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SML1342

Sigma-Aldrich

API-1

Synonym(s):

4-Amino-5,8-dihydro-5-oxo-8-b-D-ribofuranosyl-pyrido[2,3-d]pyrimidine-6-carboxamide, NSC 177223, NSC177223

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5 MG
$139.00

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5 MG
$139.00

About This Item

Empirical Formula (Hill Notation):
C13H15N5O6
CAS Number:
36707-00-3
Molecular Weight:
337.29
MDL number:
MFCD18086904
UNSPSC Code:
12352200
PubChem Substance ID:
329825799
NACRES:
NA.77

$139.00

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assay

≥95% (HPLC)

Quality Level

100

form

powder

color

white to beige

solubility

DMSO: 1 mg/mL, clear (warmed)

storage temp.

−20°C

SMILES string

O=C1C(C(N)=O)=CN([C@@H]2O[C@H](CO)[C@@H](O)[C@H]2O)C3=C1C(N)=NC=N3

InChI

1S/C13H15N5O6/c14-10-6-7(20)4(11(15)23)1-18(12(6)17-3-16-10)13-9(22)8(21)5(2-19)24-13/h1,3,5,8-9,13,19,21-22H,2H2,(H2,15,23)(H2,14,16,17)/t5-,8-,9-,13-/m1/s1

InChI key

SPBWHPXCWJLQRU-FITJORAGSA-N

Biochem/physiol Actions

API-1 is a potent and specific Akt/PKB inhibitor.
API-1 is a potent and specific Akt/PKB inhibitor. API-1 binds to pleckstrin homology (PH) domain of Akt and blocks Akt membrane translocation. The compound inhibits all three members of the family Akt1/PKBa, Akt2/PKBb and Akt3/PKBg. API-1 does not inhibit the activation of PKC, SGK, PKA, STAT3, Erk-1/2 or JNK.

pictograms

Skull and crossbones
GHS06

signalword

Danger

hcodes

H301

Hazard Classifications

Acute Tox. 3 Oral

Storage Class

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
115M4709V

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Juhua Zhuang et al.
Oncology research, 26(8), 1257-1265 (2018-02-22)
Hepatocellular carcinoma (HCC) as one of the most refractory cancers leads to high mortality worldwide. Long noncoding RNAs have been widely acknowledged as important biomarkers and therapeutic targets in HCC. In this study, we investigated the effects of long noncoding
Joshua R Huot et al.
Cells, 10(7) (2021-08-08)
It has been demonstrated that inhibiting Notch signaling through γ-secretase inhibitor (GSI) treatment increases myogenesis, AKT/mTOR signaling, and muscle protein synthesis (MPS) in C2C12 myotubes. The purpose of this study was to determine if GSI-mediated effects on myogenesis and MPS

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