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Restrict the search for
sulfisoxazole acetyl
to a specific field?
Status:
Investigational
Class (Stereo):
CHEMICAL (ACHIRAL)
Caracemide is a nonspecific inhibitor of macromolecules affecting the synthesis of DNA, RNA, and proteins. Caracemide is an active inhibitor of ribonucleotide reductase as evidenced in the Novikoff tumor model. These inhibitory effects are concentration-dependent with 70 percent of DNA synthesis inhibited by a drug concentration of 1 mkM with a 4 h incubation. However, RNA and protein synthesis inhibition require a concentration of 50-100 mkM. DNA strand breaks were observed only at high in vivo concentrations of 100 mkM. The antineoplastic activity of caracemide was observed in the P388 murine model and in mammary (MX-I) and colon (CX-1) human tumor xenographs implanted in the subrenal capsules of athymic mice. In the MX-1 mammary tumor, a single daily injection provided greater activity than an intermittent schedule. Caracemide was inactive against murine L1210 leukemia, B16 melanoma, Lewis lung carcinoma, CD8FI mammary carcinoma and Colon 38. The toxicity on phase I studies was frequent but generally mild. Of note, significant central nervous system dysfunction manifested by lethargy, depression, and confusion occurred in some and was not predictable. In phase I studies Caracemide failed to demonstrate efficacy in patients with advanced renal cell cancer and advanced large bowel cancer.
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Class (Stereo):
CHEMICAL (ABSOLUTE)
Triletide is a tripeptide derivative which shows cytoprotective and antiulcerogenic activity. It is a thromboxane synthase inhibitor. Analysis of both individual and pooled data indicated that triletide was well absorbed after oral administration, with a lag time of 0.3 hours and the blood peak was reached after about 1.1 to 1.3 hours. Metabolization to desmethyl, desacetyl, desmethyl-desacetyl and hydroxylated derivatives plays a major role in the biotransformation of the drug and thus in its disappearance from blood, the distribution half-life being about 1 hour. A greater proportion of patients given the combination cimetidine and triletide was found to be endoscopically healed after treatment in comparison with those who had cimetidine alone (53% vs 40%). Intensity of symptoms decreased significantly faster and to a significantly greater extent in the same patients, as did antacid intake. Triletide appears to be equally well tolerated as, but significantly more effective than, aluminium hydroxide and magnesium hydroxide in relieving symptoms and promoting healing in patients with mild to moderate duodenal ulcer. There were no complaints of possible side-effects with either triletide treatment and no evidence of any significant changes in blood pressure, heart rate or routine haematology and haematochemistry investigations.
Status:
Investigational
Source:
INN:melogliptin [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Melogliptin (EMD 675992 or GRC 8200) is an orally bioavailable dipeptidyl peptidase IV (DPP IV) inhibitor. Melogliptin was undergoing phase II clinical trials at Glenmark Pharmaceuticals and Merck KGaA for the treatment of type 2 diabetes. The completed 12 week Phase IIb clinical trial in 494 patients with type 2 diabetes melogliptin improved glycemic control in patients with type 2 diabetes mellitus and exhibited excellent safety and tolerability profile.
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Burapitant (SSR-240,600) is a drug developed by Sanofi-Aventis which was one of the first compounds developed that acts as a potent and selective antagonist for the NK1 receptor. Burapitant inhibited the binding of radioactive substance P to tachykinin NK1 receptors in human lymphoblastic IM9 cells, human astrocytoma U373MG cells, and human brain cortex. It also showed a subnanomolar affinity for guinea pig NK1 receptors but was less potent on rat and gerbil NK1 receptors. Burapitant inhibited [Sar(9),Met(O2)(11)]substance P-induced inositol monophosphate formation in human astrocytoma U373MG cells. Burapitant (0.1-10 mg/kg i.p. or p.o.) antagonized the excitatory effect of i.c.v. infusion of [Sar(9),Met(O2)(11)]substance P (SP) on the release of acetylcholine in the striatum of anesthetized and awake guinea pigs. This antagonistic action was still observed after repeated administration of Burapitant (5 days, 10 mg/kg p.o., once a day). Burapitant (10 mg/kg i.p.) inhibited the phosphorylation of the cAMP response element-binding protein in various brain regions induced by i.c.v. administration of [Sar9,Met(O2)(11)]SP. While burapitant itself did not proceed beyond early clinical trials and was never developed for clinical use in humans, promising animal results from this and related compounds have led to a number of novel drugs from this class that has now been introduced into medical use.
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:taniborbactam [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
N-(4-Ethylphenyl)-3-(Hydroxymethyl)-N-Isobutyl-4-(Tetrahydro-2h-Pyran-4-Ylmethoxy)Benzenesulfonamide (also known as GSK2981278) is a highly potent and selective inverse agonist of RORγ under development for the topical treatment of psoriasis. Preclinical data showed that GSK2981278 significantly inhibited the production of the Th17 signature cytokines in multiple in vitro and human tissue‐based systems. GSK2981278 may block the transcriptional activity of RORγt, leading to local suppression of cytokine expression and ultimately, improvement in psoriasis. Unfortunately in phase I clinical trial clinical assessment results showed no improvement of psoriatic lesions following treatment with GSK2981278.
Status:
Investigational
Source:
NCT04671303: Phase 2 Interventional Unknown status Lung Cancer
(2021)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
AST-1306, also known as Allitinib, is an orally active potent, selective, irreversible inhibitor of the HER family of receptor tyrosine kinases. AST-1306 inhibits the enzymatic activities of wild-type epidermal growth factor receptor (EGFR) and ErbB2 as well as EGFR resistant mutant in both cell-free and cell-based systems. AST1306 potently suppressed tumor growth in ErbB2-overexpressing adenocarcinoma xenograft and FVB-2/N(neu) transgenic breast cancer mouse models. Allitinib is in Phase I clinical trial for the treatment of advanced solid tumors. Serious adverse effects detected were: diarrhea, dehydration and hyperbilirubinemia.
Status:
Investigational
Source:
NCT03525392: Phase 1 Interventional Terminated Pancreatic Ductal Adenocarcinoma
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
INN:sirpiglenastat [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
