Clinical data | |
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Other names | α-Hydroxylinoleic acid; 2-Hydroxylinoleic acid; ABTL-0812 |
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Chemical and physical data | |
Formula | C18H32O3 |
Molar mass | 296.451 g·mol−1 |
3D model ( JSmol) | |
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ABTL0812 (α-hydroxylinoleic acid) is a small-molecule, experimental cancer drug being developed by Ability Pharmaceuticals. [1]
In 2015, Ability announced that it had received orphan drug designation (ODD) for pediatric cancer neuroblastoma from the European Medical Agency (EMA) and the US Food and Drug Administration (FDA). [1] Also in 2016 a preclinical study confirmed that ABTL0812 was well tolerated. [2] In December 2016 the company announced ODD for the treatment of pancreatic cancer. [1]
One mechanism of action is the activation of the PPAR receptors and the TRIB3 gene, leading to inhibition of the Akt/mTOR pathway. This pathway is excessively activated in most human cancers, supporting tumor growth. It is a principal target of various new anti-tumour drugs. Tumor cells are killed viva autophagy, rather than apoptosis. [3] [4]
ABTL0812 activates the PPAR receptors, inducing TRIB3 over-expression. TRIB3 binds to the Akt oncogene and inhibits the Akt/mTOR axis. [3]
ABTL0812 showed efficacy in Phase I clinical trials in patients with advanced cancer, with low toxicity and high tolerability. [3]
Clinical data | |
---|---|
Other names | α-Hydroxylinoleic acid; 2-Hydroxylinoleic acid; ABTL-0812 |
Legal status | |
Legal status |
|
Identifiers | |
| |
CAS Number | |
PubChem CID | |
UNII | |
Chemical and physical data | |
Formula | C18H32O3 |
Molar mass | 296.451 g·mol−1 |
3D model ( JSmol) | |
|
ABTL0812 (α-hydroxylinoleic acid) is a small-molecule, experimental cancer drug being developed by Ability Pharmaceuticals. [1]
In 2015, Ability announced that it had received orphan drug designation (ODD) for pediatric cancer neuroblastoma from the European Medical Agency (EMA) and the US Food and Drug Administration (FDA). [1] Also in 2016 a preclinical study confirmed that ABTL0812 was well tolerated. [2] In December 2016 the company announced ODD for the treatment of pancreatic cancer. [1]
One mechanism of action is the activation of the PPAR receptors and the TRIB3 gene, leading to inhibition of the Akt/mTOR pathway. This pathway is excessively activated in most human cancers, supporting tumor growth. It is a principal target of various new anti-tumour drugs. Tumor cells are killed viva autophagy, rather than apoptosis. [3] [4]
ABTL0812 activates the PPAR receptors, inducing TRIB3 over-expression. TRIB3 binds to the Akt oncogene and inhibits the Akt/mTOR axis. [3]
ABTL0812 showed efficacy in Phase I clinical trials in patients with advanced cancer, with low toxicity and high tolerability. [3]