Possible New Combination Chemotherapy for Patients with Advanced Prostate Cancer

For more than a decade, oncologists using cytotoxic chemotherapy to treat patients with advanced metastatic castration-resistant prostate cancer (mCRPC) have relied on the sequential use of single agent taxanes such as docetaxel and cabazitaxel. For example, docetaxel is commonly used as the "first-line" therapy, while cabazitaxel is used as the "second-line" therapy. A role for combination therapy using two or more chemotherapy agents at the same time has not been well studied. This week, however, results of a clinical trial presented at the American Society of Clinical Oncology meeting by researchers at The University of Texas MD Anderson Cancer Center may change the perspective on a role for combination chemotherapy in advanced disease.

 Carboplatin  Cabazitaxel   Docetaxel

The study compared the effectiveness of cabazitaxel alone versus cabazitaxel combined with carboplatin -- a type of platinum chemotherapy -- in patients with metastatic castrate-resistant prostate cancer (mCRPC). To date, 160 men have been randomized to treatment with either the single or dual chemotherapy drug regimen. Each patient received up to 10 cycles of chemotherapy.

To monitor the effects of treatment, MD Anderson researchers tracked several variables including Progression Free Survival, as well as changes in blood levels of prostate-specific antigen (PSA) and bone-specific alkaline phosphatase (BAP, a marker of prostate cancer in bone cells). In addition, safety and toxicity were monitored for both patient groups.

Analysis and comparison of the data demonstrated that median PFS was significantly longer for patients receiving combination versus single agent chemotherapy (6.7 months vs 4.4 months, respectively, p = 0.01). Furthermore, reductions in both PSA and BAP were greater for the combination therapy group. PSA reductions greater than 50 percent occurred 60 percent of the time with combined chemotherapy vs. 44 percent with the single drug. PSA reductions greater than 90 percent occurred 28 percent of the time with two chemotherapy drugs vs. 20 percent with one. In addition, BAP reductions greater than 50 percent for combination vs. single drug were 63 percent and 25 percent respectively.

Side effects, such as fatigue, anemia and neutropenia were comparable for both the single-drug regimen and two-drug regimen. In addition, there were no significant toxicity events.

"We believe cabazitaxel-carboplatin combination chemotherapy may become the clinical standard for advanced prostate cancer once additional safety, efficacy and overall survival data is generated," explained Paul Corn, M.D., Ph.D., an associate professor of genitourinary medical oncology at MD Anderson. "Dr. Ana Aparicio's lab is currently developing tumor-specific biomarkers to identity patients with an aggressive variant of prostate cancer most likely to benefit from this approach."

Possible New Combination Chemotherapy for Patients with Advanced Prostate Cancer 

Targeted drug can ‘diminish the suffering’ of myelofibrosis

Investigators further found that pacritinib could be used safely in patients with myelofibrosis who have thrombocytopenia, a life-threating loss of blood platelets that can lead to deadly bleeding. The only currently approved therapy for myelofibrosis   ruxolitinib   is not recommended in patients who have severe thrombocytopenia.

 Pacritinib  Ruxolitinib

Ruben A. Mesa, M.D., chair of Hematology and Medical Oncology at Mayo Clinic in Arizona, will present these results at a press conference held during the 2015 American Society of Clinical Oncology (ASCO) annual meeting in Chicago.

"Use of pacritinib can alleviate the burden and diminish the suffering that this cancer causes," says Dr. Mesa. "For many of the patients who used it, pacritinib is a very good drug. The agent was significantly superior to other medical treatments.

"It is too early to know if pacritinib has an impact on survival, but that is clearly our expectation," he adds.

Mayo researchers led by Dr. Mesa were also part of a phase 2 trial that found pacritinib offered significant benefit in treating the disorder.

Myelofibrosis is a chronic bone-marrow disorder that can lead to lowering of blood counts, scarring in the bone marrow, severe symptoms and enlargement of the spleen. Myelofibrosis can be life threatening for afflicted patients because of the debilitation the disease causes and/or progression to acute leukemia, Dr. Mesa says.

Myelofibrosis is one of three blood cancers classified as myeloproliferative neoplasms (MPNs), and MPN affects about 350,000 people in the U.S., he says.

In this study, two-thirds of the 327 patients with primary and secondary myelofibrosis were treated with pacritinib. The other one-third were treated with best available therapy (BAT), but were able to cross over to use of pacritinib if their cancer was largely nonresponsive. BAT was chosen by the patient's physician, but did not include ruxolitinib because many patients were not eligible for it due to existing thrombocytopenia.

Pacritinib, an oral drug, is known as a JAK2/FLT3 inhibitor. JAK2 is a protein that acts like an on-off growth switch in blood cells.

"The JAK2 pathway is abnormally turned on in patients, which leads to this chronic leukemia. This drug turns off that switch," Dr. Mesa says.

PERSIST-1 investigators found that medium duration of treatment on the study was 16-plus months, and that by six months, spleen size was reduced in 25 percent of evaluable patients treated with pacritinib compared to 6 percent in the BAT group. Almost 80 percent of BAT patients crossed over to use of pacritinib, and 21 percent of all pacritinib patients had achieved a reduction in spleen volume of 35 percent or more. Symptoms of the cancer were reduced in more than 46 percent of pacritinib-treated patients compared to 9 percent in patients given BAT.

Targeted drug can ‘diminish the suffering’ of myelofibrosis 

Promising preliminary results for AKB-9778 in diabetic macular oedema

AKB-9778, a small molecule competitive inhibitor of vascular endothelial-protein tyrosine phosphatase (VE-PTP), has a good safety and efficacy profile in patients with diabetic macular oedema, suggests a preliminary dose-escalation study. 

By blocking VE-PTP, AKB-9778 promotes the activation of Tie2, a protein involved in the regulation of vascular permeability, explain the researchers. In preclinical studies, AKB-9778 has been shown to suppress vascular leakage as well as neovascularisation of the retina and choroid, they add.

In this phase Ib trial, four groups of six patients were treated with open-label AKB-9778 self-administered twice daily via subcutaneous injections at doses of 5.0 mg, 15.0 mg, 22.5 mg or 30.0 mg for 4 weeks.

Participants treated with the higher 22.5 mg and 30.0 mg doses, but not those given the 5.0 mg and 15.0 mg doses, experienced headache, dizziness and vasovagal events such as presyncope or syncope – adverse events that are consistent with the anticipated vasodilatory activity of AKB-9778, say the researchers.

“Modest decreases” in resting systolic blood pressure were also observed in the 22.5 mg and 30.0 mg groups, they report, adding that these effects and the adverse events were “transient” and “generally resolved” shortly after dosing.

At 4 weeks, best-corrected visual acuity (BCVA) improved from intake in the 15.0 mg, 22.5 mg and 30.0 mg groups; of 18 participants, 10 achieved an improvement of five to 10 letters, one improved by 11 letters and two by over 15 letters.

Moreover, seven patients who received AKB-9778 at doses of 15.0 mg or more showed decreases in study eye central subfield thickness (CST) from baseline, with reductions of over 100 μm in five patients and of 50 to 100 μm in two patients.

Promising preliminary results for AKB-9778 in diabetic macular oedema

JAK2 inhibitor ruxolitinib shows promise in treating CMML patients

In continuation of my update on Ruxolitinib

Chronic myelomonocytic leukemia (CMML) is a rare type of myelodysplastic, myeloproliferative neoplasm characterized by increased numbers of peripheral monocytes and less than 20 percent blasts. CMML has few treatment options and patients only survive on average for 12 to 24 months. Preclinical studies suggest that JAK2 inhibitors may be an effective treatment option for CMML. Eric Padron, M.D., assistant member of the Malignant Hematology Program at Moffitt Cancer Center will report on the first phase 1 study of the JAK2 inhibitor ruxolitinib in CMML patients at the 2015 American Society of Clinical Oncology Annual Meeting in Chicago.

The Moffitt team and their collaborators performed a dose-escalation study of ruxolitinib in 19 CMLL patients. Ruxolitinib displayed minimal toxicity, with no dose-limiting toxicities observed and only one grade 3 or higher adverse event.

Efficacy data suggest that ruxolitinib is a promising treatment option for CMML patients. Out of fifteen patients who were evaluable for response, 3 displayed hematologic improvement and 1 patient had a partial response. Nine of the patients entered the trial with an enlarged spleen, and 5 of these patients had a greater than 50 percent reduction in their spleen size.

Ruxolitinib may be particularly beneficial for patients who have B symptoms, as 10 out of 11 patients with disease related symptoms had a clinically meaningful or complete resolution of their symptoms.

The researchers determined a phase 2 recommended dose of 20 mg twice a day, and a phase 2 study of ruxolitinib in CMML patients is planned.

JAK2 inhibitor ruxolitinib shows promise in treating CMML patients

Metformin can reduce risk of open-angle glaucoma in people with diabetes

In continuation of my update on metformin

Taking the medication metformin hydrochloride was associated with reduced risk of developing the sight-threatening disease open-angle glaucoma in people with diabetes, according to a study published online by JAMA Ophthalmology.

Medications that mimic caloric restriction such as metformin can reduce the risk of some late age-onset disease. It is unknown whether these caloric mimetic drugs affect the risk of age-associated eye diseases such as macular degeneration, diabetic retinopathy, cataract or glaucoma.

Researcher Julia E. Richards, Ph.D., of the University of Michigan, Ann Arbor, and co-authors examined metformin use and the risk of open-angle glaucoma (OAG) using data from a large U.S. managed care network from 2001 through 2010.

Of 150,016 patients with diabetes, 5,893 (3.9 percent) developed OAG. Throughout the study period, 60,214 patients (40.1 percent) filled at least one metformin prescription; 46,505 (31 percent) filled at least one sulfonylurea prescription; 35,707 (23.8 percent) filled at least one thiazolidinedione prescription; 3,663 (2.4 percent) filled at least one meglitinide prescription; and 33,948 (22.6 percent) filled at least one insulin prescription. Some patients filled prescriptions for multiple medications.

Metformin can reduce risk of open-angle glaucoma in people with diabetes

Amgen announces AMG 416 Phase 3 results for treatment of secondary hyperparathyroidism in CKD patients

Amgen announced THE pooled data from two pivotal Phase 3, global, randomized, placebo-controlled trials evaluating AMG 416, a novel calcimimetic, for the treatment of secondary hyperparathyroidism (SHPT) in patients with chronic kidney disease (CKD) receiving hemodialysis. Both studies met the primary endpoint, demonstrating that a greater proportion of patients in the AMG 416 groups achieved a greater than 30 percent reduction in parathyroid hormone (PTH) during the Efficacy Assessment Phase compared with placebo. The data were presented today at the 52nd ERA-EDTA Congress in London.

"Secondary hyperparathyroidism is a complex and challenging condition that can be difficult to manage, as it may require patients to take demanding drug regimens multiple times a day," said John Cunningham, lead author of the studies, professor of Nephrology at the University College London Medical School and consultant physician at The Royal Free Hospital, London. "Providing patients with chronic kidney disease on hemodialysis with a calcimimetic that can be administered intravenously on the same schedule as dialysis has the potential to fulfill an unmet need in this patient population."

AMG 416 is a novel calcimimetic agent in clinical development for the treatment of SHPT in patients with CKD who are receiving hemodialysis. In the registrational programs, AMG 416 is administered intravenously at the end of dialysis. AMG 416 acts by binding to and activating the calcium-sensing receptor on the parathyroid gland, thereby causing decreases in PTH. Sustained elevations in PTH are known to lead to significant clinical consequences for patients with CKD.

In the two Phase 3 placebo-controlled studies, an aggregate of 1,023 patients with moderate-to-severe SHPT (PTH greater than 400 pg/mL) on hemodialysis were randomized to receive intravenous AMG 416 or placebo three times a week. The primary endpoint of both studies was the proportion of patients achieving greater than 30 percent reduction in PTH during the Efficacy Assessment Phase, defined as weeks 20 through 27. Secondary endpoints included the proportion of patients with PTH less than or equal to 300 pg/mL, and percent reductions in PTH, albumin adjusted calcium (cCa), phosphate (P) and cCa x P. In the AMG 416 group, 74.7 percent of patients achieved a greater than 30 percent reduction from baseline in PTH compared with 8.9 percent in the placebo arm.

Amgen announces AMG 416 Phase 3 results for treatment of secondary hyperparathyroidism in CKD patients

Study expands understanding of the production of ET-743 compound

In continuation of my update on Trabectedin

For decades, scientists have known that ET-743, a compound extracted from a marine invertebrate called a mangrove tunicate, can kill cancer cells. The drug has been approved for use in patients in Europe and is in clinical trials in the U.S.

Scientists suspected the mangrove tunicate, which is a type of a sea squirt, doesn't actually make ET-743. But the precise origins of the drug, which is also known as trabectedin, were a mystery.

By analyzing the genome of the tunicate along with the microbes that live inside it using advanced sequencing techniques, researchers at the University of Michigan were able to isolate the genetic blueprint of the ET-743's producer--which turns out to be a type of bacteria called Candidatus Endoecteinascidia frumentensis.

The findings greatly expand understanding of the microbe and of how ET-743 is produced, the researchers reported online May 27 in the journal Environmental Microbiology. They're optimistic that the insights will help make it possible to culture the bacteria in the laboratory without its host.

"These symbiotic microbes have long been thought to be the true sources of many of the natural products that have been isolated from invertebrates in the ocean and on the land. But very little is known about them because we're not able to get most of them to grow in a laboratory setting," said study senior author David Sherman, the Hans W. Vahlteich Professor of Medicinal Chemistry in the College of Pharmacy and a faculty member of the U-M Life Sciences Institute, where his lab is located.

"Currently, many of these compounds can only be harvested in small amounts from host animals, which is unsustainable from an economic and environmental perspective," said Michael Schofield, one of two first authors on the study and a member of the Sherman lab before she graduated from U-M this spring. "Our hope is that understanding the genomes of these micro-organisms and the chemical reactions that occur inside of them will provide new avenues to economical and sustainable production of the medicinal molecules they make."

ET-743 is currently made using a complicated, partially synthetic process.

"A major challenge of sequencing genomes from samples containing a mixture of different organisms is figuring out which DNA sequences go with which organisms. We used bioinformatic approaches that allowed us to tease that apart," said Sunit Jain, a bioinformatics specialist in the U-M Department of Earth and Environmental Sciences, and the study's other first author.

Study expands understanding of the production of ET-743 compound

Omega-3 fatty acids improve cognitive flexibility in older adults at risk of late-onset Alzheimer's disease

A study of older adults at risk of late-onset Alzheimer's disease found that those who consumed more omega-3 fatty acids did better than their peers on tests of cognitive flexibility -- the ability to efficiently switch between tasks -- and had a bigger anterior cingulate cortex, a brain region known to contribute to cognitive flexibility.

 

[alpha-linolenic acid (ALA), an essential omega-3 fatty acid, (18:3Δ9c,12c,15c, which means a chain of 18 carbons with 3 double bonds on carbons numbered 9, 12, and 15)].

The analysis suggests, but does not prove, that consuming DHA and EPA, two omega-3 fatty acids found in fish, enhanced cognitive flexibility in these adults in part by beefing up the anterior cingulate cortex, the researchers report in the journal Frontiers in Aging Neuroscience.

"Recent research suggests that there is a critical link between nutritional deficiencies and the incidence of both cognitive impairment and degenerative neurological disorders, such as Alzheimer's disease," said University of Illinois neuroscience, psychology, and speech and hearing science professor Aron Barbey, who led the study with M.D./Ph.D. student Marta Zamroziewicz. "Our findings add to the evidence that optimal nutrition helps preserve cognitive function, slow the progression of aging and reduce the incidence of debilitating diseases in healthy aging populations."

The researchers focused on aspects of brain function that are sometimes overlooked in research on aging, Zamroziewicz said. "A lot of work in cognitive aging focuses on memory, but in fact cognitive flexibility and other executive functions have been shown to better predict daily functioning than memory does," she said.

"Executive function" describes processes like planning, reasoning, paying attention, problem solving, impulse control and task switching.

"These functions tend to decline earlier than other cognitive functions in aging," Zamroziewicz said.

The new research built on previous studies that found associations between omega-3 fatty acid consumption, cognitive flexibility and the size of the anterior cingulate cortex.

"There's been some work to show that omega-3 fatty acids benefit cognitive flexibility, and there's also been work showing that cognitive flexibility is linked to this specific brain region, the anterior cingulate. But there's been very little work actually connecting these pieces," Zamroziewicz said.

The new study focused on 40 cognitively healthy older adults between the ages of 65 and 75 who are carriers of a gene variant (APOE e4) that is known to contribute to the risk of developing late-onset Alzheimer's disease.

The researchers tested participants' cognitive flexibility, measured levels of the fatty acids EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) in their blood, and imaged their brains using MRI. Statistical analyses teased out the relationships between these factors.

"We wanted to confirm that higher omega-3 fatty acids related to better cognitive flexibility, and we did in fact see that," Zamroziewicz said. "We also wanted to confirm that higher omega-3 fatty acids related to higher volume in the anterior cingulate cortex, and we saw that. Finally, we were able to show that higher volume in the anterior cingulate cortex was an intermediary in the relationship between omega-3 fatty acids and cognitive flexibility."

 Docosahexaenoic acid

  Eicosapentaenoic acid

Omega-3 fatty acids improve cognitive flexibility in older adults at risk of late-onset Alzheimer's disease

Green tea components may help prevent prostate cancer development in at-risk men

In continuation from my update on epigallocatechin

Prostate cancer is the second most common type of cancer in men and is predicted to result in an estimated 220,00 cases in the United States in 2015. In recent years, an emphasis has been placed on chemoprevention - the use of agents to prevent the development or progression of prostate cancer. A team of researchers led by Nagi B. Kumar, Ph.D., R.D., F.A.D.A. at Moffitt Cancer Center recently published results of a randomized trial that assessed the safety and effectiveness of the active components in green tea to prevent prostate cancer development in men who have premalignant lesions. The results will be presented at the 2015 American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago.

Twenty percent of green tea is consumed in Asian countries where prostate cancer death rates are among the lowest in the world and the risk of prostate cancer appears to be increased among Asian men who abandon their original dietary habits upon migrating to the U.S.

Laboratory studies have shown that substances in green tea called, "catechins" inhibit cancer cell growth, motility and invasion, and stimulate cancer cell death. Green tea catechins also prevent and reduce tumor growth in animal models. Epigallocatechin-3-gallate (EGCG) is the most abundant and potent catechin found in green tea responsible for these cancer prevention effects.

The goal of this trial was to evaluate if a one-year intervention with green tea catechins could suppress prostate cancer development in men who had high-grade intraepithelial neoplasia (HGPIN) or atypical small acinar proliferation (ASAP). The researchers used decaffeinated green tea capsules called Polyphenon E that contained a mixture of catechins that predominantly contained EGCG at a dose of 200 mgs twice a day.

Green tea components may help prevent prostate cancer development in at-risk men

Existing anti-stroke drug can be effective in treating middle-ear infections

In continuation of my update on Vinpocetine

An existing anti-stroke drug is an effective treatment for middle-ear infections, showing the ability to suppress mucus overproduction, improve bacterial clearance and reduce hearing loss, according to researchers at Georgia State University and the University of Rochester.

The findings, published May 13 in the Journal of Immunology, could result in a novel, non-antibiotic treatment for otitis media, or middle-ear infection, possibly through topical drug delivery. Vinpocetine, the drug involved in the study, has long been used to treat neurological disorders such as stroke.

The study found topical administration of Vinpocetine suppressed inflammation and the overproduction of mucus induced by Streptococcus pneumonia bacteria, improved hearing loss in the middle ear and significantly improved bacterial clearance in animal studies.

"Our encouraging preliminary data suggest that the repurposed drug Vinpocetine may play a critical role in inhibiting inflammation and enhancing antimicrobial defenses in otitis media," said Dr. Jian-Dong Li, director of the Institute for Biomedical Sciences at Georgia State and a Georgia Research Alliance Eminent Scholar in Inflammation and Immunity. "Our proposed studies may lead to developing novel, non-antibiotic therapeutic strategies to control immunopathology, reduce mucus overproduction, improve hearing loss and enhance host defense for otitis media."

Otitis media is the most common childhood bacterial infection and the leading cause of conductive hearing loss. Streptococcus pneumonia is one of the most common bacterial pathogens causing middle-ear infection.

In the United States, there are 24.5 million visits to physicians' offices each year because of otitis media and more than $5 billion is spent annually for the care of this disease, according to studies in Pediatric Annals and Otolaryngology - Head and Neck Surgery.

Existing anti-stroke drug can be effective in treating middle-ear infections

Brigatinib drug shows promise against ALK non-small cell lung cancer in phase I/II clinical trial

Phase I/II clinical trial results reported at the American Society for Clinical Oncology (ASCO) Annual Meeting 2015 show promising results for investigational drug brigatinib against ALK+ non-small cell lung cancer (NSCLC), with 58 of 78 ALK+ patients responding to treatment, including 50 of 70 patients who had progressed after previous treatment with crizotinib, the first licensed ALK inhibitor. Progression-free survival (PFS) in patients previously treated with crizotinib was 13.4 months.

"Although still only in an early phase trial, brigatinib is showing an objective response rate in approximately 70 percent of ALK-positive patients post-crizotinib and it's showing about a year of progression-free survival. These results are among the best in the field, offering a lot of hope to people with ALK-positive lung cancer," says D. Ross Camidge, MD, PhD, director of thoracic oncology at the University of Colorado Cancer Center and the trial's principal investigator.

In addition, robust data is emerging on drug activity in patients with brain involvement of the disease. Many lung cancer trials have traditionally excluded patients with brain metastases at baseline, expecting that the presence of metastases would create negative results that could in turn create the appearance of drug failure. Following early recognition of the importance of the brain as a potential differentiator between the activity of new drugs, the brigatinib trial includes patients with untreated brain metastases, showing a greater than 30 percent decrease in size of brain tumors in 8 of 15 patients with brain tumors greater than 10 mm and disappearance of brain metastases in 11 of 33 patients with smaller lesions only. Brain metastases remained controlled for a median 15.6 months.

Based on these promising early results, brigatinib, developed by Ariad Pharmaceuticals, Inc., recently received Breakthrough Therapy designation by the U.S. Food and Drug Administration (FDA) for the treatment of patients with ALK+ metastatic NSCLC whose tumors are resistant to crizotinib (below structure)

Brigatinib drug shows promise against ALK non-small cell lung cancer in phase I/II clinical trial

Scorpion venom has toxic effects against cancer cells

When the toxin invades channels in the cells with this disease produces cellular damage until killing them.

In the venom from the Centruroides tecomanus scorpion from Colima, south-west state of Mexico, over a hundred proteins have been found and identified a "possible" toxic effect against cancer cells, reveals a scientific study.

The preliminary investigation is carried out by specialists of the Faculty of Chemistry at the University of Colima (UCOL), who have identified peptides (amino acid molecules) that destroy cancer cells in vitro.

Laura Leticia Valdez Velazquez, head of research, said that when the toxin, derived from scorpion venom, invades channels in the cells with this disease it produces cellular damage until killing them.

"We have identified a highly selective group of peptides, which indicates that they could specifically bind to cancer cells and cause their death," she indicates.

Centruroides tecomanus species is one of the most poisonous scorpions of the country. The UCOL already has the genetic sequences of the protein components of the venom.

The scientific team took advantage of the great number of scorpions found in Colima. They began with the collection and extraction of poison, inoculating and immunizing rabbits as part of the teaching career in Pharmaceutical Chemistry Biologist. From this they decided to study the venom with the support of Lourival Possani, from the Institute of Biotechnology of the National Autonomous University od Mexico (UNAM).

The researcher explains that UCOL undertook the task of characterizing each component from the arachnid toxins, one of the most poisonous of the continent. Currently it has identified a group of peptides (about 10) in order to evaluate the have greater toxic effect against lymphoma cells.

"The venom toxins act on ion channels of the cancer cell damaging them. Our interest is for the cell to be selectively removed. We have found that these peptides have affinity with these cells, that is, they could specifically bind to them and induce cancer death".

Scorpion venom has toxic effects against cancer cells

This Little Known Chinese Herb Kills 12,000 Cancer Cells For Every Healthy Cell | Collective-Evolution

A little known Chinese herb might be eligible for the growing list of cancer killers via alternative methods of treatment. According to  studies published  in Life Sciences, Cancer Letters and Anticancer Drugs, artemesinin, a derivative of the wormwood plant commonly used in Chinese medicine, can kill off  cancer cells, and do it at a rate of 12,000 cancer cells for every healthy cell.

Henry Lai and his team of researchers from the University of Washington synthesized the compound, which uses a cancer cells appetite for iron to make them the target. The great thing about artemisinin is that alone it can selectively kill cancer cells while leaving normal cells unharmed.

“By itself, artemisinin is about 100 times more selective in killing cancer cells as opposed to normal cells. Artemisinin is 34,000 times more potent in killing the cancer cells as opposed to their normal cousins. So the tagging process appears to have greatly increased the potency of artemisinin’s cancer-killing properties.” – Henry Lai

Despite the compound being licensed to Holley Pharmaceuticals, it has yet to be used for cancer treatment in humans.

“We call it a Trojan horse because the cancer cell recognizes transferrin as a natural, harmless protein. So the cell picks up the compound without knowing that a bomb (artemisinin) is hidden inside.”  – Henry Lai

The wormwood extract was used many centuries ago in China for healing purposes. The treatment became lost over time and has now been rediscovered thanks to an ancient manuscript containing medical remedies. It kills 12,000 cancer cells for every healthy cell, which means it could be turned into a drug with minimal side effects.

“The compound is currently being licensed by the University of Washington to Artemisia Biomedical Inc., a company that Lai, Sasaki and Narendra Singh, UW associate professor of bioengineering, founded in Newcastle, Washington for development and commercialization. Human trials are at least several years away. Artemisinin is readily available, Sasaki said, and he hopes their compound can eventually be cheaply manufactured to help cancer patients in developing countries.”

This Little Known Chinese Herb Kills 12,000 Cancer Cells For Every Healthy Cell | Collective-Evolution

Chemical compound shows promise in treating rheumatoid arthritis

Montana State University researchers and their collaborators have published their findings about a chemical compound that shows potential for treating rheumatoid arthritis.

The paper ran in the June issue of the Journal of Pharmacology and Experimental Therapeutics (JPET), and one of its illustrations is featured on the cover. JPET
is a leading scientific journal that covers all aspects of pharmacology, a field that investigates the effects of drugs on biological systems and vice versa.

"This journal is one of the top journals that reports new types of therapeutics that are being developed," said Mark Quinn, senior author on the paper and a professor in MSU's Department of Microbiology and Immunology. The department is part of the College of Agriculture and the
College of Letters and Science.

Rheumatoid arthritis is a chronic autoimmune disorder that affects an estimated 1.3 million people in the world, Quinn said. Characterized by stiff, swollen joints, it's a progressive disease that occurs when the body's immune system attacks its own cells. Inflammation in the lining of the joints leads to loss of bone and cartilage. People who have rheumatoid arthritis lose mobility and joint function without adequate treatment.

New kinds of drugs have been developed for treating the disease, Quinn said. Called biological drugs, or "biologics," they are made from genetically engineered proteins or antibodies that act on substances in the immune system. When used to treat rheumatoid arthritis, they interrupt signals that fuel the inflammatory process. Two such drugs are ENBREL and HUMIRA.

Biologics can be expensive, however, and some people don't respond to
them, Quinn said. Some people respond at first, but not forever.

"There is a real need to develop new kinds of drugs that are different," Quinn said. "They could be combined with other available drugs or replace drugs that aren't working for patients."

Researchers in his laboratory and elsewhere identified a new chemical compound, called IQ-1S, in a previous study, Quinn said. Then they conducted a new study to understand how the   small-molecule  compound
works against rheumatoid arthritis. They explained their findings in the JPET paper.  

Ref : http://jpet.aspetjournals.org/content/353/3/505.abstract?sid=8b8e3977-7bbd-40f4-ab43-f37402878df0

Chemical compound shows promise in treating rheumatoid arthritis: 

Salix Pharmaceuticals receives FDA approval for Xifaxan 550 mg to treat IBS-D in adults

In continuation of my update on xifaxan

Valeant Pharmaceuticals International, Inc. (NYSE: VRX) (TSX: VRX) announced that its wholly owned subsidiary, Salix Pharmaceuticals, Inc., has received approval from the U.S. Food and Drug Administration (FDA) for Xifaxan® 550 mg for the treatment of IBS-D in adults. The FDA approval of Xifaxan 550 mg is based on data from three phase 3 studies, TARGET 1, TARGET 2 and TARGET 3. Xifaxan 550 mg was studied in over 3,000 patients and demonstrated the efficacy and safety of repeat treatment following completion of a two-week course of treatment. A full course of Xifaxan 550 mg for IBS-D is available in a convenient 2 week pack of 42 pills.

"As a gastroenterologist who helps patients navigate the symptoms of IBS-D, I see the need for treatments that directly address those most bothersome, such as diarrhea and abdominal pain" said Dr. Mark Pimentel, director of the Gastrointestinal Motility Program and Laboratory at Cedars-Sinai in Los Angeles. "Today's approval gives a new option to these patients and providers."

Salix Pharmaceuticals receives FDA approval for Xifaxan 550 mg to treat IBS-D in adults