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[18F]FE@SUPPY: a suitable PET tracer for the adenosine A3 receptor? An in vivo study in rodents

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[18F]FE@SUPPY: a suitable PET tracer for the adenosine A3 receptor? An in vivo study in rodents. / Haeusler, Daniela; Kuntner, Claudia; Nics, Lukas; Savli, Markus; Zeilinger, Markus; Wanek, Thomas; Karagiannis, Panagiotis; Lanzenberger, Rupert R; Langer, Oliver; Shanab, Karem; Spreitzer, Helmut; Wadsak, Wolfgang; Hacker, Marcus; Mitterhauser, Markus.

In: EUR J NUCL MED MOL I, Vol. 42, No. 5, 04.2015, p. 741-9.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Haeusler, D, Kuntner, C, Nics, L, Savli, M, Zeilinger, M, Wanek, T, Karagiannis, P, Lanzenberger, RR, Langer, O, Shanab, K, Spreitzer, H, Wadsak, W, Hacker, M & Mitterhauser, M 2015, '[18F]FE@SUPPY: a suitable PET tracer for the adenosine A3 receptor? An in vivo study in rodents', EUR J NUCL MED MOL I, vol. 42, no. 5, pp. 741-9. https://doi.org/10.1007/s00259-014-2976-3

APA

Haeusler, D., Kuntner, C., Nics, L., Savli, M., Zeilinger, M., Wanek, T., Karagiannis, P., Lanzenberger, R. R., Langer, O., Shanab, K., Spreitzer, H., Wadsak, W., Hacker, M., & Mitterhauser, M. (2015). [18F]FE@SUPPY: a suitable PET tracer for the adenosine A3 receptor? An in vivo study in rodents. EUR J NUCL MED MOL I, 42(5), 741-9. https://doi.org/10.1007/s00259-014-2976-3

Vancouver

Haeusler D, Kuntner C, Nics L, Savli M, Zeilinger M, Wanek T et al. [18F]FE@SUPPY: a suitable PET tracer for the adenosine A3 receptor? An in vivo study in rodents. EUR J NUCL MED MOL I. 2015 Apr;42(5):741-9. https://doi.org/10.1007/s00259-014-2976-3

Bibtex

@article{4d0e1015a14b46abb9a773001aa081b7,
title = "[18F]FE@SUPPY: a suitable PET tracer for the adenosine A3 receptor? An in vivo study in rodents",
abstract = "PURPOSE: The adenosine A3 receptor (A3R) is involved in cardiovascular, neurological and tumour-related pathologies and serves as an exceptional pharmaceutical target in the clinical setting. A3R antagonists are considered antiinflammatory, antiallergic and anticancer agents, and to have potential for the treatment of asthma, COPD, glaucoma and stroke. Hence, an appropriate A3R PET tracer would be highly beneficial for the diagnosis and therapy monitoring of these diseases. Therefore, in this preclinical in vivo study we evaluated the potential as a PET tracer of the A3R antagonist [(18)F]FE@SUPPY.METHODS: Rats were injected with [(18)F]FE@SUPPY for baseline scans and blocking scans (A3R with MRS1523 or FE@SUPPY, P-gp with tariquidar; three animals each). Additionally, metabolism was studied in plasma and brain. In a preliminary experiment in a mouse xenograft model (mice injected with cells expressing the human A3R; three animals), the animals received [(18)F]FE@SUPPY and [(18)F]FDG. Dynamic PET imaging was performed (60 min in rats, 90 min in xenografted mice). In vitro stability of [(18)F]FE@SUPPY in human and rat plasma was also evaluated.RESULTS: [(18)F]FE@SUPPY showed high uptake in fat-rich regions and low uptake in the brain. Pretreatment with MRS1523 led to a decrease in [(18)F]FE@SUPPY uptake (p = 0.03), and pretreatment with the P-gp inhibitor tariquidar led to a 1.24-fold increase in [(18)F]FE@SUPPY uptake (p = 0.09) in rat brain. There was no significant difference in metabolites in plasma and brain in the treatment groups. However, plasma concentrations of [(18)F]FE@SUPPY were reduced to levels similar to those in rat brain after blocking. In contrast to [(18)F]FDG uptake (p = 0.12), the xenograft model showed significantly increased uptake of [(18)F]FE@SUPPY in the tissue masses from CHO cells expressing the human A3R (p = 0.03). [(18)F]FE@SUPPY was stable in human plasma.CONCLUSION: Selective and significant tracer uptake of [(18)F]FE@SUPPY was found in xenografted mice injected with cells expressing human A3R. This finding supports the strategy of evaluating [(18)F]FE@SUPPY in {"}humanized animal models{"}. In conclusion, preclinical evaluation points to the suitability of [(18)F]FE@SUPPY as an A3R PET tracer in humans.",
author = "Daniela Haeusler and Claudia Kuntner and Lukas Nics and Markus Savli and Markus Zeilinger and Thomas Wanek and Panagiotis Karagiannis and Lanzenberger, {Rupert R} and Oliver Langer and Karem Shanab and Helmut Spreitzer and Wolfgang Wadsak and Marcus Hacker and Markus Mitterhauser",
year = "2015",
month = apr,
doi = "10.1007/s00259-014-2976-3",
language = "English",
volume = "42",
pages = "741--9",
journal = "EUR J NUCL MED MOL I",
issn = "1619-7070",
publisher = "Springer",
number = "5",

}

RIS

TY - JOUR

T1 - [18F]FE@SUPPY: a suitable PET tracer for the adenosine A3 receptor? An in vivo study in rodents

AU - Haeusler, Daniela

AU - Kuntner, Claudia

AU - Nics, Lukas

AU - Savli, Markus

AU - Zeilinger, Markus

AU - Wanek, Thomas

AU - Karagiannis, Panagiotis

AU - Lanzenberger, Rupert R

AU - Langer, Oliver

AU - Shanab, Karem

AU - Spreitzer, Helmut

AU - Wadsak, Wolfgang

AU - Hacker, Marcus

AU - Mitterhauser, Markus

PY - 2015/4

Y1 - 2015/4

N2 - PURPOSE: The adenosine A3 receptor (A3R) is involved in cardiovascular, neurological and tumour-related pathologies and serves as an exceptional pharmaceutical target in the clinical setting. A3R antagonists are considered antiinflammatory, antiallergic and anticancer agents, and to have potential for the treatment of asthma, COPD, glaucoma and stroke. Hence, an appropriate A3R PET tracer would be highly beneficial for the diagnosis and therapy monitoring of these diseases. Therefore, in this preclinical in vivo study we evaluated the potential as a PET tracer of the A3R antagonist [(18)F]FE@SUPPY.METHODS: Rats were injected with [(18)F]FE@SUPPY for baseline scans and blocking scans (A3R with MRS1523 or FE@SUPPY, P-gp with tariquidar; three animals each). Additionally, metabolism was studied in plasma and brain. In a preliminary experiment in a mouse xenograft model (mice injected with cells expressing the human A3R; three animals), the animals received [(18)F]FE@SUPPY and [(18)F]FDG. Dynamic PET imaging was performed (60 min in rats, 90 min in xenografted mice). In vitro stability of [(18)F]FE@SUPPY in human and rat plasma was also evaluated.RESULTS: [(18)F]FE@SUPPY showed high uptake in fat-rich regions and low uptake in the brain. Pretreatment with MRS1523 led to a decrease in [(18)F]FE@SUPPY uptake (p = 0.03), and pretreatment with the P-gp inhibitor tariquidar led to a 1.24-fold increase in [(18)F]FE@SUPPY uptake (p = 0.09) in rat brain. There was no significant difference in metabolites in plasma and brain in the treatment groups. However, plasma concentrations of [(18)F]FE@SUPPY were reduced to levels similar to those in rat brain after blocking. In contrast to [(18)F]FDG uptake (p = 0.12), the xenograft model showed significantly increased uptake of [(18)F]FE@SUPPY in the tissue masses from CHO cells expressing the human A3R (p = 0.03). [(18)F]FE@SUPPY was stable in human plasma.CONCLUSION: Selective and significant tracer uptake of [(18)F]FE@SUPPY was found in xenografted mice injected with cells expressing human A3R. This finding supports the strategy of evaluating [(18)F]FE@SUPPY in "humanized animal models". In conclusion, preclinical evaluation points to the suitability of [(18)F]FE@SUPPY as an A3R PET tracer in humans.

AB - PURPOSE: The adenosine A3 receptor (A3R) is involved in cardiovascular, neurological and tumour-related pathologies and serves as an exceptional pharmaceutical target in the clinical setting. A3R antagonists are considered antiinflammatory, antiallergic and anticancer agents, and to have potential for the treatment of asthma, COPD, glaucoma and stroke. Hence, an appropriate A3R PET tracer would be highly beneficial for the diagnosis and therapy monitoring of these diseases. Therefore, in this preclinical in vivo study we evaluated the potential as a PET tracer of the A3R antagonist [(18)F]FE@SUPPY.METHODS: Rats were injected with [(18)F]FE@SUPPY for baseline scans and blocking scans (A3R with MRS1523 or FE@SUPPY, P-gp with tariquidar; three animals each). Additionally, metabolism was studied in plasma and brain. In a preliminary experiment in a mouse xenograft model (mice injected with cells expressing the human A3R; three animals), the animals received [(18)F]FE@SUPPY and [(18)F]FDG. Dynamic PET imaging was performed (60 min in rats, 90 min in xenografted mice). In vitro stability of [(18)F]FE@SUPPY in human and rat plasma was also evaluated.RESULTS: [(18)F]FE@SUPPY showed high uptake in fat-rich regions and low uptake in the brain. Pretreatment with MRS1523 led to a decrease in [(18)F]FE@SUPPY uptake (p = 0.03), and pretreatment with the P-gp inhibitor tariquidar led to a 1.24-fold increase in [(18)F]FE@SUPPY uptake (p = 0.09) in rat brain. There was no significant difference in metabolites in plasma and brain in the treatment groups. However, plasma concentrations of [(18)F]FE@SUPPY were reduced to levels similar to those in rat brain after blocking. In contrast to [(18)F]FDG uptake (p = 0.12), the xenograft model showed significantly increased uptake of [(18)F]FE@SUPPY in the tissue masses from CHO cells expressing the human A3R (p = 0.03). [(18)F]FE@SUPPY was stable in human plasma.CONCLUSION: Selective and significant tracer uptake of [(18)F]FE@SUPPY was found in xenografted mice injected with cells expressing human A3R. This finding supports the strategy of evaluating [(18)F]FE@SUPPY in "humanized animal models". In conclusion, preclinical evaluation points to the suitability of [(18)F]FE@SUPPY as an A3R PET tracer in humans.

U2 - 10.1007/s00259-014-2976-3

DO - 10.1007/s00259-014-2976-3

M3 - SCORING: Journal article

C2 - 25601336

VL - 42

SP - 741

EP - 749

JO - EUR J NUCL MED MOL I

JF - EUR J NUCL MED MOL I

SN - 1619-7070

IS - 5

ER -