecular gatekeepers further reduces the chances of unwanted side effects occurring in parts of the body that had not been targeted for treatment.
Meanwhile other groups are borrowing from different biological processes to develop their own genetic switches and added control mechanisms. Eventually the ability to deliver several switch-controlled genes—each one able to be dialed up or down as needed—should make gene therapy safe and effective enough that it can become part of mainstream medicine. Or at least that is the idea. Preliminary tests in humans suggest that the switch approach could work as intended. So far it has been studied mostly in cancer and will likely make its biggest mark there first.
First trials
In particular, investigators are studying the switch approach as a way of making cancer immunotherapy less of a harrowing ordeal for patients. Cancer immunotherapies, which have made a lot of headlines of late, aim either to reawaken an immune response that has been lulled to sleep by chemical signals from a malignancy or to jump-start an entirely new and more powerful anticancer response than a patient's immune system can achieve on its own. Trouble is, a rebooted immune system can easily slip into overdrive, triggering life-threatening fevers and the potentially lethal buildup of fluids throughout the body.
Gene switches are now being evaluated, for example, in small trials of carefully chosen patients with recurrent melanoma (a type of skin cancer) and breast cancer. Doctors inject one or two tumors in these individuals with genes designed to boost production of cytokines—signaling molecules (such as interferon and various interleukins) that the immune system uses to monitor and adjust the fight against tumors. Investigators believe that they may not need to treat all the malignant lesions in each patient, because once the immune system is properly primed to tackle one nest of cancerous cells, it should start searching for others elsewhere in the body without the need for further prompting.
Cytokines trigger a wide range of physiological reactions—from opening up blood vessels so that immune cells can rush to the scene of an infection to activating ruthless killer T cells, which, among other things, specialize in destroying cancerous cells. But to date, doctors have not been able to treat patients successfully with one of the most powerful cytokines, known as interleukin-12, or IL-12.
This failure stems in part from IL-12's propensity for unleashing a “cytokine storm,” in which the immune system seemingly goes on a rampage against the body. In the bloodstream, IL-12 can cause a sharp drop in blood pressure, difficulties with lung function, and heart problems, which together can easily lead to organ failure and death. And yet, says Laurence Cooper, a physician-scientist at the University of Texas M.D. Anderson Cancer Center and CEO of biotech company Ziopharm Oncology, “there is a ton of literature on its effectiveness in the tumor microenvironment. IL-12 is the holy grail of immunotherapy.” The idea, then, is to deliver as much IL-12 as possible to a single tumor but not so much that a cytokine storm occurs. Here is where the switch technology could prove revolutionary.
Researchers insert the switch-enabled IL-12 genes into an individual's tumor, where they take up residence in many cells, including the immune cells that are already there, giving the latter a boost. Because the switch can be activated only by the presence of the ligand, physicians can increase the levels of cytokine in the tumor very deliberately by slowly increasing the amount of drug they give their patient. If a cytokine storm starts to develop, they can skip the next scheduled dose, thereby averting the worst of the damage.
Ziopharm, which is working with Intrexon to develop switch-enabled cytokine treatment in people, reports encouraging results so far. Kirk acknowledges that they might have chosen to test their approach on something less potent than the IL-12 gene—where the slightest misstep could prove fatal. But he says, “We chose one of the hardest genes because we wanted to pressure-test the switch.” In other words, when it counts most, does a switch that has been turned off remain completely off?
Results from two safety studies conducted at several medical centers (and totaling fewer than 40 patients) suggest that the answer is yes. Although no one was cured, the switch-controlled regimen appeared to be reasonably safe. As anticipated, a few patients did begin showing signs of a dangerous overreaction, but it dissipated soon after they stopped taking the ecdysone pills.
The researchers also found hints that the therapy could be helpful. In one of the studies, they injected the gene-plus-switch combination into 12 people with metastatic breast cancer. Each of them had already endured an average of eight previous cancer treatments, with diminishing hopes of survival. For various reasons, investigators were able to evaluate the new therapy's effect in only seven patients, however. The IL-12 treatment shrank some of their tumors, and in three people, the disease appeared to remain stable, at least for the short duration of the trial. The second safety study, in 26 patients who had been treated an average of six different times for metastatic melanoma, showed an uptick in cytokine levels and other cancer-fighting activity. In May 2015 Ziopharm initiated another study using switch-enabled IL-12 as an experimental treatment for glioblastoma multiforme, a particularly aggressive type of brain cancer.
Riboswitches
Richard Mulligan of Harvard Medical School has been working on a different kind of switch. His approach features small naturally occurring RNA molecules called ribozymes. First described in the 1980s, ribozymes are like enzymes in that they catalyze chemical reactions in the body, but most enzymes are proteins, and ribozymes consist of RNA. In a feature useful for switches, some ribozymes also have the ability to cut themselves up and induce genetic molecules to which they have been attached to self-destruct.
Mulligan's constructs give rise to a ribozyme linked not to a classic gene but to a messenger RNA (mRNA) molecule. When cells make proteins, they first copy the DNA in a gene into messenger RNA (a mobile, single-stranded transcript), after which the mRNA gets translated into the protein. From the cell's point of view, the addition of a stretch of DNA or its corresponding mRNA should result in the same outcome—production of a specific protein.
As a first step, researchers assemble and inject a strand of DNA that codes for a “self-cleaving” ribozyme plus the selected therapeutic protein. If a human cell transcribed this synthetic DNA into mRNA, the ribozyme portion would cut itself, causing the rest of the mRNA molecule to appear defective; the surrounding cellular machinery would then break the mRNA apart and cause the entire process of building a protein to grind to a halt. It would be as if the gene had been turned off.
Starting in 2000, Ronald R. Breaker and his colleagues at Yale University showed how to protect the mRNA but also to turn off protein synthesis when desired. The trick was to link the ribozyme to an additional molecule called an aptamer, which is a kind of sensor that is designed to be activated by a drug. In the presence of the drug (and only in the presence of the drug), the sensor changes shape in a way that prevents the ribozyme from destroying the mRNA. With the full length of mRNA intact, the cell makes the protein. When the drug that acts on the sensor is withdrawn, the ribozyme and the mRNA self-destruct.
By 2004 Mulligan and his colleagues were regularly equipping his ribozyme switches with carefully customized drug-sensitive sensors, and he continues to hone the technology today. The sensors can be designed with great specificity, Mulligan says, further reducing the chances of unwanted side effects. As with ecdysone, the mRNA that is connected to the riboswitch would allow production of the protein only if the patient swallowed the appropriate pill. Take the pill, and you have, in effect, turned on a gene. Stop the pill, and the gene stays off.
Multiple switches
Although single gene switches are not yet perfected, investigators can envision a not too distant future in which multiple switches become the norm, allowing increasingly precise control of gene therapy. Combining switch-enabled gene therapy with other anticancer regimens may also bear tremendous fruit.
Already M.D. Anderson's Cooper, for example, is combining a couple of switch-enabled genes with a cell-based cancer treatment. The genes will contribute interleukin-12 and another cytokine, interleukin-15; lab tests suggest that IL-15 makes IL-12 even more effective at rallying immune cells. The third part of this experimental treatment—the cells—is a group of genetically engineered immune cells called CAR T cells that are better able to direct their firepower on cancerous tissue than naturally occurring immune cells can. Adding switch-bearing IL-12 and IL-15 genes to the CAR T cells should allow Cooper to boost the cells' potency and effectiveness. Because the gene switches and their respective activators will allow him to adjust the levels of IL-12 and IL-15 independently, he should be able to fine-tune the treatment to produce the best results with the least amount of IL-12, thereby further reducing the risk of unleashing a cytokine storm. With a touch of whimsy, Cooper calls this new suite of engineered cells “remote-control CARs.”
Many technical hurdles must still be overcome, but the potential arc of progress is beginning to take shape. If inserting new genes into our bodies in the 1990s was Genetic Engineering 1.0, then the switch-based control of our genes is Genetic Engineering 2.0. Someday many of the pills that doctors give patients may be used to switch on various transferred genes at precisely the right place and time in the body instead of flooding every organ and tissue with the powerful pharmaceutical agents that act both where they are needed and elsewhere, causing side effects. Many drugs will no longer be manufactured in giant vats and so-called bioreactors in pharmaceutical facilities. Instead new gene treatments will allow patients to churn out a molecule exactly where and when it is needed most in the body.
Added 200 more shares to initial position created last week, the charts are screaming for a quick rebound above 10$
oil price is affecting the market which in turn affects biotechs. biotech will continue to go up in the long run, imo. it's taking a breather for now.
That's not helping. Bios have been getting killed for the last two plus quarters. So many other companies are down much more than ZIOP. According to the CC the other day it looks like there could be real tremendous upside in the long term.
3 yrs out this should be well over $20 IMO
it's the market being down is the problem. It was up nicely at 8.50++ in the AM when XBI was up 1%+. The market dropped further which added pressure to biotechs. most of the other biotech stocks I'm watching dropped from 2.5%+ to the negative territory now but bounced back a bit now.
but i think once the market recovers, we'll have a nice year end rally which also helps biotechs.
Last time it dipped this low it went on a pretty nice run. I just wish it could stay at that level if it starts a reversal and can hit teens again.
Is that the RSI now?
I never saw it that low.
we'll see. market most likely will be down tomorrow. the dropped to 7.07 around 8/24 was due to the drop in the Chinese market which affected ZIOP greatly. If it wasn't for the drop in the Chinese market, it wouldn't have dropped that far before going back to 14 and reaching new high.
not all gaps filled...
i know this will fill the 6-7 gap range before 10
what makes you think that? this will go back to 10 in the near term for sure. if you want it to fill, then it's no longer ZIOP that you know and the sentiment is very bad
looks to fill 6 dollar gap before taking off again
That's what I'm doing too. Forget about it.
It's a shorts wet dream.
I've never traded it. We all could be up alot of money if we did. I wish I picked up some puts when it hit 14+
It's been a tough month all around.
Do ya follow ADXS? That was 30 in June and it's less than ZIOP now.
Heavily shorted as well.
I think we will be ok in the long term.
When we least expect it is when something really great will happen.
Best of luck!
Unbelievable how this stock is manipulated. I guess it is a swing traders dream?
Let's hope so.
dang, back down to where it was a few months ago before it ran back to 14 bucks. thinking it will go back to 10+ in a month
probably someone painted that, i don't know.
after hours?
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http://www.ziopharm.com/
http://finance.yahoo.com/q/h?s=ZIOP
ZIOPHARM Oncology, Inc., a biopharmaceutical company, engages in the development and commercialization of a portfolio of in-licensed cancer drugs. It focuses primarily on the licensing and development of proprietary drug candidate families that are related to cancer therapeutics that are already on the market or in development. The company�s product candidates include ZIO-101, ZIO-201, and ZIO-301, which are in phase I and/or II studies. ZIO-101, organic arsenic is in a phase I/II trial in patients with advanced myeloma, as well as a phase I trial in advanced cancers; ZIO-201, stabilized isophosphoramide mustard is in a phase I/II trial in patients with advanced sarcoma, as well as in a phase I trials in advanced cancers; and ZIO-301, an anti-cancer agent that targets mitosis like the taxanes is in a phase I trial. ZIOPHARM was founded in 2003 and is based in New York, New York.
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