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Chemical Structure| 305834-79-1 Chemical Structure| 305834-79-1

Structure of SC-79
CAS No.: 305834-79-1

Chemical Structure| 305834-79-1

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SC79 is a specific Akt agonist capable of crossing the blood-brain barrier. It activates cytosolic Akt and inhibits Akt membrane translocation by specifically binding to the PH domain of Akt.

4.5 *For Research Use Only! Not for Human Use. We Do Not Sell to Patients.

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Product Citations

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Wang, Yi ; Zhao, Tong ; Huang, Chuyue ; Liu, Fei ; Zhang, Yang ; Kong, Desong , et al.

Abstract: Background: Banxia Xiexin decoction (BXD) is a traditional Chinese medicine with anti-colorectal cancer (CRC) activity. However, its bioactive constituents and its mechanism of action remain unclear. Herein, we explored the mechanism of action of BXD against CRC using a network pharmacology approach. Methods: First, the targets of the main chemical components of BXD were predicted and collected through a database, and the intersection of compound targets and disease targets was obtained. Subsequently, protein–protein interaction network analysis, Gene Ontology enrichment, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed to explore the potential mechanisms underlying the effects of BXD on CRC. Finally, a CRC cell model and a CRC xenograft model in nude mice were utilized to further determine the mechanism of action. Results: A compound-therapeutic target network of BXD was constructed, revealing 146 cellular targets of BXD. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling axis was identified as the main target of BXD. Using in vitro and in vivo models, the activity of BXD against CRC was found to be mediated through ferritinophagy by targeting the PI3K/AKT/mTOR axis, leading to intracellular iron accumulation, reactive oxygen species activation, and finally ferroptosis. Conclusions: Through the application of network pharmacology and in vitro/in vivo validation experiments, we discovered that BXD exerts anti-CRC effects via the ferritinophagy pathway. Furthermore, we elucidated the potential mechanism underlying its induction of ferritinophagy. These findings demonstrate the significant potential of traditional drugs in managing CRC and support their wider clinical application in combination chemotherapy, targeted therapy, and immunotherapy.

Keywords: Banxia Xiexin decoction ; Colorectal cancer ; Network pharmacology ; PI3K/AKT/mTOR

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Wan, Rong ; Pan, Lujuan ; Wang, Qi ; Shen, Guanliang ; Guo, RuoNan ; Qin, Yueqiu , et al.

Abstract: Copper, an indispensable trace element for the human body, serves not only as a crucial auxiliary factor in redox reactions within the organism but also as a significant constituent of numerous key metabolic enzymes. The COMMD family plays a vital role in regulating copper at both the cellular and systemic levels, particularly in the realm of tumor research, an area notably deficient in gastric cancer investigations. With the advancement of precision medical techniques, individualized and precise screening and treatment have become paramount considerations in the contemporary medical landscape for gastric cancer therapy. In light of this, we meticulously scrutinized existing transcriptomic datasets for gastric cancer, validating the expression levels and prognostic value of COMMD family genes. Simultaneously, employing the ssGSEA algorithm, we devised the COMMDs score. Enrichment analysis, gene mutations, and clinical features were incorporated into the assessment of this score. Furthermore, we contextualized the COMMDs score within the framework of the immune microenvironment, evaluating the relationship between the COMMDs family and immune factors as well as immune cells. The results suggest a correlation between the COMMDs score and various immune-related features. Based on this foundation, multiple machine learning approaches indicated Logistic Regression, with a remarkable ROC of 0.972, as the optimal diagnostic model. To accentuate the translational medical value of the COMMDs family, we selected COMMD10 as a differential gene in gastric cancer for further validation. Functional experiments revealed a decline in the proliferative and migratory capabilities of gastric cancer cells upon silencing COMMD10. Additionally, through pathway intervention, we unveiled the PI3K-AKT pathway as a potential mechanism through which COMMD10 influences gastric cancer activity. In summary, our study affirms the prospective role of the COMMDs family as potential markers for the diagnosis and treatment of gastric cancer in the future.

Keywords: Gastric Cancer ; Machine Learning ; COMMDs Family ; Immunotherapy ; TME

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Fang, Xuehong ; Zhu, Yuzhen ; Zhang, Taomin ; Li, Qian ; Fan, Lvhua ; Li, Xiaodan , et al.

Abstract: Although lung cancer treatment strategies have improved in recent years, the 5-year overall survival of non-small cell lung cancer (NSCLC) remains less than 15%. Chemotherapy is considered the most promising option in the comprehensive treatment of NSCLC. Fucoxanthin (FX) is a natural product derived from brown algae and has extensive applications in medicine. Previous studies reported that FX effectively inhibits the growth of NSCLC cells in vitro and in vivo. However, the mechanism underlying the anti-NSCLC effect of FX remains unknown. In this study, NSCLC cell lines and a xenograft nude mouse model were used to examine the anti-NSCLC activities of FX in vitro and in vivo. Network pharmacology analysis and inhibitors or activators of the PI3K/Akt signaling pathway were used to explore the anti-NSCLC mechanisms of FX. The results indicated that FX could inhibit proliferation, migration, and invasion, arrest cell cycle at the G0/G1 phase, and induce apoptosis of NSCLC cells in vitro. Additionally, FX suppressed tumor growth in vivo. The PI3K/Akt signaling pathway was found to be involved in the anti-NSCLC activity of FX. In conclusion, FX inhibits malignant biological behaviors of NSCLC by suppressing the phosphorylation of both PI3K and AKT, and subsequently inactivating PI3K/AKT signaling pathway.

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Alternative Products

Product Details of SC-79

CAS No. :305834-79-1
Formula : C17H17ClN2O5
M.W : 364.78
SMILES Code : O=C(OCC)C(C#N)C1C(C(OCC)=O)=C(N)OC2=CC=C(Cl)C=C12
English Name :Ethyl 2-amino-6-chloro-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate
MDL No. :MFCD02681303
InChI Key :DXVKFBGVVRSOLI-UHFFFAOYSA-N
Pubchem ID :2810830

Safety of SC-79

Related Pathways of SC-79

PI3K-AKT

Isoform Comparison

Biological Activity

In Vitro:

Cell Line
Concentration Treated Time Description References
AML12 cells 5 μg/ml 24 h To study the effect of SC-79 on AML12 cells, results showed that SC-79 activated the Akt2 signaling pathway. Cell Mol Gastroenterol Hepatol. 2022;14(3):669-692.
EndoC-βH1 cells 8 μg/mL 48 h SC79 increased PDX1 protein levels, but METTL3 silencing blocked this increase, indicating that m6A regulates PDX1 protein levels synergistically with AKT. Nat Metab. 2019 Aug;1(8):765-774.
SCC9 cells 5 μg/mL Activate AKT, partially reverse the effects of METTL1 knockout on HNSCC cells Cancer Commun (Lond). 2022 Mar;42(3):223-244.
SCC15 cells 5 μg/mL Activate AKT, partially reverse the effects of METTL1 knockout on HNSCC cells Cancer Commun (Lond). 2022 Mar;42(3):223-244.
MHCC-97H cells 4 µg/ml 1 h SC79 partially restored the suppressed effect on cell proliferation induced by YTHDF1 inhibition Exp Hematol Oncol. 2021 Jun 4;10(1):35.
Primary leiomyoma cells 10 μM 15 min, 30 min, 60 min, 120 min, 360 min SC79 treatment enhanced AKT phosphorylation after 30 min treatment and reached significance after 1h. β-catenin phosphorylation at Ser 552 increased at 30 min and peaked at two h post-treatment, which was accompanied by increased levels of active β-catenin (non-phosphorylated β-catenin at Ser 45) and its downstream target, Axin2. Fertil Steril. 2020 Dec;114(6):1339-1349.
MCF-7 cells 5 µg/mL 1 h To test the effect of SC-79 on the AKT signaling pathway, results showed that SC-79 activated the AKT signaling pathway. Genome Res. 2017 Jun;27(6):1087-1097.
MH-S cells 10 nM 4 h SC-79 was used as an Akt activator to study its effect on signaling pathway activation in MH-S cells. Sci Signal. 2018 Jun 26;11(536):eaao2387.

In Vivo:

Species
Animal Model
Administration Dosage Frequency Description References
Mice Col2a1-cre; Mapk7f/fmouse model Intraperitoneal injection 0.04 mg/g Once daily for 8 weeks Activated the AKT signaling pathway, partially alleviating the impaired chondrocyte hypertrophy and vertebral defects caused by Mapk7 deletion. Genes Dis. 2023 Mar 24;11(2):964-977
Mice C57BL/6J mice Intraperitoneal injection 20 mg/kg Once a week for 14 days To study the effect of SC-79 on liver fat deposition in mice, results showed that SC-79 enhanced Akt2 activity, leading to increased liver fat deposition. Cell Mol Gastroenterol Hepatol. 2022;14(3):669-692.
C57BL/6 male mice Iron deficiency mouse model Intraperitoneal injection 20 mg/kg Every 5 days for one month To evaluate the effect of SC-79 on bone density in iron-deficient mice, results showed that SC-79 significantly reversed the bone density decline caused by iron deficiency Cell Mol Life Sci. 2024 Aug 19;81(1):360.
Mice Mettl1cKO mice Intraperitoneal injection 0.04 mg/g 4 weeks after 4NQO treatment and fed for 20 weeks Activate AKT, increase the lesion number, lesion area, malignancy, proliferation, and metastasis of HNSCC in Mettl1cKO mice Cancer Commun (Lond). 2022 Mar;42(3):223-244.
C57BL/6 mice Bleomycin-induced pulmonary fibrosis model Intraperitoneal injection 40 mg/kg Once daily for 3 days SC-79 significantly improved bleomycin-induced pulmonary fibrosis symptoms, including tissue pathological changes, collagen deposition, and loss, by activating the AKT signaling pathway. Cell Death Dis. 2021 Oct 13;12(10):938

Protocol

Bio Calculators
Preparing Stock Solutions 1mg 5mg 10mg

1 mM

5 mM

10 mM

2.74mL

0.55mL

0.27mL

13.71mL

2.74mL

1.37mL

27.41mL

5.48mL

2.74mL

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