M1 receptor agonists(Muscarinic acetylcholine receptor M1 agonists), M2 receptor antagonists(Muscarinic acetylcholine receptor M2 antagonists), M3 receptor antagonists(Muscarinic acetylcholine receptor M3 antagonists)

Therapeutic Areas

Nervous System DiseasesUrogenital Diseases

Active Indication-

Inactive Indication

Alzheimer DiseaseUrinary Incontinence

Originator Organization

H. Lundbeck A/S

Active Organization-

Inactive Organization

Allergan Ltd. (Ireland)

H. Lundbeck A/SForest Laboratories, Inc.

Drug Highest PhaseDiscontinuedPhase 2

First Approval Date-

Regulation-

Structure/Sequence

Molecular FormulaC9H15N5

InChIKeyRNMOMKCRCIRYCZ-UHFFFAOYSA-N

CAS Registry120241-31-8

View All Structures (2)

100 Clinical Results associated with Alvameline Tartrate

100 Translational Medicine associated with Alvameline Tartrate

100 Patents (Medical) associated with Alvameline Tartrate

Literatures (Medical) associated with Alvameline Tartrate

01 Sep 1997·Experimental NeurologyQ2 · MEDICINE

Chronic Administration of a Partial Muscarinic M1Receptor Agonist Attenuates Decreases in Forebrain Choline Acetyltransferase Immunoreactivity Following Experimental Brain Trauma

Q2 · MEDICINE

Article

Author: Hamm, Robert J. ; Pike, Brian R.

Lu 25-109-T is a partial muscarinic M1 receptor agonist with antagonistic effects at presynaptic M2 autoreceptors and has been shown to improve cognitive function following traumatic brain injury (TBI) in rats. This investigation examined the effects of TBI on basal forebrain choline acetyltransferase immunoreactivity (ChAT-IR) following daily administration of saline or 15 mumol/kg Lu 25-109-T. Rats received a moderate (2.1 +/- 0.1 atm) level of central fluid percussion TBI or were surgically prepared but not injured and were injected (sc) with saline or drug on Days 1-15 postinjury. Rats were sacrificed following the last daily injection, and sections were collected through the basal forebrain and processed for ChAT-IR. TBI caused a significant reduction in ChAT-IR neuronal density in saline- and Lu 25-109-T-treated rats with a 13% and 5% decrease in the medial septal nucleus (MSN), a 48 and 23% decrease in the vertical limb nucleus of the diagonal band (VDB), and a 51 and 28% decrease in the nucleus basalis magnocellularis (NBM), respectively. However, Lu 25-109-T significantly attenuated the injury-induced reductions in ChAT-IR. Loss in ChAT-IR neuronal density is not thought to result from cell death as parallel cresyl violet-stained sections indicated no decrease in neuronal cell density in the MSN, VDB, or NBM. These results support the hypothesis that increasing cholinergic tone during the recovery period after TBI will restore cholinergic function impaired by brain trauma.

01 Aug 1997·Pharmacology Biochemistry and BehaviorQ4 · PSYCHOLOGY

Activating the Posttraumatic Cholinergic System for the Treatment of Cognitive Impairment Following Traumatic Brain Injury

Q4 · PSYCHOLOGY

Article

Author: Brian R Pike ; Robert J Hamm

Cognitive impairment after traumatic brain injury (TBI) is correlated with decreased cholinergic markers of neuronal viability. The purpose of this experiment was to test the hypothesis that pharmacological activation of the muscarinic cholinergic system during the recovery period after TBI will improve cognitive performance. LU 25-109-T is a partial muscarinic M1 agonist that also acts as an antagonist at presynaptic M2 autoreceptors (thus increasing ACh release). Injured rats were injected subcutaneously daily for 15 days with either 0.0, 3.6, or 15 mumol/kg of LU 25-109-T beginning 24 h after a receiving a moderate (2.1 +/- 0.1 atm) level of central fluid percussion brain injury. Cognitive performance was assessed on days 11-15 postinjury in a Morris water maze (MWM). Injured rats treated with 15 mumol/kg, but not those treated with 3.6 mumol/kg, showed a significant improvement (p < 0.01) in MWM performance as compared with injured vehicle-treated rats. This result supports the hypotheses that a decrease in posttraumatic cholinergic neurotransmission contributes to TBI-induced cognitive deficits and that increasing cholinergic tone during the recovery period following TBI will improve cognitive performance.

01 Jan 1968·Farmatsevtychnyi zhurnal

[Spectrophotometric determination of dibazol and mercazolyl].

Article

Author: Verzina, G V ; Shakh, Ts I

100 Deals associated with Alvameline Tartrate

External Link

KEGG	Wiki	ATC	Drug Bank
-	Alvameline Tartrate	-	-

R&D Status

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Alzheimer Disease	Phase 2	DK	H. Lundbeck A/S	-
Urinary Incontinence	Phase 2	US	Forest Laboratories, Inc.	-
Urinary Incontinence	Phase 2	-	H. Lundbeck A/S	-
Urinary Incontinence	Phase 2	-	Allergan Ltd. (Ireland)	-

Clinical Result

Indication

Phase

Evaluation

View All Results

Translational Medicine

Boost your research with our translational medicine data.

view full example data

Deal

Boost your decision using our deal data.

view full example data

Core Patent

Boost your research with our Core Patent data.

view full example data

Clinical Trial

Identify the latest clinical trials across global registries.

view full example data

Approval

Accelerate your research with the latest regulatory approval information.

view full example data

Regulation

Understand key drug designations in just a few clicks with Synapse.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis