Betulinic glycine amide
Betulinic glycine amide (compound 5a) is a pentacyclic triterpenoid and derivative of Betulinic acid (HY-10529). Betulinic glycine amide has been used as a precursor in the synthesis of betulinic acid derivatives with anticancer and antiviral activity.
For research use only. We do not sell to patients.
- CAS No.: 174740-40-0
- Formula: C32H51NO4
- Molecular Weight:513.75
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| CHO | EC50 |
>10 μM
Compound: 33
|
Agonist activity at TGR5 expressed in CHO cells by CRE-driven luciferase reporter gene assay
Agonist activity at TGR5 expressed in CHO cells by CRE-driven luciferase reporter gene assay
|
[PMID: 19911773] |
| KB | ED50 |
>20 μg/mL
Compound: 16
|
In vitro cytotoxicity (antitumor activity) against human epidermoid carcinoma of mouth cell line (KB)
In vitro cytotoxicity (antitumor activity) against human epidermoid carcinoma of mouth cell line (KB)
|
[PMID: 10328313] |
| SK-MEL-2 | ED50 |
4.2 μg/mL
Compound: 16
|
In vitro cytotoxicity (antitumor activity) against human melanoma (MEL-2) cell lines
In vitro cytotoxicity (antitumor activity) against human melanoma (MEL-2) cell lines
|
[PMID: 10328313] |
Chemical Information
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CAS No. 174740-40-0
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Molecular Weight 513.75
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Formula C32H51NO4
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SMILES
OC(CNC([C@]12[C@@]([C@@H](CC2)C(C)=C)([H])[C@]3([H])[C@@](CC1)([C@]4([C@]([C@@]5([C@@](C(C)([C@H](CC5)O)C)([H])CC4)C)([H])CC3)C)C)=O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)