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Restrict the search for
tolterodine
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There is one exact (name or code) match for tolterodine
Status:
US Approved Rx
(2000)
Source:
NDA021228
(2000)
Source URL:
First approved in 1998
Source:
NDA020771
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Tolterodine is competitive muscarinic receptors M3 and M2 antagonist. It was sold under trade names detrol for the treatment of overactive bladder with symptoms of urge urinary incontinence. Both urinary bladder contraction and salivation are mediated via cholinergic muscarinic receptors. After oral administration, tolterodine is metabolized in the liver, resulting in the formation of the 5-hydroxymethyl derivative, a major pharmacologically active metabolite. The 5-hydroxymethyl metabolite, which exhibits an antimuscarinic activity similar to that of tolterodine, contributes significantly to the therapeutic effect. Both tolterodine and the 5-hydroxymethyl metabolite exhibit a high specificity for muscarinic receptors, since both show negligible activity and affinity for other neurotransmitter receptors and other potential cellular targets, such as calcium channels. Tolterodine has a pronounced effect on bladder function. The main effects of tolterodine at 1 and 5 hours were an increase in residual urine, reflecting an incomplete emptying of the bladder, and a decrease in detrusor pressure. These findings are consistent with an antimuscarinic action on the lower urinary tract.
Status:
US Approved Rx
(2000)
Source:
NDA021228
(2000)
Source URL:
First approved in 1998
Source:
NDA020771
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Tolterodine is competitive muscarinic receptors M3 and M2 antagonist. It was sold under trade names detrol for the treatment of overactive bladder with symptoms of urge urinary incontinence. Both urinary bladder contraction and salivation are mediated via cholinergic muscarinic receptors. After oral administration, tolterodine is metabolized in the liver, resulting in the formation of the 5-hydroxymethyl derivative, a major pharmacologically active metabolite. The 5-hydroxymethyl metabolite, which exhibits an antimuscarinic activity similar to that of tolterodine, contributes significantly to the therapeutic effect. Both tolterodine and the 5-hydroxymethyl metabolite exhibit a high specificity for muscarinic receptors, since both show negligible activity and affinity for other neurotransmitter receptors and other potential cellular targets, such as calcium channels. Tolterodine has a pronounced effect on bladder function. The main effects of tolterodine at 1 and 5 hours were an increase in residual urine, reflecting an incomplete emptying of the bladder, and a decrease in detrusor pressure. These findings are consistent with an antimuscarinic action on the lower urinary tract.
Status:
US Approved Rx
(2023)
Source:
ANDA204973
(2023)
Source URL:
First approved in 2008
Source:
NDA022030
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Desfesoterodine is an active metabolite of antimuscarinic drugs for the treatment of overactive bladder fesoterodine and tolterodine. In contrast to the cytochrome P450 (CYP) 2D6-mediated metabolism of tolterodine, desfesoterodine formation from fesoterodine occurs via ubiquitous nonspecific esterases. Serum levels of the desfesoterodine in humans are generally comparable to those of tolterodine following oral administration of the parent compound. The pharmacological in vitro and in vivo profiles of desfesoterodine are almost identical to those of tolterodin. The potent antimuscarinic action of desfesoterodine on the urinary bladder was confirmed in the in vivo studies and, like tolterodine, desfesoterodine was significantly more potent in inhibiting bladder contractions than salivation in the anaesthetised cat. Desfesoterodine is more potent than tolterodine in vivo. The apparent difference in potency in vivo might be explained by the degree of serum protein binding of the two compounds. The fraction of unbound drug in serum is larger for desfesoterodine than for tolterodine. Desfesoterodine may contribute to the therapeutical action of tolterodine.
Status:
US Approved Rx
(2010)
Source:
ANDA091575
(2010)
Source URL:
First approved in 2004
Source:
SANCTURA by ALLERGAN
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Trospium is an antispasmodic, antimuscarinic agent indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency. Receptor assays showed that trospium has negligible affinity for nicotinic receptors as compared to muscarinic receptors at concentrations obtained from therapeutic doses. Trospium antagonizes the effect of acetylcholine on muscarinic receptors in cholinergically innervated organs. Its parasympatholytic action reduces the tonus of smooth muscle in the bladder. Trospium is marketed under the brand name Sancturain the US, Tropez OD in India,Trosec in Canada, Regurin and Flotros in the United Kingdom and Spasmex in Germany, Russia, Turkey, Argentina, Chile and Israel.
Status:
US Approved Rx
(2024)
Source:
ANDA204374
(2024)
Source URL:
First approved in 2004
Source:
NDA021518
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Solifenacin is a competitive muscarinic acetylcholine receptor antagonist. The binding of acetylcholine to these receptors, particularly the M3 receptor subtype, plays a critical role in the contraction of smooth muscle. By preventing the binding of acetylcholine to these receptors, solifenacin reduces smooth muscle tone in the bladder, allowing the bladder to retain larger volumes of urine. It is FDA approved for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency. Common adverse reactions include constipation, Xerostomia. Inhibitors of CYP3A4 may increase the concentration of Solifenacin. Vice versa, CYP3A4 Inducers decrease concentration.
Status:
US Approved Rx
(2001)
Source:
NDA021146
(2001)
Source URL:
First marketed in 1921
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Atropine inhibits the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves, and on smooth muscles which respond to endogenous acetylcholine but are not so innervated. As with other antimuscarinic agents, the major action of atropine is a competitive or surmountable antagonism which can be overcome by increasing the concentration of acetylcholine at receptor sites of the effector organ (e.g., by using anticholinesterase agents which inhibit the enzymatic destruction of acetylcholine). The receptors antagonized by atropine are the peripheral structures that are stimulated or inhibited by muscarine (i.e., exocrine glands and smooth and cardiac muscle). Responses to postganglionic cholinergic nerve stimulation also may be inhibited by atropine but this occurs less readily than with responses to injected (exogenous) choline esters. Atropine is relatively selective for muscarinic receptors. Its potency at nicotinic receptors is much lower, and actions at non-muscarinic receptors are generally undetectable clinically. Atropine does not distinguish among the M1, M2, and M3 subgroups of muscarinic receptors.
Status:
US Approved OTC
Source:
21 CFR 331.11(m) antacid:tartrate-containing tartrate (acid or salt)
Source URL:
First marketed in 1921
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Tartaric acid is found in many plants such as grapes, tamarinds, pineapples, mulberries and so on. Wine lees (called mud in the US), the sediment collected during the fermentation of grapes, contains potassium bitartrate (potassium hydrogen tartrate) as its major component. L-(+)-tartaric acid is an enantiomer of tartaric acid. Twenty five years before the tetrahedral structure for carbon was proposed in 1874 to explain the optical activity and other properties of organic compounds, Louis Pasteur discovered the existence of enantiomerism in tartaric acid. L-(+)-tartaric acid is widely used in food and beverage as acidity regulator with E number E334.
