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Biomedical subjects

U Thatte

Publications and source records attributed to U Thatte.

8 recordsLinked to original sources

AN-1792 (Elan).

Elan is developing AN-1792 as a potential immunotherapy for Alzheimer's disease (AD). It is currently in phase I trials [350904]. Phase II/III trials, running in parallel in the US and UK, are expected to start by the end of 2001 [375061], [383226], [401966]. American Home Products (AHP) are collaborating with Elan on research and development of an immunotherapy directed towards the beta-amyloid peptide, including AN-1792 and other potential products [361702]. In September 2000, an agreement was established between Elan, AHP and Cambridge Antibody Technology (CAT), whereby CAT are investigating anti-beta-amyloid human antibodies [394844]. In July 2000, Merrill Lynch predicted a possible late-2001 entry into pivotal trials with a potential NDA filing in 2004 [375966]. The clinical program is expected to take approximately four years [339630]. In April 2001, ABN Amro Hoare Govett stated that, if data from the large phase II trial expected to start late in 2001 satisfied FDA requirements, then Elan might be able to file an NDA in 2003, with a potential launch in 2005 [407412].

Adjuvants, Immunologic↗

NS-2330 (Neurosearch).

NeuroSearch is developing NS-2330, a compound that increases the activity of dopamine, norepinephrine and acetylcholine, as a potential therapy for Alzheimer's disease (AD) and Parkinson's disease (PD) [260782]. It is in phase II for AD [355341], and by March 2001 was also in a phase II tolerability trial in PD patients with dyskinesia. Phase III studies are expected to begin in the third quarter of 2002 [413151]. At this time, NeuroSearch was in licensing negotiations with a number of companies and had expected an agreement to be concluded within the first half of 2001 [401800]. In June 2001, NeuroSearch decided to continue the in-house development of NS-2330 provided that a capital increase could be effected on satisfactory terms [412065], [413151]. In August 2001, the company confirmed that it had raised these funds and phase III studies were planned for the third quarter of 2002 [420708]. In September 2001, WestLB Panmure predicted that NS-2330 had 12 and 15% probabilities of reaching market for its PD and AD indications, respectively. It also predicted that the drug would be launched in 2008 and 2007 for these indications, with market shares of 12.5 and 25%, respectively [423585].

Acetylcholine↗

Modulation of programmed cell death by medicinal plants.

Programmed cell death (apoptosis), a form of cell death, described by Kerr and Wyllie some 20 years ago, has generated considerable interest in recent years. The mechanisms by which this mode of cell death (seen both in animal and plant cells), takes place have been examined in detail. Extracellular signals and intracellular events have been elaborated. Of interest to the clinician, is the concentrated effort to study pharmacological modulation of programmed cell death. The attempt to influence the natural phenomenon of programmed cell death stems from the fact that it is reduced (like in cancer) or increased (like in neurodegenerative diseases) in several clinical situations. Thus, chemicals that can modify programmed cell death are likely to be potentially useful drugs. From foxglove, which gave digitalis to the Pacific Yew from which came taxol, plants have been a source of research material for useful drugs. Recently, a variety of plant extracts have been investigated for their ability to influence the apoptotic process. This article discusses some of the interesting data. The ability of plants to influence programmed cell death in cancerous cells in an attempt to arrest their proliferation has been the topic of much research. Various cell-lines like HL60, human hepatocellular carcinoma cell line (KIM-1), a cholangiocarcinoma cell-line (KMC-1), B-cell hybridomas, U937 a monocytic cell-line, HeLa cells, human lymphoid leukemia (MOLT-4B) cells and K562 cells have been studied. The agents found to induce programmed cell death (measured either morphologically or flow cytometrically) included extracts of plants like mistletoe and Semicarpus anacardium. Isolated compounds like bryonolic acid (from Trichosanthes kirilowii var. Japonica, crocin (from saffron) and allicin (from Allium sativum) have also been found to induce programmed cell death and therefore arrest proliferation. Even Chinese herbal medicine "Sho-saiko-to" induces programmed cell death in selected cancerous cell lines. Of considerable interest is the finding that Panax ginseng prevents irradiation-induced programmed cell death in hair follicles, suggesting important therapeutic implications. Nutraceuticals (dietary plants) like soya bean, garlic, ginger, green tea, etc. which have been suggested, in epidemiological studies, to reduce the incidence of cancer may do so by inducing programmed cell death. Soy bean extracts have been shown to prevent development of diseases like polycystic kidneys, while Artemisia asiatica attenuates cerulein-induced pancreatitis in rats. Interestingly enough, a number of food items as well as herbal medicines have been reported to produce toxic effects by inducing programmed cell death. For example, programmed cell death in isolated rat hepatocytes has been implicated in the hepatitis induced by a herbal medicine containing diterpinoids from germander. Other studies suggest that rapid progression of the betel- and tobacco-related oral squamous cell carcinomas may be associated with a simultaneous involvement of p53 and c-myc leading to inhibition of programmed cell death. Several mechanisms have been identified to underlie the modulation of programmed cell death by plants including endonuclease activation, induction of p53, activation of caspase 3 protease via a Bcl-2-insensitive pathway, potentiate free-radical formation and accumulation of sphinganine. Programmed cell death is a highly conserved mechanism of self-defense, also found to occur in plants. Hence, it is natural to assume that chemicals must exist in them to regulate programmed cell death in them. Thus, plants are likely to prove to be important sources of agents that will modulate programmed cell death.

Animals↗

Phenserine (Axonyx/NIH).

The National Institute on Aging (part of the National Institutes of Health) and Axonyx are investigating phenserine, a phenylcarbamate derivative of physostigmine, as a potential therapy for Alzheimer's disease (AD). The first phase I trial has been completed and, pending the results of a second phase Ib multiple dose study, a phase II efficacy study is scheduled for the fourth quarter of 2000 with completion expected during 2001. Axonyx filed an IND in 1998, which was approved in November 1999, and the company began phase I trials in December 1999 in the US. A second phase I trial, in a group of healthy, elderly volunteers, was initiated in February 2000. Phenserine reduces the production of the amyloid precursor protein and beta-amyloid in vitro. When added to human neuronal cells, Phenserine decreased the production of beta-amyloid peptide by 30%. Phenserine also showed small, non dose-dependent effects on learning in studies in aged rats and lower toxicity than physostigmine. Phenserine has a long duration of action (t(1/2) = 8 to 10 h).

Journal Article↗

CPC-211 (Questcor).

CPC-211 is under development by Questcor (formerly Cypros) as a potential treatment for stroke and closed head injury. Phase II trials have commenced for both indications. In June 1999, it was granted Orphan Drug status [329979]. In July 1998, CPC-211 received expedited development status by the FDA, following a review of the company's data and clinical plan for the development of CPC-211 to treat acute head injury [291130]. CPC-211 stimulates the action of pyruvate dehydrogenase, reducing the build up of lactic acid which may cause brain damage after stroke. It diverts the lactate production into acetyl-CoA which is a beneficial metabolite. CPC-211 crosses the blood-brain barrier. Preclinical studies involving both stroke and head injury models have shown that CPC-211 (25 to 200 mg/kg iv) effected a significant reduction in brain lactate levels [328231].

Journal Article↗

The Mexican poppy poisons the Indian mustard facts and figures.

Argemone seeds are mixed with mustard seeds either accidentally or purposefully, and, ingestion of this contaminated oil can lead to often fatal "epidemic dropsy". The liver, heart, kidney and lungs are the major target organs of the toxins (the alkaloids, sanguinarine and dihydrosanguinarine) and damage is mostly caused by free radical (singlet oxygen and hydroxyl radical) to the cell membranes. Treatment at present is mainly symptomatic but therapy with anti-secretory agents for glaucoma and anti-oxidants/free radical scavengers for systemic manifestations appear to be logical.

Chemical and Drug Induced Liver Injury↗

Apoptosis: clinical relevance and pharmacological manipulation.

Apoptosis, often synonymously used with the term 'programmed cell death', is an active, genetically controlled process that removes unwanted or damaged cells. Suppression, overexpression or mutation of a number of genes which orchestrate the apoptotic process are associated with disease. The diseases in which apoptosis has been implicated can be grouped into 2 broad groups: those in which there is increased cell survival (i.e. associated with inhibition of apoptosis) and those in which there is excess cell death (where apoptosis is overactive). Diseases in which there is an excessive accumulation of cells include cancer, autoimmune disorders and viral infections. Deprivation of trophic factors is known to induce apoptosis in cells dependent on them for survival. This fact has been exploited in the use of antiandrogens or antiestrogens in the management of prostate or breast cancer. Haemopoietic growth factors like granulocyte-macrophage colony stimulating factor (GM-CSF) or interleukin-3 prevent apoptosis in target cells and modulation of levels of these factors has been tried in the prevention of chemotherapy-induced myelosuppression. Until recently, it was thought that cytotoxic drugs killed target cells directly by interfering with some life-maintaining function. However, of late, it has been shown that exposure to several cytotoxic drugs with disparate mechanisms of action induces apoptosis in both malignant and normal cells. Physiological regulation of cell death is essential for the removal of potentially autoreactive lymphocytes during development and the removal of excess cells after the completion of an immune response. Recent work has clearly demonstrated that dysregulation of apoptosis may underlie the pathogenesis of autoimmune diseases by allowing abnormal autoreactive lymphocytes to survive. AIDS and neurodegenerative disorders like Alzheimer's or Parkinson's disease represent the most widely studied group of disorders where an excess of apoptosis has been implicated. Amyotrophic lateral sclerosis, retinitis pigmentosa, epilepsy and alcoholic brain damage are other neurological disorders in which apoptosis has been implicated. Apoptosis has been reported to occur in conditions characterised by ischaemia, e.g. myocardial infarction and stroke. The liver is a site where apoptosis occurs normally. This process has also been implicated in a number of liver disorders including obstructive jaundice. Hepatic damage due to toxins and drugs is also associated with apoptosis in hepatocytes. Apoptosis has also been identified as a key phenomenon in some diseases of the kidney, i.e. polycystic kidney, as well as in disorders of the pancreas like alcohol-induced pancreatitis and diabetes.

Acquired Immunodeficiency Syndrome↗