Page last updated: 2024-11-13

akb-9778

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

AKB-9778: an inhibitor of vascular endothelial-protein tyrosine phosphatase [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID46700782
CHEMBL ID3931971
SCHEMBL ID679459
MeSH IDM000606692

Synonyms (29)

Synonym
SCHEMBL679459
carbamic acid, n-((1s)-2-oxo-1-(phenylmethyl)-2-(((1s)-2-(4-(sulfoamino)phenyl)-1-(2-(2-thienyl)-4-thiazolyl)ethyl)amino)ethyl)-, c-methyl ester
1008510-37-9
razuprotafib
razuprotafib [inn]
n-(4-((2s)-2-((2s)-2-((methoxycarbonyl)amino)- 3-phenylpropanamido)-2-(2-(thiophen-2-yl)-1,3-thiazol4-yl)ethyl)phenyl)sulfamic acid
razuprotafib [usan]
razuprotafib [who-dd]
0WAX4UT396 ,
who 10271
unii-0wax4ut396
razuprotafib [usan:inn]
akb-9778
AT18581
CHEMBL3931971
n-(4-{(2s)-2-{(2s)-2-[(methoxycarbonyl)amino]-3-phenylpropanamido}-2-[2-(thiophen-2-yl)-1,3-thiazol-4-yl]ethyl}phenyl)sulfamic acid
HY-109041
razuprotafib (usan)
D11540
us10220048, compound aa34
bdbm359124
CS-0031483
MS-30484
[4-[(2s)-2-[[(2s)-2-(methoxycarbonylamino)-3-phenylpropanoyl]amino]-2-(2-thiophen-2-yl-1,3-thiazol-4-yl)ethyl]phenyl]sulfamic acid
gtpl11336
akb9778
compound aa34 [us10220048]
Z4869073504
AKOS040742534

Research Excerpts

Toxicity

ExcerptReferenceRelevance
"Administration of interleukin (IL)-2 has led to a durable response in patients with advanced renal cancer and melanoma but is restricted for clinical application because of adverse effects, including the vascular leak syndrome (VLS)."( The VE-PTP Inhibitor AKB-9778 Improves Antitumor Activity and Diminishes the Toxicity of Interleukin 2 (IL-2) Administration.
Li, G; Liang, X; Lotze, MT; Peters, K; Sachdev, U, 2019
)
0.83

Compound-Compound Interactions

AKB-9778 combined with suppression of vascular endothelial growth factor (VEGF) causes a significantly greater reduction in DME than that seen with VEGF alone.

ExcerptReferenceRelevance
"To assess the effect of AKB-9778 alone or in combination with ranibizumab in subjects with diabetic macular edema (DME)."( Enhanced Benefit in Diabetic Macular Edema from AKB-9778 Tie2 Activation Combined with Vascular Endothelial Growth Factor Suppression.
Boyer, D; Brigell, M; Campochiaro, PA; Dugel, P; Gambino, L; Khanani, A; Kherani, S; Patel, S; Peters, K; Singer, M; Withers, B, 2016
)
1
"Activation of Tie2 by subcutaneous injections of AKB-9778 combined with suppression of vascular endothelial growth factor (VEGF) causes a significantly greater reduction in DME than that seen with suppression of VEGF alone."( Enhanced Benefit in Diabetic Macular Edema from AKB-9778 Tie2 Activation Combined with Vascular Endothelial Growth Factor Suppression.
Boyer, D; Brigell, M; Campochiaro, PA; Dugel, P; Gambino, L; Khanani, A; Kherani, S; Patel, S; Peters, K; Singer, M; Withers, B, 2016
)
0.94
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Protein Targets (1)

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Receptor-type tyrosine-protein phosphatase betaHomo sapiens (human)IC50 (µMol)0.00000.00000.00000.0000AID1339822
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (6)

Processvia Protein(s)Taxonomy
protein dephosphorylationReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
phosphate-containing compound metabolic processReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
glial cell migrationReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
dephosphorylationReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
angiogenesisReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
peptidyl-tyrosine dephosphorylation involved in inactivation of protein kinase activityReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (3)

Processvia Protein(s)Taxonomy
transmembrane receptor protein tyrosine phosphatase activityReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
protein bindingReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
cadherin bindingReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (4)

Processvia Protein(s)Taxonomy
plasma membraneReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
specific granule membraneReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
tertiary granule membraneReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
receptor complexReceptor-type tyrosine-protein phosphatase betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Research

Studies (12)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's0 (0.00)29.6817
2010's9 (75.00)24.3611
2020's3 (25.00)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 26.41

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be moderate demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index26.41 (24.57)
Research Supply Index2.83 (2.92)
Research Growth Index4.57 (4.65)
Search Engine Demand Index29.35 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (26.41)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials4 (33.33%)5.53%
Reviews2 (16.67%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other6 (50.00%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]