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Restrict the search for
clindamycin phosphate
to a specific field?
Status:
Possibly Marketed Outside US
Source:
21 CFR 356
(2016)
Source URL:
First approved in 2016
Source:
21 CFR 356
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Phytonadiol sodium diphosphate is an antihaemorrhagic agent.
Status:
Possibly Marketed Outside US
Source:
21 CFR 356
(2016)
Source URL:
First approved in 2016
Source:
21 CFR 356
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Phytonadiol sodium diphosphate is an antihaemorrhagic agent.
Status:
Possibly Marketed Outside US
Source:
21 CFR 352
(2015)
Source URL:
First approved in 2015
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Possibly Marketed Outside US
Source:
21 CFR 352
(2015)
Source URL:
First approved in 2015
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Possibly Marketed Outside US
Source:
M021
(2014)
Source URL:
First approved in 2014
Source:
M021
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
21 CFR 356
(2014)
Source URL:
First approved in 2014
Source:
21 CFR 355
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
21 CFR 352
(2013)
Source URL:
First approved in 2013
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
21 CFR 348
(2013)
Source URL:
First approved in 2013
Source:
21 CFR 348
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
NCT03833089: Phase 4 Interventional Active, not recruiting Ventricular Arrhythmias and Cardiac Arrest
(2019)
Source URL:
First approved in 2012
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
21 CFR 352
(2011)
Source URL:
First approved in 2011
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Cyclic adenosine monophosphate (cAMP, cyclic AMP or 3'-5'-cyclic adenosine monophosphate) is a molecule that is important in many biological processes; it is derived from adenosine triphosphate (ATP) by adenylate cyclase located on the inner side of the plasma membrane and anchored at various locations in the interior of the cell. Around 1960 Earl W. Sutherland, Jr. showed that cyclic adenosine monophosphate (cAMP) serves as the secondary messenger within the cell. Cyclic AMP works by activating protein kinase A (PKA, or cAMP-dependent protein kinase). PKA is normally inactive as a tetrameric holoenzyme, consisting of two catalytic and two regulatory units with the regulatory units blocking the catalytic centers of the catalytic units. Cyclic AMP binds to specific locations on the regulatory units of the protein kinase, and causes dissociation between the regulatory and catalytic subunits, thus enabling those catalytic units to phosphorylate substrate proteins. It was discovered, that melanocytes require the RAS/RAF/MEK/ERK and the cyclic AMP (cAMP) signaling pathways to maintain the fine balance between proliferation and differentiation. cAMP suppressed CRAF activity in melanocytes and that was essential to suppress the oncogenic potential of CRAF in the cells. When RAS was mutated in melanoma, the cells switched their signaling from BRAF to CRAF. That switch was accompanied by dysregulated cAMP signaling, a step that was necessary to allow CRAF to signal to MEK. Thus, a fundamental switch in RAF isoform usage occurs when RAS was mutated in melanoma, and that occurs in the context of disrupted cAMP signaling. These data have important implications for the development of therapeutic strategies to treat this life-threatening disease.
