H1-receptor antagonists terfenadine and loratadine inhibit spontaneous growth of neoplastic mast cells.

Hadzijusufovic E, Peter B, Gleixner KV, Schuch K, Pickl WF, Thaiwong T, Yuzbasiyan-Gurkan V, Mirkina I, Willmann M, Valent P.

Department for Companion Animals and Horses, Clinic for Internal Medicine and Infectious Diseases, University of Veterinary Medicine Vienna, Vienna, Austria.
Abstract

OBJECTIVE: In mast cell (MC) neoplasms, clinical problems requiring therapy include local aggressive and sometimes devastating growth of MCs and mediator-related symptoms. A key mediator of MCs responsible for clinical symptoms is histamine. Therefore, use of histamine receptor (HR) antagonists is an established approach to block histamine effects in these patients.

MATERIALS AND METHODS: We screened for additional beneficial effects of HR antagonists and asked whether any of these agents would also exert growth-inhibitory effects on primary neoplastic MCs, the human MC line HMC-1, and on two canine MC lines, C2 and NI-1.

RESULTS: We found that the HR1 antagonists terfenadine and loratadine suppress spontaneous growth of HMC-1, C2, and NI-1 cells, as well as growth of primary neoplastic MCs in all donors tested (human patients, n = 5; canine patients, n = 8). The effects of both drugs were found to be dose-dependent (IC(50): terfenadine, 1-20 μM; loratadine, 10-50 μM). Both agents also produced apoptosis in neoplastic MCs and augmented apoptosis-inducing effects of two KIT-targeting drugs, PKC412 and dasatinib. The other HR1 antagonists (fexofenadine, diphenhydramine) and HR2 antagonists (famotidine, cimetidine, ranitidine) tested did not exert substantial growth-inhibitory effects on neoplastic MCs. None of the histamine receptor blockers were found to modulate cell-cycle progression in neoplastic MCs.

CONCLUSIONS: The HR1 antagonists terfenadine and loratadine, in addition to their antimediator activity, exert in vitro growth-inhibitory effects on neoplastic MCs. Whether these drugs (terfenadine) alone, or in combination with KIT inhibitors, can also affect in vivo neoplastic MC growth remains to be determined.
Copyright © 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.

PMID: 20570632 [PubMed - indexed for MEDLINE]

OMG Im so glad you told me about the Allegra.. I am one of the people that took Seldane and it almost gave me a heart attack!! I was only about 32 and woke up at night with serere chest pains.. I dont think I will ever take Allegra now..

Im sorry bout that article, I usually try to add the url to each one.. I'll  look and find it...
Hugs,
Ramona

Interesting to learn of this, and hear your comments.

I quit Seldane -- sometime in the early Nineties -- as it made me feel like I was having a heart attack.  I think maybe I did, to some degree (and the same symptoms happened to me with Diflucan).

Then when I tried Allegra, I had a terrible reaction to it, too, on the first dose.  I don't remember what the reaction was, exactly, but I made a mental note to never touch it again. Their being related, is an interesting connection for me.

So, if I am understanding this rightly, the drug Seldane is the helpful one according to this article, yet it says that the Allegra drug is not.

Then the especially good one, in this particular case, is Claritin?   I'll consider adding that one to my mix.

Is there an Rx version of Claritin, like there is with Zyrtec (Zyzal)?