H2 receptor antagonists and human granulopoiesis

M. Aglietta; A. Stacchini; F. Sanavio; W. Piacibello

doi:10.1007/BF02004513

H2 receptor antagonists and human granulopoiesis

M. Aglietta, A. Stacchini, F. Sanavio, W. Piacibello

Istituto Oncologico Candiolo

Research output: Contribution to journal › Article › peer-review

Abstract

The effect of 2 H₂ receptor antagonists (ranitidine and cimetidine) on the in vitro growth of human granulomonopoietic precursors (CFU-GM) was studied. Ranitidine, although having an anti H₂ receptor activity much greater than that of cimetidine, displays the same toxicity for CFU-GM.

Original language	English
Pages (from-to)	375-376
Number of pages	2
Journal	Experientia
Volume	41
Issue number	3
DOIs	https://doi.org/10.1007/BF02004513
Publication status	Published - Mar 1985

Keywords

cimetidine
granulomonopoietic precursors, inhibition of
Granulopoiesis, human
H receptor antagonists
ranitidine

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)

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10.1007/BF02004513

Cite this

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abstract = "The effect of 2 H2 receptor antagonists (ranitidine and cimetidine) on the in vitro growth of human granulomonopoietic precursors (CFU-GM) was studied. Ranitidine, although having an anti H2 receptor activity much greater than that of cimetidine, displays the same toxicity for CFU-GM.",

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author = "M. Aglietta and A. Stacchini and F. Sanavio and W. Piacibello",

year = "1985",

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doi = "10.1007/BF02004513",

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AU - Aglietta, M.

AU - Stacchini, A.

AU - Sanavio, F.

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AB - The effect of 2 H2 receptor antagonists (ranitidine and cimetidine) on the in vitro growth of human granulomonopoietic precursors (CFU-GM) was studied. Ranitidine, although having an anti H2 receptor activity much greater than that of cimetidine, displays the same toxicity for CFU-GM.

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KW - granulomonopoietic precursors, inhibition of

KW - Granulopoiesis, human

KW - H receptor antagonists

KW - ranitidine

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H2 receptor antagonists and human granulopoiesis

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

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