Today, Herrmann says, "The theranostic concept has gained new momentum with the recent success of peptide receptor radioligand therapy (PRRT) ...
Today, Herrmann says, "The theranostic concept has gained new momentum with the recent success of peptide receptor radioligand therapy (PRRT) ...
Bioniz is a clinical-stage biopharmaceutical company leading the discovery and development of first-in-class multi-cytokine inhibitory peptide ...
Source: http://www.fiercebiotech.com/
AbbVie has unveiled a clutch of pacts in fields including immuno-oncology and genomics. The deals give AbbVie access to MerTK inhibitors, a source of peptide targets and genome sequencing data on 45,000 people.
All of the deals cover early-stage research, and as such it will be years before they have a notable effect on AbbVie’s fortunes. But, collectively, the pacts hint at the areas in which AbbVie sees its future resting and how it plans to go about realizing its ambitions. Two of the alliances relate to immuno-oncology, one is in the field of immunology and the fourth sees AbbVie gain access to a source of genomic data to support its future R&D efforts.
The genomics pact is perhaps the most striking. AbbVie has teamed up with the recently founded Genomics Medicine Ireland (GMI) to sequence the genomes of 45,000 volunteers. GMI and AbbVie will enroll people with “several types of immune-mediated diseases, neurological disorders and cancer” and individuals unaffected by these conditions in the sequencing program. AbbVie plans to pair these genotypic data to phenotypic information to identify new therapeutic targets and biomarkers.
Read more: http://www.fiercebiotech.com/node/470886
Funnel-web spider venom may one day be used to save the lives of stroke patients, new research shows.
A peptide found inside the venom of the Fraser Island funnel-web spider has been found to slow the death of brain cells in rats after they suffer an induced stroke.
Stroke is one of Australia's biggest killers and cause of disability. According to the Stroke Foundation, there will be more than 55,000 new and recurrent strokes this year.
Every 10 minutes an Australian suffers a stroke, when the brain is starved of blood by either a blocked artery (the most common) or a haemorrhage in the brain itself.
Professor King told Fairfax Media that, in cells starved of oxygen, the peptide in the venom (Hi1a) blocks the signal that initiates programmed cell death, keeping the neurons alive.
The research, published on Tuesday in the Proceedings of the National Academy of Sciences, showed that the Hi1a peptide was effective in rats even eight hours after a stroke.
"This could provide a good window of protection for treatment of the stroke to occur," Professor King said.
His hope is that any drug developed from the funnel-web venom can be applied by paramedics before the patient's arrival at hospital.
"There are two main stroke types and neurologists can't treat patients until they know which one they are dealing with," he said.
His hope is that any drug developed from the funnel-web venom will keep neurons alive after both types of stroke as patients are taken to hospital.
"Time is neurons saved," he said.
While Professor King is optimistic there is a "clear path forward to clinical trials in two years", others in the field are more cautious.
"It's a very exciting discovery and a very big effect," said Neil Spratt from the University of Newcastle John Hunter Hospital. "However, two years is very, very ambitious."
Professor Spratt, a neurologist who leads the stroke translation laboratory at the University of Newcastle, said the study relied on injecting the peptide directly into the rats' brains. "We can't do that with a stroke patient," he said.
"They are right to be excited but how they get any drug into the brain is a hurdle they need to cross," said Professor Pratt, who was not connected with the study.
His caution was echoed by University of Sydney clinician Craig Anderson. "It's a very interesting and promising study," he said. "But even if it has application, nothing will be developed for decades.
"What looks promising in rats can fall away by the wayside," he warned.
Professor King said where previous rat studies had failed was the short time span of efficacy studied. "None of the other studies in rats showed efficacy after eight hours," he said.
Professor Anderson, a director of neurological and mental health at The George Institute, said: "The key to reducing damage is restoring blood flow as quickly as possible, so the direction of this research will be on top of proven therapies."
Stroke Foundation clinical council chair Bruce Campbell said: "This research is very interesting, however more work needs to be done."
Professor King said the peptide had been found in the Fraser Island funnel-web. "There are 35 species of funnel-web," he said. "We assume there will be similar peptides in others, such as the Sydney funnel-web."
A POTENTIAL new drug to tackle a highly aggressive type of breast cancer has been discovered by a Bradford researcher.
Professor Mohamed El-Tanani from the University of Bradford’s Institute for Cancer Therapeutics has also developed a way of delivering the drug directly to the cancer cells.
Laboratory tests have shown when the drug is added to hard-to-treat breast cancer cells, the cells actively take it in and their growth rate is reduced.
The drug is a peptide, a fragment of a protein, which Prof El-Tanani found out is able to block out another protein called RAN which helps cancer cells to divide and grow.
High levels of RAN have been linked to aggressive tumour growth, cancer spread and are resistance to chemotherapy often ending in poor prognosis in a number of cancers, including triple negative breast cancer (TNBC).
Between 10 to 20 per cent of breast cancers are found to be triple negative which means they do not respond to hormones oestrogen and progesterone or the protein HER2, limiting the range of treatment options and increasing the risk of it coming back if cured.
Prof El-Tanani has been working with colleagues from Ulster University, Sunderland and Queen’s University Belfast to come up with a special way of getting the new protein drug to the cancer cells and attacking them.
The researchers have found that by putting the drug in a tiny particle first, which acts like a capsule, once it is injected it preserves it long enough to be carried to the cells before being released. Tests have shown the protein drug breaks down too early to work if injected by itself.
“By developing a nanoparticle that can help this peptide enter triple negative breast cancer cells and block RAN we’ve brought this potential new treatment a step closer to the clinic,” said Professor El-Tanani.
He added: “We knew we’d need a novel delivery mechanism for this drug because peptides on their own are unstable and they can degrade too quickly to be effective. Using a nanoparticle as a delivery mechanism was the perfect solution.”
Professor El-Tanani is also working on a number of other potential RAN inhibitors, including a drug that has been already pre-clinically validated in breast and lung cancer and is ready for clinical trials. The University of Bradford is looking for funding and investor support to support more development of those drugs.
Abstract: A novel neuroendocrine peptide, pituitary adenylate cyclase activating peptide (PACAP), was found to have an important role in carbohydrate or lipid metabolism and was susceptible to dipeptidyl peptidase IV degradation. It can not only mediate glucose-dependent insulin secretion and lower blood glucose by activating VPAC2 receptor, but also raise blood glucose by promoting glucagon production by VPAC1 receptor activation. Therefore, its therapeutic application is restricted by the exceedingly short-acting half-life and the stimulatory function for glycogenolysis. Herein, we generated novel peptide-conjugated selenium nanoparticles (SeNPs; named as SCD), comprising a 32-amino acid PACAP-derived peptide DBAYL that selectively binds to VPAC2, and chitosan-modified SeNPs (SeNPs-CTS, SC) as slow-release carrier. The circulating half-life of SCD is 14.12 h in mice, which is 168.4- and 7.1-fold longer than wild PACAP (~5 min) and DBAYL (~1.98 h), respectively. SCD (10 nmol/L) significantly promotes INS-1 cell proliferation, glucose uptake, insulin secretion, insulin receptor expression and also obviously reduces intracellular reactive oxygen species levels in H2O2-injured INS-1 cells. Furthermore, the biological effects of SCD are stronger than Exendin-4 (a clinically approved drug through its insulinotropic effect), DBAYL, SeNPs or SC. A single injection of SCD (20 nmol/kg) into db/db mice with type 2 diabetes leads to enhanced insulin secretion and sustained hypoglycemic effect, and the effectiveness and duration of SCD in enhancing insulin secretion and reducing blood glucose levels are much stronger than Exendin-4, SeNPs or SC. In db/db mice, chronic administration of SCD by daily injection for 12 weeks markedly improved glucose and lipid profiles, insulin sensitivity and the structures of pancreatic and adipose tissue. The results indicate that SC can play a role as a carrier for the slow release of bioactive peptides and SCD could be a hopeful therapeutic against type 2 diabetes through the synergy effects of DBAYL and SeNPs.
A research team from the UK has developed a prospective new drug for confronting the highly aggressive “triple negative” breast cancer (TNBC), as well as a nanoparticle for delivering the drug directly into the cancer cells.
Professor Mohamed El-Tanani from the Institute for Cancer Therapeutics at the University of Bradford has discovered the new drug, which is a peptide, that is, a protein fragment. Professor El-Tanani has demonstrated, using computer models, that the peptide inhibits a protein known as RAN which helps the division and growth of cancer cells.
Higher levels of RAN are known to cause aggressive growth of tumor, spreading of cancer, resistance to chemotherapy, and poor prognosis in many types of cancers, such as the TNBC.
We knew we’d need a novel delivery mechanism for this drug because peptides on their own are unstable and they can degrade too quickly to be effective. Using a nanoparticle as a delivery mechanism was the perfect solution.
Professor Mohamed El-Tanani, University of Bradford
The research team worked in collaboration with researchers from Ulster University, Sunderland, and Queen’s University Belfast to develop a nanoparticle with the ability to encapsulate the peptide. The nanoparticle was made of a biodegradable polymer.
The researchers analyzed a number of different polymers to determine the most effective nanoparticle that could help the entry of the protein into the cancer cells to attack the cancer cells.
Laboratory tests demonstrated that when the nanoparticle that included the peptide was added to the TNBC cells, the cells actively took it in. Consequently, the growth rate of the cancer cells reduced, their replication stopped, and nearly two-thirds of the cancer cells died within a time period of 24 hours. The researchers compared the effect of this with the addition of just the peptide, or an empty nanoparticle, which did not have any effect on the growth of the cells.
The research team also validated the point that the drug destroyed the cancer cells through the same mechanism that they had viewed in the computer models, that is, it blocked the action of RAN which has a significant role in the division and growth of the cancer cells.
Prior research carried out by Professor El-Tanani has indicated that when RAN is blocked, the resistance to chemotherapy in small cell lung cancer can be prevented or even reversed.
Almost 10% - 20% of breast cancers are known to be triple negative. This implies that this type of cancer does not have any receptors neither for the progesterone or estrogen hormones nor for the protein HER2, limiting the array of treatments available, and hence leading to poorer prognosis and heightened recurrence risk.
By developing a nanoparticle that can help this peptide enter triple negative breast cancer cells and block RAN we’ve brought this potential new treatment a step closer to the clinic. We’re already working on in vivo tests of the nanoparticle in a triple negative breast cancer model and are thinking ahead to taking this drug into clinical trials.
Professor Mohamed El-Tanani, University of Bradford
Professor El-Tanani has also been researching on a range of other probable RAN inhibitors, which include a “repurposed” drug already pre-clinically validated in lung and breast cancer and now ready for clinical trials. The University of Bradford has been actively soliciting additional investor support and funding to aid the development of such drugs.
The outcomes of this research have been published in the International Journal of Pharmaceutics.
Abstract: Differentiating between chronic obstructive pulmonary disease (COPD) patients with normal (PiMM) or deficient (PiZZ) genetic variants of alpha-1 antitrypsin (A1AT) is important not only for understanding the pathobiology of disease progression but also for improving personalized therapies. This pilot study aimed to investigate whether urinary peptides reflect the A1AT-related phenotypes of COPD. Urine samples from 19 clinically stable COPD cases (7 PiMM and 12 PiZZ A1AT) were analyzed by capillary electrophoresis coupled to mass spectrometry. We identified 66 peptides (corresponding to 36 unique proteins) that differed between PiZZ and PiMM COPD. Among these, peptides from the collagen family were the most abundant and divergent. A logistic regression model based on COL1A1 or COL5A3 peptides enabled differentiation between PiMM and PiZZ groups, with a sensitivity of 100% and specificity of 85.71% for COL1A1 and a sensitivity of 91.67% and specificity of 85.71% for COL5A3. Furthermore, patients with PiZZ presented low levels of urinary peptides involved in lipoproteins/lipids and retinoic acid metabolism, such as apolipoprotein A-I and C4, retinol-binding protein 4 and prostaglandin-H2 d-isomerase. However, peptides of MDS1 and EVII complex locus, gelsolin and hemoglobin alpha were found in the urine of COPD cases with PiZZ, but not with PiMM. These capillary electrophoresis coupled to mass spectrometry-based results provide the first evidence that urinary peptide content differs between PiMM and PiZZ patients with COPD.
The report "Biosimilars Market by Product (Recombinant Non-glycosylated Proteins (Insulin, rHGH, Interferon), glycosylated (mAb, EPO), Peptides (Glucagon, Calcitonin)), Manufacturing (In-House, CMO) & Application (Oncology, Blood Disorders) - Global Forecast to 2021", provides a detailed overview of the major drivers, restraints, challenges, opportunities, current market trends, and strategies impacting the biosimilars market along with the estimates and forecasts of the revenue and market share analysis.
The global biosimilars market is expected to reach USD 10.90 Billion by 2021 from USD 3.39 Billion in 2016, at a CAGR of 26.3% during the forecast period. The major factors driving the growth of this market are the increasing demand for biosimilar drugs due to their cost-effectiveness, growing pressure to curtail healthcare expenditure, rising geriatric population, strategic collaborations resulting in enhanced productivity and clinical trial activities for biosimilars, and increasing government support and initiatives to develop and promote biosimilars.
Download PDF Brochure @ http://www.marketsandmarkets.com/pdfdownload.asp?id=40
This report segments the market on the basis of product, manufacturing type, application, and region. On the basis of product, the biosimilars market is segmented into recombinant non-glycosylated proteins, recombinant glycosylated proteins, and recombinant peptides. In 2016, the recombinant non-glycosylated proteins segment is expected to account for the largest share of the market. New product launches, cost-effectiveness, growing incidence of diabetes, and presence of many biosimilar versions of insulin in the pipeline are the factors driving the growth of this segment.
Based on manufacturing type, the biosimilars market is segmented into in-house manufacturing and contract manufacturing organizations. In 2016, the contract manufacturing segment is expected to account for the largest share of the market.
Based on application, the biosimilars market is segmented into oncology, blood disorders, chronic and autoimmune diseases, growth hormone deficiency, infectious diseases, and other applications. The oncology segment is expected to grow at the highest CAGR during the forecast period. The rising incidence of cancer, high cost of biologics, pressure to reduce healthcare expenditure, and low cost of biosimilars are factors contributing to the growth of this segment.
Based on region, the global biosimilars market is segmented into North America, Europe, Asia, and RoW. Asia is expected to grow at the highest CAGR during the forecast period. This can be attributed to factors such as the low per capita consumption, rapid growth in economies, rise in technological innovation, trade links, and the rise in medical tourism.
The key players in the biosimilars market include Pfizer Inc. (U.S.), Sandoz International GmbH (Germany), Teva Pharmaceuticals Industries Ltd. (Israel), Amgen Inc. (U.S.), Biocon Ltd. (India), Dr. Reddy’s Laboratories (India), F. Hoffmann-La Roche Ltd. (Switzerland), Celltrion Inc. (South Korea), and Samsung Bioepis (South Korea).
A compound extracted from marine snail venom may be a potent alternative to opioids for pain relief, new research suggests.
Scientists at the University of Utah found that Rg1A, a compound isolated from the venom of Conus regius, a marine cone snail common in the Caribbean Sea, acts on a different pain pathway than those targeted by opioids.
“Rg1A4 works by an entirely new pathway, which opens the door for new opportunities to treat pain,” said J. Michael McIntosh, MD, study co-author and professor and director of research of psychiatry at the University of Utah in Salt Lake City, in a press release. “We feel that drugs that work by this pathway may reduce burden of opioid use.”
Prior research has suggested that antagonists of alpha9 alpha10 nicotinic acetylcholine receptors (nAChRs) might be a potential nonopioid target in the pathophysiology of chronic pain (Curr Pharm Des 2014;20:6042-6047). Rg1A is effective at blocking these receptors in rodents, but similar results have not been achieved in humans, according to the researchers.
They used synthetic chemistry to engineer 20 analogs of the compound to ensure they had one that would be effective in people. They found that the peptide Rg1A4 exhibited a “high potency for both human and rodent α9α10 nAChRs, and was at least 1,000-fold more selective for α9α10 nAChRs vs. all other molecular targets tested.”
The researchers tested the efficacy of this peptide by exposing rodents to a chemotherapy drug that causes extreme cold sensitivity and hypersensitivity to touch. They found that rodents that received Rg1A4—or were genetically engineered to not have this pain pathway—did not experience pain compared with those not given the compound.
Dr. McIntosh noted that even though the compound only remains in the body for about four hours, it “was still working 72 hours after the injection, still preventing pain.”
The lingering effect highlights this compound’s potential for preventing chronic pain from developing, and may be a treatment for patients with established pain who have run out of other options, according to the researchers.
Using marine snail venom to develop pain treatment is not a new concept. Researchers have had positive results using venom from another member of the Conoidea family (Integr Comp Biol 2016;56:962-972). The venom of the Conus magus marine snail has been used to develop ziconotide (Prialt, Jazz), which is used to treat chronic pain in HIV and cancer patients.
—Carina Elfving
Based on a press release from the University of Utah.