Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation

Search Page

Filters

My NCBI Filters

Results by year

Table representation of search results timeline featuring number of search results per year.

Year Number of Results
1991 1
1997 1
1999 4
2001 1
2002 1
2003 1
2005 1
2024 0

Text availability

Article attribute

Article type

Publication date

Search Results

10 results

Results by year

Filters applied: . Clear all
Page 1
Pharmacokinetics and central nervous system toxicity of declopramide (3-chloroprocainamide) in rats and mice.
Hua J, Pero RW, Kane R. Hua J, et al. Anticancer Drugs. 1999 Jan;10(1):79-88. doi: 10.1097/00001813-199901000-00010. Anticancer Drugs. 1999. PMID: 10194550
Declopramide (3-chloroprocainamide) has been identified in previous studies as a representative of a new class of chemosensitizers. ...One of the main metabolites of declopramide was identified as N-acetyl declopramide. Taken together, these dat …
Declopramide (3-chloroprocainamide) has been identified in previous studies as a representative of a new class of chemo …
N-Chlorination and oxidation of procainamide by myeloperoxidase: toxicological implications.
Uetrecht JP, Zahid N. Uetrecht JP, et al. Chem Res Toxicol. 1991 Mar-Apr;4(2):218-22. doi: 10.1021/tx00020a015. Chem Res Toxicol. 1991. PMID: 1664258
In the presence of chloride ion, a much greater degree of metabolism occurred, and the major product (40% of the starting procainamide) was a reactive species that could not be isolated. This metabolite spontaneously rearranged to 3-chloroprocainamide, and from its …
In the presence of chloride ion, a much greater degree of metabolism occurred, and the major product (40% of the starting procainamide) was …
Comparison of antitumor activity of declopramide (3-chloroprocainamide) and N-acetyl-declopramide.
Hua J, Sheng Y, Bryngelsson C, Kane R, Pero RW. Hua J, et al. Anticancer Res. 1999 Jan-Feb;19(1A):285-90. Anticancer Res. 1999. PMID: 10226556
Previous studies have suggested that some of the antitumor activity of declopramide (3-chloroprocainamide) could be due to its metabolites. One metabolite has been identified as N-acetyl-declopramide (N-acetyl-3-chloroprocainamide). The a …
Previous studies have suggested that some of the antitumor activity of declopramide (3-chloroprocainamide) could be due …
Toxicity, antitumor and chemosensitizing effects of 3-chloroprocainamide.
Hua J, Pero RW. Hua J, et al. Acta Oncol. 1997;36(8):811-6. doi: 10.3109/02841869709001362. Acta Oncol. 1997. PMID: 9482687
3-Chloroprocainamide (3-CPA), an analog of metoclopramide (MCA), dose-dependently inhibited tumor growth in scid mice xenografted with a human brain astrocytoma (T24) when given intramuscularly to mice every third day for 14-20 days. 3-CPA was shown to have the same …
3-Chloroprocainamide (3-CPA), an analog of metoclopramide (MCA), dose-dependently inhibited tumor growth in scid mice xenograf …
Newly discovered anti-inflammatory properties of the benzamides and nicotinamides.
Pero RW, Axelsson B, Siemann D, Chaplin D, Dougherty G. Pero RW, et al. Mol Cell Biochem. 1999 Mar;193(1-2):119-25. Mol Cell Biochem. 1999. PMID: 10331648
Our data have shown that nicotinamide and two N-substituted benzamides, metoclopramide (MCA) and 3-chloroprocainamide (3-CPA), gave dose dependent inhibition of lipopolysacharide induced TNFalpha in the mouse within the dose range of 10-500 mg/kg. ...
Our data have shown that nicotinamide and two N-substituted benzamides, metoclopramide (MCA) and 3-chloroprocainamide (3-CPA), …
Mechanism of action for N-substituted benzamide-induced apoptosis.
Olsson AR, Lindgren H, Pero RW, Leanderson T. Olsson AR, et al. Br J Cancer. 2002 Mar 18;86(6):971-8. doi: 10.1038/sj.bjc.6600136. Br J Cancer. 2002. PMID: 11953831 Free PMC article.
We have analysed the mechanism of action for induction of apoptosis by N-substituted benzamides using declopramide as a lead compound. We show here that declopramide at doses above 250 microM in the mouse 70Z/3 pre-B cell line or in the human promyeolocytic cancer c …
We have analysed the mechanism of action for induction of apoptosis by N-substituted benzamides using declopramide as a lead compound …
Differential usage of IkappaBalpha and IkappaBbeta in regulation of apoptosis versus gene expression.
Lindgren H, Olsson AR, Pero RW, Leanderson T. Lindgren H, et al. Biochem Biophys Res Commun. 2003 Jan 31;301(1):204-11. doi: 10.1016/s0006-291x(02)03012-7. Biochem Biophys Res Commun. 2003. PMID: 12535663
In this study we use the N-substituted benzamides declopramide (3-CPA) and N-acetyl declopramide (Na-3-CPA) to investigate the involvement of the transcription factor NF-kappaB in the induction of apoptosis and surface immunoglobulin kappa (Igkappa) expression in th …
In this study we use the N-substituted benzamides declopramide (3-CPA) and N-acetyl declopramide (Na-3-CPA) to investigate the …
N-substituted benzamides inhibit nuclear factor-kappaB and nuclear factor of activated T cells activity while inducing activator protein 1 activity in T lymphocytes.
Lindgren H, Pero RW, Ivars F, Leanderson T. Lindgren H, et al. Mol Immunol. 2001 Aug;38(4):267-77. doi: 10.1016/s0161-5890(01)00060-8. Mol Immunol. 2001. PMID: 11566320
Treatment of the Jurkat cells with procainamide did not influence the transcription factor profile of stimulated cells, while treatment with a derivative having an acetyl group in position 4 of the aromatic ring inhibited NF-kappaB and nuclear factor of activated T cells (NFAT) a …
Treatment of the Jurkat cells with procainamide did not influence the transcription factor profile of stimulated cells, while treatment with …
N-substituted benzamides inhibit NFkappaB activation and induce apoptosis by separate mechanisms.
Liberg D, Lazarevic B, Pero RW, Leanderson T. Liberg D, et al. Br J Cancer. 1999 Nov;81(6):981-8. doi: 10.1038/sj.bjc.6690796. Br J Cancer. 1999. PMID: 10576654 Free PMC article.
We found that while procainamide was biologically inert in our system, the addition of a chloride in the 3' position of the benzamide ring created a compound (declopramide) that induced rapid apoptosis. Furthermore, declopramide also inhibited NFkappaB activation by …
We found that while procainamide was biologically inert in our system, the addition of a chloride in the 3' position of the benzamide ring c …
N-substituted 4-aminobenzamides (procainamide analogs): an assessment of multiple cellular effects concerning ion trapping.
Morissette G, Moreau E, C-Gaudreault R, Marceau F. Morissette G, et al. Mol Pharmacol. 2005 Dec;68(6):1576-89. doi: 10.1124/mol.105.016527. Epub 2005 Sep 23. Mol Pharmacol. 2005. PMID: 16183854
Procainamide and related triethylamine-substituted 4-aminobenzamides, such as metoclopramide and declopramide, exert cellular effects potentially exploitable in oncology at millimolar concentrations (DNA demethylation, nuclear factor-kappaB inhibition, apoptosis) and displ …
Procainamide and related triethylamine-substituted 4-aminobenzamides, such as metoclopramide and declopramide, exert cellular effects …