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Restrict the search for
sulfisoxazole acetyl
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Status:
Designated
Source:
EU-Orphan Drug:EU/3/16/1654
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Designated
Source:
FDA ORPHAN DRUG:49690
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Leupeptin is produced by various species of Actinomycetes. It strongly inhibits proteolysis by plasmin, trypsin and papin. Leupeptin is well absorbed through oral route. Leupeptin has been known to cause various neuropathological changes in vivo resembling those of aging or neurodegenerative processes in the human brain, including the accumulation of neuronal processes and neuronal cytoskeletal abnormalities leading to neurofibrillary tangle (NFT)-like formations. In in vitro experiments, leupeptin protects the heart from myocardial stunning. Leupeptin was found to inhibit tumorigenesis in mouse skin induced by a single, noncarcinogenic dose of 7,12- dimethylbenz(a)anthracene followed by repeated application of croton oil. Tumors that had already been induced were scarcely affected by leupeptin.
Status:
Designated
Source:
FDA ORPHAN DRUG:49690
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Leupeptin is produced by various species of Actinomycetes. It strongly inhibits proteolysis by plasmin, trypsin and papin. Leupeptin is well absorbed through oral route. Leupeptin has been known to cause various neuropathological changes in vivo resembling those of aging or neurodegenerative processes in the human brain, including the accumulation of neuronal processes and neuronal cytoskeletal abnormalities leading to neurofibrillary tangle (NFT)-like formations. In in vitro experiments, leupeptin protects the heart from myocardial stunning. Leupeptin was found to inhibit tumorigenesis in mouse skin induced by a single, noncarcinogenic dose of 7,12- dimethylbenz(a)anthracene followed by repeated application of croton oil. Tumors that had already been induced were scarcely affected by leupeptin.
Status:
Designated
Source:
FDA ORPHAN DRUG:224206
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
JNJ-28312141 is an orally active colony-stimulating factor-1 receptor and FMS-related receptor tyrosine kinase-3 inhibitor. In preclinical models, JNJ-28312141 caused regression of ITD-FLT3–dependent MV-4-11 AML xenografts. The drug also suppressed the growth of H460 non-small cell lung adenocarcinoma xenografts and inhibited osteoclastogenesis and osteolysis in a rat model of metastatic bone disease.
![Structure of ALTERNATIVE DEFINITION for [Acetyl Hexapeptide-1]](/img/cb4f646c-a9b2-4c7f-f4a2-02132eabc703.svg?size=200&context=yjouujxlqo)
![Structure of 4H-1,2,4-Triazolium, 1-[(2R,3R)-3-[4-(4-cyanophenyl)-2-thiazolyl]-2-(2,5-difluorophenyl)-2-hydroxybutyl]-4-[1-[[[[3-[[[2-[[(1,1-dimethylethoxy)carbonyl]methylamino]acetyl]oxy]methyl]-2-pyridinyl]methylamino]carbonyl]oxy]ethyl]-, iodide (1:1)](/img/2b4c7574-f3b0-456f-ad07-b57caf7a5f03.svg?size=200&context=yjouujxlqo)
![Structure of ALTERNATIVE DEFINITION for [Acetyl Octapeptide-3]](/img/2b6b3529-73d0-4b29-9573-62c8931767ae.svg?size=200&context=yjouujxlqo)