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Development Status

Investigational

3

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Primary Target

Mitogen-activated protein kinase 11

2

Mitogen-activated protein kinase 12

2

Mitogen-activated protein kinase 13

2

Mitogen-activated protein kinase 14

2

cAMP-dependent protein kinase (PKA)

2

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Highest Phase

Phase II

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Approval Year

Unknown

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Condition

Colorectal cancer

2

Metastatic colorectal cancer

2

Multiple myeloma

2

Plasma cell neoplasm

2

Recurrent or refractory multiple myeloma

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Treatment Modality

Primary

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CNS Activity

CNS Penetrant

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Originator

Robins, R.K.|Revankar, G.R.|Chang, Y.

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CV Therapeutics

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Chemical

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CAS

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FDA UNII

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PUBCHEM

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ChEMBL

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DRUG BANK

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Principal Form

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Salts, Hydrates, Esters, etc.

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8-Chloro-ATP

Z846LF5DED

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Status:

Investigational

Class (Stereo):

CHEMICAL (ABSOLUTE)

Targets:

p38 MAPK pathway

Mitogen-activated protein kinase 13

cAMP-dependent protein kinase (PKA)

Mitogen-activated protein kinase 12

Mitogen-activated protein kinase 14

Mitogen-activated protein kinase 11

Conditions:

Metastatic colorectal cancer

Recurrent or refractory multiple myeloma

Colorectal cancer

Multiple myeloma

Plasma cell neoplasm

8-Chloroadenosine-3',5'-cyclic-monophosphate (8-Cl-cAMP), an analog of c-AMP, is a novel antineoplastic agent. It has been shown to be effective against different human cancer cell lines modulating the cellular signal transduction pathway, thereby ca...

using growth inhibition, cell differentiation, and apoptosis. 8-Cl-cAMP preferentially binds to the R2 subunit of protein kinase A (PKA) and induces rapid R2 up-regulation and eventual R1 subunit down-regulation. It has potent inhibitory effects on a wide variety of human cancer cell lines, with an IC50 ranging from 0.1 to 20 uM. The IC50 falls with the length of drug exposure. It can suppress c-myc and c-ras proto-oncogenes in vitro and in vivo. It was shown that 8-Cl-cAMP induces cell growth inhibition through AMP-activated protein kinase (AMPK) activation with p38 MAPK acting downstream of AMPK in this signaling pathway. 8-Cl-cAMP induced apoptosis, apparently through activation of the p38 MAPK pathway by inducing progressive phosphorylation of the p38 mitogen-activated protein kinase (MAPK), via activation of AMPK by its metabolite 8-Cl-adenosine. 8-Cl-cAMP does not significantly inhibit the growth of NIH 3T3 cells, rat kidney fibroblasts, mammary epithelial cells, or peripheral blood lymphocytes, nor does it inhibit the growth of parental cells whose progeny have been transformed. Such selectivity makes it an attractive candidate for cancer therapy suggesting that it should not cause the toxicity of conventional cytotoxic agents but should inhibit tumor growth. 8-Cl-cAMP has been evaluated in phase I/II clinical trials.

TECADENOSON

GZ1X96601Z

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Status:

Investigational

Class (Stereo):

CHEMICAL (ABSOLUTE)

Targets:

Equilibrative nucleoside transporter 1

Adenosine A2b receptor

Adenosine A1 receptor

Equilibrative nucleoside transporter 2

Adenosine A2a receptor

Conditions:

Atrial fibrillation

Tecadenoson is a novel selective A1 adenosine receptor agonist that is currently being evaluated for the conversion of paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm. Adenosine is a naturally occurring compound that stimulates all ade...

nosine receptor subtypes in the body, including the A2 adenosine receptor which lowers blood pressure. In non-clinical trials, tecadenoson selectively stimulated the A1 adenosine receptor in the Atrioventricular node (AV node) and slowed the speed of electrical conduction across the AV node, reducing the number of electrical impulses that reached the ventricle, without affecting blood pressure. Clinical studies to date with intravenous tecadenoson suggest that it may slow the speed of AV nodal conduction by selectively stimulating the A1 adenosine receptor, and may avoid blood pressure lowering by not stimulating the A2 adenosine receptor. Thus, it may be possible to use intravenous tecadenoson to convert patients from PSVT to normal sinus rhythm without lowering blood pressure or causing adverse events related to vasodilation such as flushing, palpitations or a headache.

TOCLADESINE

BQ94Z7E5OR

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Search for Structure

Status:

Investigational

Class (Stereo):

CHEMICAL (ABSOLUTE)

Targets:

p38 MAPK pathway

Mitogen-activated protein kinase 13

cAMP-dependent protein kinase (PKA)

Mitogen-activated protein kinase 12

Mitogen-activated protein kinase 14

Mitogen-activated protein kinase 11

Conditions:

Metastatic colorectal cancer

Recurrent or refractory multiple myeloma

Colorectal cancer

Multiple myeloma

Plasma cell neoplasm

8-Chloroadenosine-3',5'-cyclic-monophosphate (8-Cl-cAMP), an analog of c-AMP, is a novel antineoplastic agent. It has been shown to be effective against different human cancer cell lines modulating the cellular signal transduction pathway, thereby ca...

using growth inhibition, cell differentiation, and apoptosis. 8-Cl-cAMP preferentially binds to the R2 subunit of protein kinase A (PKA) and induces rapid R2 up-regulation and eventual R1 subunit down-regulation. It has potent inhibitory effects on a wide variety of human cancer cell lines, with an IC50 ranging from 0.1 to 20 uM. The IC50 falls with the length of drug exposure. It can suppress c-myc and c-ras proto-oncogenes in vitro and in vivo. It was shown that 8-Cl-cAMP induces cell growth inhibition through AMP-activated protein kinase (AMPK) activation with p38 MAPK acting downstream of AMPK in this signaling pathway. 8-Cl-cAMP induced apoptosis, apparently through activation of the p38 MAPK pathway by inducing progressive phosphorylation of the p38 mitogen-activated protein kinase (MAPK), via activation of AMPK by its metabolite 8-Cl-adenosine. 8-Cl-cAMP does not significantly inhibit the growth of NIH 3T3 cells, rat kidney fibroblasts, mammary epithelial cells, or peripheral blood lymphocytes, nor does it inhibit the growth of parental cells whose progeny have been transformed. Such selectivity makes it an attractive candidate for cancer therapy suggesting that it should not cause the toxicity of conventional cytotoxic agents but should inhibit tumor growth. 8-Cl-cAMP has been evaluated in phase I/II clinical trials.

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