Amonafide L-malate
Based on 5 publication(s) in Google Scholar
Amonafide L-malate is a topoisomerase II inhibitor and DNA intercalator that induces Apoptotic signaling by blocking the binding of Topo II to DNA.
For research use only. We do not sell to patients.
- CAS No.: 618863-54-0
- Formula: C20H23N3O7
- Molecular Weight:417.41
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Amonafide L-malate
MoreAll Topoisomerase Isoforms
More
Biological Activity
Description
|
Topoisomerase II |
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
-
CAS No. 618863-54-0
-
Molecular Weight 417.41
-
Formula C20H23N3O7
-
SMILES
OC(C[C@H](O)C(O)=O)=O.O=C1C2=CC(N)=CC3=C2C(C(N1CCN(C)C)=O)=CC=C3
-
Synonyms
AS-1413 L-malate
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (5)
-
Journal Impact Factor
-
Most Recent
-
ACS Appl Mater Interfaces
Drastic Modulation of Molecular Packing and Intrinsic Dissolution Rates by Meniscus-Guided Coating of Extremely Confined Pharmaceutical Thin Films. [Abstract]2021 Dec 1;13(47):56519-56529. PMID: 34783517 -
Anal Chem
Metal-Enhanced Aggregation-Induced Emission Strategy for the HIV-I RNA-Binding Ligand Assay. [Abstract]2022 Mar 22;94(11):4695-4702. PMID: 35258935 -
J Am Heart Assoc
Amonafide Targeting NTSR1-PI3K/AKT/mTOR Signaling Attenuates Vascular Remodeling in Pulmonary Arterial Hypertension. [Abstract]2026 May 19;15(10):e045580. PMID: 42132175 -
PLoS One
Drug repositioning for pan-cancers of the digestive system: Identification of amonafide and BX795 as potential therapeutics via integrative Omics analysis. [Abstract]2025 Jun 16;20(6):e0325700. PMID: 40522954 -
Cancer Manag Res
UNBS5162 and amonafide inhibits tumor progression in human melanoma by the AKT/mTOR pathway. [Abstract]2019 Mar 22:11:2339-2348. PMID: 30962721
Protocols
-
Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
-
Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Purity & Documentation
References
[1]. Allen SL, et al. Amonafide: a potential role in treating acute myeloid leukemia. Expert Opin Investig Drugs. 2011 Jul;20(7):995-1003. [Content Brief]
[2]. Andersson BS, et al. In vitro toxicity and DNA cleaving capacity of benzisoquinolinedione (nafidimide; NSC 308847) in human leukemia. Cancer Res. 1987 Feb 15;47(4):1040-4. [Content Brief]
[3]. Ajani JA, et al. In vitro activity of amonafide against primary human tumors compared with the activity of standard agents. Invest New Drugs. 1988 Jun;6(2):79-85. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)