Home » Posts tagged 'AYURVEDA' (Page 9)
Tag Archives: AYURVEDA
DRUG APPROVALS BY DR ANTHONY MELVIN CRASTO
.....FOR BLOG HOME CLICK HEREFlag and hits
ORGANIC SPECTROSCOPY
SUBSCRIBE
Subscribe in a reader
Enter your email address:
Delivered by FeedBurner
Subscribe to New Drug Approvals by Email
Recent Comments
 | shivkr2 on SPSR Excellence Award 2025 – S… |
 | Bonkasaurus on Infigratinib phosphate |
 | PALOVAROTENE | ORGAN… on Palovarotene |
| Pfizer just purchase… on Temanogrel | |
| Pfizer To Cash In On… on Temanogrel |
Cabergoline therapy for cushing disease throughout pregnancy
CABERGOLINE
Obstet Gynecol. 2013 Aug;122(2 Pt 2):485-7. doi: 10.1097/AOG.0b013e31829e398a.
http://www.ncbi.nlm.nih.gov/pubmed/23884269
.
Woo I, Ehsanipoor RM.
Source
Department of Gynecology and Obstetrics and Division of Maternal-Fetal Medicine, Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Abstract
BACKGROUND:
Cushing disease during pregnancy is rare and is associated with significant maternal and fetal morbidity and mortality. Transsphenoidal pituitary surgery is the first-line therapy; however, in cases of failed surgery or in patients who are not surgical candidates, medical therapy has been used to control symptoms.
CASE:
A 29-year-old woman with Cushing disease and a noncurative transsphenoidal pituitary surgery was successfully treated with cabergoline, a dopamine agonist. After approximately 1 year of therapy, she became pregnant. She was maintained on high-dose cabergoline throughout her pregnancy and had an uncomplicated antenatal course. She went into spontaneous labor at 38 weeks of gestation and delivered a healthy female neonate.
CONCLUSION:
Cabergoline can be used to manage Cushing disease successfully during pregnancy with an opportunity for a favorable outcome.
Cabergoline (brand names Dostinex and Cabaser), an ergot derivative, is a potent dopamine receptor agonist on D2 receptors. In vitro, rat studies show cabergoline has a direct inhibitory effect on pituitary lactotroph (prolactin) cells.[1] It is frequently used as a first-line agent in the management of prolactinomas due to higher affinity for D2 receptor sites, less severe side effects, and more convenient dosing schedule than the older bromocriptine.
History
Cabergoline was invented by scientists working for the Italian drug company Farmitalia-Carlo Erba SpA in Milan in 1981/82,[2] who were experimenting with semisynthetic derivatives of the ergot alkaloids. Farmitalia-Carlo Erba was acquired by Pharmacia in 1992, which in turn was acquired by Pfizer in 2002. The drug was approved by the FDA on December 23, 1996. It went generic in late 2005 following US patent expiration.
Intellectual property
Farmitalia filed a patent application for Cabergoline in 1982, and U.S. Patent 4,526,892 issued in July 1985.
Pharmacology
Although cabergoline is commonly described principally as a dopamine D2 receptor agonist, it also possesses significant affinity for the D3, D4, 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C, α2B– receptors, and moderate/low affinity for the D1 and 5-HT7 receptors. Cabergoline functions as an agonist at all of these receptors except for 5-HT7 and α2B–, where it acts as an antagonist.[3]
Following a single oral dose, resorption of cabergoline from the gastrointestinal (GI) tract is highly variable, typically occurring within 0.5 to 4 hours. Ingestion with food does not alter its absorption rate. Human bioavailability has not been determined since the drug is intended for oral use only. In mice and rats the absolute bioavailability has been determined to be 30 and 63 percent, respectively. Cabergoline is rapidly and extensively metabolized in the liver and excreted in bile and to a lesser extent in urine. All metabolites are less active than the parental drug or inactive altogether. The human elimination half-life is estimated to be 63 to 68 hours in patients with Parkinson’s disease and 79 to 115 hours in patients with pituitary tumors. Average elimination half-life is 80 hours.
The therapeutic effect in treatment of hyperprolactinemia will typically persist for at least 4 weeks after cessation of treatment.
Mechanism of action
Cabergoline is a long-acting dopamine D2 receptor agonist and in vitro rat studies show a direct inhibitory effect on the prolactin secretion in the pituitary’s lactotroph cells. Cabergoline decreased serum prolactin levels in reserpinized rats.
Receptor binding studies indicate a low affinity for dopamine D1 receptors, α1-adrenergic receptors, and α2-adrenergic receptors.[1]
- 1 Dostinex at www.rxlist.com”. Retrieved 2007-04-27.
- 2 US Patent 4526892 – Dimethylaminoalkyl-3-(ergoline-8′.beta.carbonyl)-ureas
- 3 Sharif NA, McLaughlin MA, Kelly CR, Katoli P, Drace C, Husain S, Crosson C, Toris C, Zhan GL, Camras C (March 2009). “Cabergoline: Pharmacology, ocular hypotensive studies in multiple species, and aqueous humor dynamic modulation in the Cynomolgus monkey eyes”. Experimental Eye Research 88 (3): 386–97. doi:10.1016/j.exer.2008.10.003. PMID 18992242.
- 4 National Institute ofMental Health. PDSD Ki Database (Internet) [cited 2013 Jul 24]. ChapelHill (NC): University of North Carolina. 1998-2013. Available from: http://pdsp.med.unc.edu/pdsp.php
- 5 Sayyah-Melli, M; Tehrani-Gadim, S; Dastranj-Tabrizi, A; Gatrehsamani, F; Morteza, G; Ouladesahebmadarek, E; Farzadi, L; Kazemi-Shishvan, M (2009). “Comparison of the effect of gonadotropin-releasing hormone agonist and dopamine receptor agonist on uterine myoma growth. Histologic, sonographic, and intra-operative changes”. Saudi medical journal 30 (8): 1024–33. PMID 19668882. edit
6 Sankaran, S.; Manyonda, I. (2008). “Medical management of fibroids”. Best Practice & Research Clinical Obstetrics & Gynaecology 22 (4): 655. doi:10.1016/j.bpobgyn.2008.03.001. PMID 18468953. edit http://www.britishfibroidtrust.org.uk/journals/bft_Sankaran.pdf
CUSHING DISEASE VIDEO
Vifor gets FDA approval for Injectafer
Switzerland’s Vifor Pharma is celebrating after getting the thumbs-up from US regulators for Injectafer for the treatment of iron deficiency anaemia.
The US Food and Drug Administration has approved the treatment, sold in Europe as Ferinject (ferric carboxymaltose) since getting the green light in 2007. Specifically, Injectafer will be available for the treatment of IDA in adults who have had an unsatisfactory response or are intolerant to oral iron.
The approval is based on two large trials conducted by Vifor’s US partner Luitpold Pharmaceuticals which studied more than 3,500 patients, of which 1,800 were treated with Injectafer.
read all at
http://www.pharmatimes.com/Article/13-07-26/Vifor_gets_FDA_approval_for_Injectafer.aspx
Ferric carboxymaltose
Chemical structure
The active substance of FERINJECT is a complex of polynuclear iron(III)-hydroxide with 4(R)-(poly-(1→4)-
O-α-D-glucopyranosyl)-oxy-2(R),3(S),5(R),6-tetrahydroxy-hexanoate. The relative molecular weight is
approximately 150,000 Da, corresponding to the empirical formula:
[FeOx(OH)y(H2O)z]n [{(C6H10O5)m (C6H12O7)}l]k, where n ≈ 103, m ≈ 8, l ≈ 11, and k ≈ 4.
CAS-Number
9007-72-1
http://www.tga.gov.au/pdf/auspar/auspar-ferric.pdf for structure
Curis phase 1 Cancer Trial for CUDC-427 Begins
CUDC-427, GDC-0917; RG-7459
Genentech Inc (Roche Holding AG)
Curis licenses GDC-0917 from Genentech
Curis Cancer Trial Begins
Curis Inc. has initiated patient dosing in a second Phase 1 dose-escalation study of CUDC-427 that is being conducted using a continuous, twice-daily oral dosing regimen in patients with advanced and refractory solid tumors or lymphoma.
FULL STORY
About CUDC-427 (GDC-0917)
CUDC-427 is an orally bioavailable small molecule that is designed to promote cancer cell death by antagonizing IAP proteins. IAP proteins are a family of functionally and structurally related proteins that promote cancer cell survival by inhibiting programmed cell death, also known as apoptosis, which is a normal process inherent in every cell. Using IAP proteins and other anti-apoptotic factors, cancer cells evade apoptosis in response to a variety of signals, including those provided by anti-cancer agents such as chemotherapy, or naturally occurring inflammatory and immune signals transmitted through members of the tumor necrosis factor, or TNF, family of factors. Evasion from apoptosis is a fundamental mechanism whereby human cancers develop resistance to standard anti-cancer treatments. IAP inhibitors such as CUDC-427 are designed to counteract the effects of IAP proteins, thus shifting the balance away from cancer cell survival and allowing apoptosis to proceed.
CUDC-427 was designed to mimic the endogenous IAP antagonist mitochondrial protein second mitochondria-derived activator of caspases/direct IAP-binding protein (Smac/DIABLO) that is released into the cytoplasm in response to pro-apoptotic stimuli. CUDC-427 has demonstrated single-agent and combination anti-tumor activity in mouse xenograft tumor models when administered orally on a daily schedule, and IND-enabling safety studies have shown it to be well tolerated when dosed daily by oral administration, potentially enabling sustained target inhibition.
In October 2010, an open-labeled, uncontrolled, dose-escalation, Phase I clinical trial of CUDC-427 (NCT01226277; IAM4914g) began in patients with refractory solid tumors or lymphoma. Genentech recently completed this Phase I clinical trial in which 42 people received daily oral doses of CUDC-427 for two weeks, followed by a one week rest period. This 21-day cycle is repeated until disease progression or study discontinuation for any other reason. The primary endpoints of the study include evaluating the safety and tolerability and the pharmacokinetics of CUDC-427 in people with solid tumors or lymphoma and determining the maximum-tolerated-dose and a potential recommended dose for further clinical studies. Secondary endpoints include a preliminary assessment of anti-tumor activity of CUDC-427 and evaluating pharmacodynamic markers. Genentech plans to present full study results at a medical conference in mid-2013. Please refer to http://www.clinicaltrials.gov for additional study details.
About Inhibitor of Apoptosis Proteins
Impairment of programmed cell death or apoptosis often contributes to the formation and progression of cancer, and evasion of apoptosis is one of the primary strategies by which cancer cells develop resistance to anticancer therapies. Inhibitor of apoptosis (IAP) proteins are a family of functionally and structurally related proteins which include X-linked IAP (XIAP), cellular IAPs (cIAP1 and cIAP2), and melanoma IAP (ML-IAP). They confer protection from death-inducing stimuli by exerting a range of biological activities that promote cancer cell survival and proliferation. Some even directly inhibit caspases, critical players in the execution of apoptosis.
Mutations, amplifications and chromosomal translocations of IAP genes are associated with various solid and hematologic cancer types, and increased IAP expression has been associated with an unfavorable prognosis and poor outcome for patients. As a consequence, IAP proteins are considered promising molecular targets for anticancer therapy.
Antibody Effective Against Norovirus
Antibody Effective Against Norovirus
Researchers have released data showing that a monoclonal antibody can neutralize human norovirus. Norovirus causes roughly 20 million cases of acute diarrhea and vomiting annually in the United States, alone. It is also responsible for roughly 800 deaths annually.
FULL STORY
What is Norovirus?
Norovirus is a stomach bug that sets in within 10 hours of transmission and usually lasts up to three days. It is completely different from the flu in that only your stomach is affected. While most people recover completely after three days, norovirus is more serious for young children, the elderly and people with other serious health conditions. Every year 70,000 people are hospitalized and 800 deaths are caused by the virus.
What are the symptoms?
The most common symptoms of norovirus include stomach pain, vomiting, diarrhea and nausea. Some people also experience a low-grade fever, headache and body ache. Because it is common to have continued vomiting and diarrhea during the three days of illness, dehydration is another concern for those affected.
How do you get it?
Norovirus is spread through direct contact with an infected person’s vomit or feces. Most commonly, unwashed hands can be attributed to spreading the virus through surfaces or food. The virus spreads quickly in enclosed spaces like cruise ships, nursing homes and schools.
What is the treatment?
Unfortunately, there are no medications to treat norovirus. Health care providers say the best thing to do is try to stay hydrated, rest and wait for the virus to run its course. People who are unable to keep fluids down may need to receive fluids intravenously.
How can you protect yourself?
Hand washing is the best defense against the norovirus, since no one is immune to the always-changing strains of the virus. However, new research has found hand sanitizers are not affective in killing the virus. Avoid direct contact with anyone who is infected and pay close attention to cleaning and preparing food. Also, anyone who is infected should not prepare food. Use disinfectants to wipe down all surfaces that have come in contact with someone who is infected. Also, launder infected clothes immediately on the longest wash cycle to help from spreading the virus.
Actavis submits ANDAs for two more generic version of Bayer’s Safyral and Fresenius Kabi’s Diprivan (propofol) injection
Actavis submits ANDAs for two more generic version of
Bayer’s Safyral and
Fresenius Kabi’s Diprivan (propofol) injection
Actavis has filed for US approval for generic versions of a contraceptive and a sedative/anaesthetic.http://www.gabionline.net/Generics/News/Actavis-submits-ANDAs-for-two-more-generics
Biosimilars applications under review by EMA – 2013 Q2
The European Medicines Agency (EMA) is the body responsible for approval of biosimilars within the EU. A legal framework for approving biosimilars was established in 2003. Approval of biosimilars is based on an abbreviated registration process, which allows biosimilars manufacturers to provide a reduced package of information compared to originator drugs, provided they can prove ‘similarity’ to the originator or ‘reference drug’.
read all at
http://www.gabionline.net/Biosimilars/General/Biosimilars-applications-under-review-by-EMA-2013-Q2
First biosimilar filgrastims launched in Japan
International nonproprietary name: Filgrastim
Chemical name: N-L- Methionyl colony-stimulating factor (human genetically engineered); non-glycated protein consisted of 175 amino acids.
Chemical name: N-L- Methionyl colony-stimulating factor (human genetically engineered); non-glycated protein consisted of 175 amino acids.
Filgrastim is a granulocyte colony-stimulating factor (G-CSF) analog used to stimulate the proliferation and differentiation of granulocytes.[1] It is produced by recombinant DNA technology. The gene for human granulocyte colony-stimulating factor is inserted into the genetic material of Escherichia coli. The G-CSF then produced by E. coli is different from G-CSF naturally made in humans.
Hematopoietic growth factor. Interacting with receptors on the surface of hematopoietic cells it regulates production and release of neutrophils from the bone marrow to the peripheral blood. Dose dependant number growth of neutrophils with normal or increased functional activity is passing for 24 hours.
Filgrastim is marketed under several brand names, including Neupogen (Amgen), Imumax(Abbott Laboratories), Grafeel (Dr. Reddy’s Laboratories), Neukine (Intas Biopharmaceuticals), Emgrast (Emcure Pharmaceuticals), Religrast (Reliance Life Sciences), Zarzio (Sandoz), Nufil (Biocon) and others.
Apricus Biosciences is currently developing and testing a product under the brand nameNupen which can deliver filgrastim through the skin to improve post-chemotherapy recovery of neutrophil counts.
Filgrastim is also used to increase the number of hematopoietic stem cells in the blood before collection by leukapheresis for use in hematopoietic stem cell transplantation.Filgrastim is used to treat neutropenia,[2] stimulating the bone marrow to increase production of neutrophils. Causes of neutropenia include chemotherapy and bone marrow transplantation.
Filgrastim should not be used in patients with known hypersensitivity to E. coli-derived proteins.
The most commonly observed adverse effect is mild-to-moderate bone pain after repeated administration and local skin reactions at the site of injection.[3] Other observed adverse effects include serious allergic reactions (including a rash over the whole body, shortness of breath, wheezing, dizziness, swelling around the mouth or eyes, fast pulse, and sweating), ruptured spleen (sometimes resulting in death), alveolar hemorrhage, acute respiratory distress syndrome, and hemoptysis.[3] Severe sickle cell crises, in some cases resulting in death, have been associated with the use of filgrastim in patients with sickle cell disorders.[4]
Drug interactions between filgrastim and other drugs have not been fully evaluated. Drugs which may potentiate the release of neutrophils‚ such as lithium‚ should be used with caution.
Increased hematopoietic activity of the bone marrow in response to growth factor therapy has been associated with transient positive bone imaging changes; this should be considered when interpreting bone-imaging results.[5]
Filgrastim has not been studied in pregnant women and its effects on unborn babies is unknown. If taking filgrastim while pregnant, it is possible that traces of the drug could be found in the baby’s blood. It is not known if the drug can get into human breast milk.
- Beveridge, R. A.; Miller, J. A.; Kales, A. N.; Binder, R. A.; Robert, N. J.; Harvey, J. H.; Windsor, K.; Gore, I. et al. (1998). “A Comparison of Efficacy of Sargramostim (Yeast-Derived RhuGM-CSF) and Filgrastim (Bacteria-Derived RhuG-CSF) in the Therapeutic Setting of Chemotherapy-Induced Myelosuppression”. Cancer Investigation 16 (6): 366–373. doi:10.3109/07357909809115775.PMID 9679526. edit
- Crawford, J.; Glaspy, J. A.; Stoller, R. G.; Tomita, D. K.; Vincent, M. E.; McGuire, B. W.; Ozer, H. (2005). “Final Results of a Placebo-Controlled Study of Filgrastim in Small-Cell Lung Cancer: Exploration of Risk Factors for Febrile Neutropenia”. Supportive Cancer Therapy 3 (1): 36–46. doi:10.3816/SCT.2005.n.023. PMID 18632435. edit
- Neupogen “Neupogen: Patient Information Leaflet”. Amgen. Retrieved 24 June 2013.
- “NEUPOGEN® Patient Guide”. Amgen. Retrieved 24 June 2013.
- “Neupogen”. RxList. 4 June 2012. Retrieved 23 June 2013.
- Budiono Santoso; Chris J. van Boxtel; Boxtel, Christoffel Jos van (2001). Drug benefits and risks: international textbook of clinical pharmacology. New York: Wiley. ISBN 0-471-89927-5.
- “Neupogen information”. Retrieved 20 October 2005.
Genentech announced positive results from the Phase 3 CLL11 study, Leukemia Trial
Afutuzumab
Obinutuzumab (GA101)
Genentech announced positive results from the Phase 3 CLL11 study. At a pre-planned interim analysis, an independent data monitoring committee determined that the study met its primary endpoint showing that GA101 plus chlorambucil helped people live significantly longer without their disease worsening (progression-free survival; PFS) compared to Rituxan (rituximab) plus chlorambucil.
The CLL11 study is being conducted in cooperation with the German CLL Study Group (GCLLSG). These final data were reached well ahead of the target completion date in 2014 as a result of the magnitude of difference seen between the two study arms.
Afutuzumab is a monoclonal antibody being developed by Hoffmann-La Roche Inc. for the treatment of lymphoma.[1] It acts as an immunomodulator.[2][3] It was renamed obinutuzumab in 2009.[4]
Class/mechanism: Glyco-engineered anti-CD20 IgG1 type II monoclonal antibody. Engineered with a modified elbow hinge residue (valine instead of leucine at Kabat position 11) and a glyco-engineered Fc region, which is postulated to enhance its immunomodulatory effect.[1]
Route: IV
Extravasation: no information
For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer.
- Robak, T (2009). “GA-101, a third-generation, humanized and glyco-engineered anti-CD20 mAb for the treatment of B-cell lymphoid malignancies”. Current opinion in investigational drugs (London, England : 2000) 10 (6): 588–96. PMID 19513948.
- Statement On A Nonproprietary Name Adopted By The Usan Council – Afutuzumab, American Medical Association.
- International Nonproprietary Names for Pharmaceutical Substances (INN), World Health Organization.
- International Nonproprietary Names for Pharmaceutical Substances (INN), World Health Organization.
| FULL STORYread all |
Alkermes unveils three new drug candidates
Alkermes has unveiled three new drug candidates, including: a monomethyl fumarate (MMF) prodrug programme for the treatment of multiple sclerosis; ALKS 7106 for the treatment of pain; and RDB 1419, a cancer immunotherapy candidate based on interleukin-2 (IL-2) and its receptors, Alkermes’ first proprietary biologic.
According to Alkermes, these drug candidates demonstrate the company’s focus on unmet medical needs in specific patient populations and show the productivity of its expanded R&D capabilities.
read all at
http://www.manufacturingchemist.com/news/article_
page/Alkermes_unveils_three_new_drug_candidates/90167
FDA Approves New Drug to Treat Nephropathic Cystinosis
CHICAGO—The U.S. Food and Drug Administration (FDA) has recently approved PROCYSBI(cysteamine bitartrate), a delayed release capsule for treating nephropathic cystinosis in adults and children 6 years and older.
Ann and Robert H. Lurie Children’s Hospital of Chicago served as one of three United States sites for the landmark study and patients came from all over North America to be seen by lead investigator, Craig B Langman, M.D., The Isaac A Abt, M.D. professor of Kidney Diseases at Northwestern University Feinberg School of Medicine and head of Kidney Diseases at Lurie Children’s
New Drug Approvals 