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Small molecule drug	1

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5-HT2A receptor(Serotonin 2a (5-HT2a) receptor)	1

We evaluated the capacity of freshly isolated blood monocytes to mediate antibody-dependent cellular-mediated cytotoxicity (ADCC) in cooperation with murine anti-tumor monoclonal antibodies (MAbs). Blood monocytes isolated from most donors by adherence selection to fibronectin-coated plastic surfaces and subsequently depleted of natural killer/killer (NK/K) cells exhibited significant ADCC activity against tumor cell lines in combination with an IgG3 antitumor MAb (BR55-2). However, significant variation in ADCC competence was observed among donors. Culture parameters influencing monocyte ADCC activity were evaluated and optimized. The influence of MAb isotype on ADCC capacity of anti-tumor MAbs was also evaluated using anti-tumor class-switch variant hybridoma proteins and a panel of anti-tumor MAbs. MAbs of the IgG2a and IgG3 subclasses exhibited high ADCC potential, whereas MAbs of the IgG2b subclass exhibited no ADCC activity. One of two IgG1 MAbs tested exhibited high ADCC activity with monocyte effectors. The role of monocytes or macrophages in tumor remission of cancer patients undergoing MAb immunotherapy is not known. However, correlative studies of monocyte ADCC capacity and responsiveness of cancer patients to MAb immunotherapy may help to establish the role of these effectors in MAb-mediated tumor remissions.

01 Jan 1988·Arthritis & Rheumatism

Interleukin‐1 activates phospholipase a₂ IN HUMAN SYNOVIAL CELLS

Article

Author: Gilman, Steven C. ; Chang, Joseph ; Mochan, Eugene ; Uhl, Joanne ; Zeigler, Pamela R.

AbstractInterleukin‐1 (IL‐1) treatment of synovial cells from rheumatoid arthritis and osteoarthritis patients resulted in a dose‐dependent secretion of phospholipase A2 (PLA2). IL‐1 also stimulated prostaglandin E2 and plasminogen activator synthesis, in parallel with PLA2 activation; all 3 were detectable within 6 hours of IL‐1 treatment and peaked by 24 hours. Synovial cell PLA2 required calcium (5 mM) and a neutral pH (7.5) for maximal activity and appears similar to the PLA2 in synovial fluid, which has been described previously. We conclude that PLA2 can be induced by IL‐1, and its secretion may contribute significantly to the inflammatory actions of IL‐1.

01 Feb 1986·British Journal of Pharmacology

Investigation into the cardioregulatory properties of the α₁‐adrenoceptor blocker indoramin

Article

Author: Todd, M. H. ; Shepperson, N. B. ; Pierce, Vanessa ; Waterfall, J. F.

The cardioregulatory properties of the α1‐adrenoceptor blocker indoramin have been compared with those of prazosin in the anaesthetized rat. The effects of autonomic blockade on heart rate responses evoked by these two agents and their effects on blood pressure and heart rate after peripheral or central administration have been compared.

Cumulative administration of indoramin (0.8–25.6 mg kg−1 i.v.) evoked significant decreases in arterial blood pressure and a concomitant bradycardia. Pithing or autonomic blockade, by pretreatment with a combination of practolol and bilateral vagotomy, prevented the bradycardia evoked by indoramin (0.8–3.2 mg kg−1 i.v.). Atropine sulphate pretreatment abolished the bradycardia until a cumulative dose of 25.6 mg kg−1 (i.v.) of indoramin had been reached. Bilateral vagotomy, intravenous administration of atropine methylnitrate or practolol pretreatment attenuated the bradycardia.

Prazosin (0.02–0.64 mg kg−1 i.v.) evoked a fall in arterial blood pressure of similar magnitude to that observed following indoramin. A bradycardia was evoked only at a relatively high dose (0.64 mg kg−1 i.v.).

Intracisternal injection of indoramin or prazosin evoked bradycardia and hypotension at a dose which had no effect after intravenous injection (25 μg). Intracerebroventricular injection of indoramin (25 μg) had no significant effect on heart rate or blood pressure compared to control values, whereas prazosin (25 μg) evoked a significant tachycardia and hypotension.

It is concluded that the bradycardia evoked by indoramin in the rat is not due to a direct action on the heart except possibly at high doses. Central α1‐adrenoceptor blockade, possibly in the brainstem region, results in a bradycardia and this may explain the lack of reflex tachycardia following the administration of indoramin.

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Pipeline

Pipeline Snapshot as of 20 May 2025

The statistics for drugs in the Pipeline is the current organization and its subsidiaries are counted as organizations,Early Phase 1 is incorporated into Phase 1, Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3

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