U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Showing 1 - 10 of 21 results

Status:
US Approved OTC
Source:
21 CFR 346.20(a) anorectal:keratolytic alcloxa
Source URL:
First approved in 1961
Source:
ALLANTOMIDE ALLANTOIN by NATIONAL DRUG
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)



Aldioxa is the generic name for the metal complex, dihydroxyaluminum allantoinate, which is hydrolyzed to allantoin and aluminium hydrate at the gastric mucosa. Aldioxa was approved in Japan to improve subjective symptoms or objective of gastric/duodenal ulcer and gastritis. It was discovered, that aldioxa ameliorates delayed gastric emptying through its antagonistic activity on the α-2 adrenergic receptor. The most commonly reported adverse reactions include constipation.
Status:
Investigational
Source:
NCT03525392: Phase 1 Interventional Terminated Pancreatic Ductal Adenocarcinoma
(2018)
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)


Conditions:

2,6-Pyridinedicarboxylic acid (PDC, Dipicolinic acid) is a major component of bacterial endospores, comprising 5-15% of the spore dry weight, and is important for spore stability and resistance properties. 2,6-Pyridinedicarboxylic acid and its derivatives are introduced as a new sensitizer system for enzyme-amplified lanthanide luminescence (EALL), a detection scheme for bioassays, which combines enzymatic amplification with time-resolved luminescence measurements of lanthanide chelates.
Status:
US Previously Marketed

Class (Stereo):
CHEMICAL (ACHIRAL)



Etidronate is a salt of etidronic acid (brand name Didronel, also known as EHDP) a diphosphonate, which is indicated for the treatment of symptomatic Paget’s disease of bone and in the prevention and treatment of heterotopic ossification following total hip replacement or due to spinal cord injury. Didronel is not approved for the treatment of osteoporosis. This drugs acts primarily on bone. It can inhibit the formation, growth, and dissolution of hydroxyapatite crystals and their amorphous precursors by chemisorption to calcium phosphate surfaces. Inhibition of crystal resorption occurs at lower doses than are required to inhibit crystal growth. Both effects increase as the dose increases. Preclinical studies indicate etidronate disodium does not cross the blood-brain barrier. Didronel is not metabolized. The amount of drug absorbed after an oral dose is approximately 3 percent. Bisphosphonates, when attached to bone tissue, are absorbed by osteoclasts, the bone cells that breaks down bone tissue. Although the mechanism of action of non-nitrogenous bisphosphonates has not been fully elucidated, available data suggest that they bind strongly to hydroxyapatite crystals in the bone matrix, preferentially at the sites of increased bone turnover and inhibit the formation and dissolution of the crystals. Other actions may include direct inhibition of mature osteoclast function, promotion of osteoclast apoptosis, and interference with osteoblast-mediated osteoclast activation. Etidronic acid may promote osteoclast apoptosis by competing with adenosine triphosphate (ATP) in the cellular energy metabolism. The osteoclast initiates apoptosis and dies, leading to an overall decrease in the breakdown of bone.
Status:
US Previously Marketed
First marketed in 1929

Class (Stereo):
CHEMICAL (ACHIRAL)


Dithranol (INN) or anthralin (USAN and former BAN) is a Hydroxyanthrone, anthracene derivative, medicine applied to the skin of people with psoriasis. It is available as creams, ointment or pastes in 0.1 to 2% strengths. The terms dithranol and anthralin are sometimes used synonymously. Anthralin cream is a topical antimitotic. It works by slowing the reproduction of skin cells, precise mechanism of anti-psoriatic action is not yet fully understood. However, numerous studies have demonstrated anti-proliferative and anti-inflammatory effects of anthralin on psoriatic and normal skin. The anti-proliferative effects of anthralin appear to result from both an inhibition of DNA synthesis as well as from its strong reducing properties. Recently, anthralin’s effectiveness as an anti-psoriatic agent has also been in part attributed to its abilities to induce lipid peroxidation and reduce levels of endothelial adhesion molecules which are markedly elevated in psoriatic patients. Unlike retinoids and PUVA, anthralin does not inhibit liver microsomal enzyme activity; consequently, the likelihood of adverse drug interactions is greatly reduced when other agents are administered concomitantly with anthralin.