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Restrict the search for
amphotericin b
to a specific field?
Status:
Investigational
Source:
Br J Cancer. Apr 2016;114(9):986-94.: Phase 1 Human clinical trial Completed Neoplasms
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
The sesquiterpene lactone thapsigargin is found in the plant Thapsia garganica L., and is one of the major constituents of the roots and fruits of this Mediterranean species. In 1978, the first pharmacological effects of thapsigargin were established and the full structure was elucidated in 1985. Thapsigargin is a potent inhibitor of Sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) and is widely used to study Ca2+-signaling. Thapsigargin is a non-cell-type specific toxin with documented ability to kill a broad spectrum of cancer cell lines as well as normal endothelial cells, fibroblasts and osteoblasts. It induces a rapid and pronounced increase in the concentration of cytosolic calcium, due to blockade of the Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase (SERCA) pump to which it binds with high affinity. The increase in cytosolic calcium leads to induction of apoptosis and ensuing cell death. A prodrug, G-202 (mipsagargin) has been designed to target the blood vessels of cancer cells; the death of these blood vessels then leads to tumor necrosis. G-202 consists of a cytotoxic analog of thapsigargin coupled to a masking peptide which inhibits its biologic activity until proteolytic cleavage at the tumor site. The first clinical trials of this drug were initiated in 2008 for the treatment Advanced Solid Tumors.
Status:
Investigational
Source:
NCT00496353: Phase 1/Phase 2 Interventional Completed Neoplasm
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
The receptor tyrosine kinase c-Met is an attractive target for therapeutic blockade in cancer. MK-2461 is a novel ATP-competitive multitargeted inhibitor of activated c-Met, was synthesized by Merck and was investigated in phase I of clinical trial for the potential treatment of patients with advanced solid tumors.
Status:
Investigational
Source:
NCT03189992: Phase 1 Interventional Unknown status Malignant Tumor of Small Intestine Metastatic to Liver
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Cinobufotalin, the bufadienolide isolated from toad venom,
has displayed antitumor activities in many in vitro systems. It has been shown that cinobufotalin induced significant apoptosis in cultured human lymphoma U-937 cells. It induced DNA fragmentation, mitochondrial membrane
potential decrease, and reactive oxygen species (ROS)
production in U-937 cells. Cinobufotalin induces cytotoxic effect in cultured lung cancer cells. Cinobufotalin (1/5 mg/kg, i.p. twice
daily, for 7 days) significantly inhibited A549 xenograft growth in
mice. Further, same cinobufotalin administration improved mice
survival at week five. Cinobufotalin administration didn’t
significantly affect mice body weight, indicating the relative safety
of this regimen. Thus, cinobufotalin inhibits A549 xenograft
growth in vivo and improves mice survival.
Status:
Investigational
Source:
NCT03547115: Phase 1 Interventional Recruiting Follicular Lymphoma (FL)
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Voruciclib (also known as P1446A-05) is a flavone-based, potent and selective CDK 4/6 inhibitor with activity in multiple BRAF-mutant and wild type cell lines. It is currently in clinical trials in combination with BRAF inhibitor (PLX4032) to treat advanced BRAF-mutant melanoma. Voruciclib has significant inhibitory activity against cutaneous and uveal melanoma. Mechanistic studies revealed that P1446A-05 inhibits phosphorylation targets of CDK members, and induces cell cycle arrest and apoptosis irrespective of melanoma genotype or phenotype. Voruciclib Hydrochloride is in phase I clinical trials by Piramal Life Sciences for the treatment of chronic lymphocytic leukaemia and malignant melanoma.
Status:
Investigational
Source:
NCT02222363: Phase 1 Interventional Terminated Refractory Cancer
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
VLX600 - is a lipophilic cation-based triazinoindolyl-hydrazone compound and mitochondrial oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. VLX600 is designed to increase the efficacy of radiotherapy and to kill cancer cells that survive traditional chemotherapy. VLX 600 is a small molecule that inhibits deubiquitinating enzymes USP14 (a ubiquitin thiolesterase) and UCHL5 (a carboxypeptidase). Upon infusion, in normal cells and proliferating tumor cells where glucose is readily available, inhibition of OxPhos by VLX600 induces a hypoxia-inducible factor 1-alpha (HIF-1alpha)-dependent shift to, and an increase in glycolysis. Glycolysis alone does not produce enough energy to support the growth of tumor cells in this environment, and the induction of autophagy occurs. In the metabolically compromised tumor microenvironment, the availability of oxygen and glucose is limited due to poor vascularization and perfusion of tumor micro-areas. Tumor cells growing in this environment are thus unable to compensate for decreased mitochondrial function by increasing glycolysis. This leads to nutrient depletion, decreased energy production, induction of autophagy, tumor cell death and an inhibition of cell proliferation in quiescent tumor cells. Mitochondrial OxPhos, which is hyperactivated in cancer cells, plays a key role in the promotion of cancer cell proliferation. VLX-600 is in phase I clinical trials for the treatment of solid tumours. This compound was originally jointly discovered and developed by Vivolux and Karolinska Institute.
Status:
Investigational
Source:
NCT01832298: Phase 1 Interventional Completed Advanced Solid Tumor
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
HaiHe Biopharma (Shanghai HaiHe Pharmaceutical) is developing simmitecan, an ester pro-drug of chimmitecan for the treatment of cancer. Simmitecan is in phase I development for solid tumours and colorectal cancer in China. Simmitecan (L-P) is a water-soluble ester prodrug of chimmitecan (L-2-Z) with potent anti-tumor activities in different experimental animals. Chimmitecan，a novel CPT derivative, exhibited potent antitumor activities both in vitro and in vivo by inhibiting topoisomerase I.
Status:
Investigational
Source:
Hum Exp Toxicol. May 1996;15(5):369-75.: Not Applicable Human clinical trial Completed N/A
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Status:
Investigational
Source:
NCT00954538: Phase 1 Interventional Completed Alzheimer's Disease
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT03577509: Phase 1 Interventional Completed Invasive Fungal Disease
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
AMPHOTERICIN B CHOLESTERYL SULFATE COMPLEX (AMPHOTEC) is an antifungal medicine. AMPHOTEC® is a sterile, pyrogen-free, lyophilized powder for reconstitution and intravenous (IV) administration. AMPHOTEC consists of a 1:1 (molar ratio) complex of amphotericin B and cholesteryl sulfate. AMPHOTEC is indicated for the treatment of invasive aspergillosis in patients where renal impairment or unacceptable toxicity precludes the use of amphotericin B deoxycholate in effective doses, and in patients with invasive aspergillosis where prior amphotericin B deoxycholate therapy has failed. The active ingredient of AMPHOTEC, amphotericin B, is a polyene antibiotic that acts by binding to sterols (primarily ergosterol) in cell membranes of sensitive fungi, with subsequent leakage of intracellular contents and cell death due to changes in membrane permeability. Amphotericin B also binds to the sterols (primarily cholesterol) in mammalian cell membranes, which is believed to account for its toxicity in animals and humans. AMPHOTEC is active against Aspergillus spp (A. fumigatus, A. flavus), Candida spp (C. albicans, C. krusei, C. parapsilosis, C. tropicalis), Cryptococcus neoformans, and Blastomyces dermatitidis. Active against most fungi with the notable exceptions of Candida lusitaniae, Trichosporon beigelii, Aspergillus terreus (some isolates), Pseudallescheria boydii, Malassezia furfur and Fusarium spp.
The lipid formulations are designed to reduce binding of amphotericin to mammalian cell membranes, therefore reducing toxicities.
Status:
Investigational
Source:
NCT01908699: Phase 3 Interventional Completed Pulmonary Arterial Hypertension
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Esuberaprost (314d) is an active enantiomer of beraprost, a prostacyclin analog. The pharmacologic action of esuberaprost is mediated by specifically binding to PGI2 receptors in smooth muscle cells (the blood vessel’s endothelium) and platelets. Upon binding, the compound widened blood vessels, preventing the formation of blood clots, and lowering blood pressure in the lungs. As a result, it was expected to improve the symptoms of pulmonary arterial hypertension. United Therapeutics announced it has ended its Phase 3 BEAT trial testing esuberaprost as an add-on therapy to its product Tyvaso (inhaled treprostinil) for clinically symptomatic patients with pulmonary arterial hypertension (PAH). According to a company press release, the study failed to reach its main endpoint of delaying the time to first clinical worsening events.
