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Restrict the search for
vitamin a palmitate
to a specific field?
Status:
Investigational
Source:
INN:relicpixant [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:cenacitinib [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:vormatrigine [INN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
INN:soxataltinib [INN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT04055649: Phase 2 Interventional Recruiting Malignant Ovarian Epithelial Tumor
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
TIC10 (TIC10 isomer or ONC201 isomer) is a potent, orally active, and stable small molecule and is an efficacious antitumor therapeutic agent that acts on tumor cells and their microenvironment to enhance the concentrations of the endogenous tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). The isomeric structure of TIC10/ONC201 is critical to its activity: anti-cancer activity is associated with the angular structure and not the linear TIC10 isomer. TIC10 transcriptionally induces a sustained up-regulation TRAIL in tumors and normal cells in a p53-independent manner. TIC10 inactivates kinases Akt and extracellular signal-regulated kinase (ERK), leading to the translocation of Foxo3a into the nucleus, where it binds to the TRAIL promoter to up-regulate gene transcription. TIC10 crosses the blood-brain barrier. TIC10 treatment caused tumor regression in the HCT116 p53−/− xenograft, RKO human colon cancer xenograft–bearing mice and human triple-negative breast cancer xenografts and significantly prolonged the survival of Eμ-myc transgenic mice, which spontaneously develop metastatic lymphoma from weeks 9 to 12 of age by 4 weeks.
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:frevecitinib [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
CX3CR1 antagonist 18a (AZD8797) is the first potent selective and orally available CX3CR1 allosteric antagonist. AZD8797 is able to non-competitively displace and block CX3CL1 from binding CX3CR1 through an allosteric binding mechanism of action. AZD8797 effects G-protein signaling and β-arrestin recruitment in a biased way. Starting treatment with AZD8797 either before or after onset of disease reduced the clinical symptoms and pathological signs of experimental autoimmune encephalomyelitis (EAE) (the model of multiple sclerosis) in a concentration-dependent manner. CX3CR1 (Fractalkine) signaling probably contributes to the growth and spread of tumors and the pain that often affects cancer patients. Kancera will now evaluate how efficiently the Fractalkine inhibitor AZD8797 may stop tumor growth and relieve severe pain.
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:tibremciclib [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
