Methotrexate analogues display enhanced inhibition of TNF-α production in whole blood from RA patients

Scand J Rheumatol. 2014;43(1):9-16. doi: 10.3109/03009742.2013.797490. Epub 2013 Aug 30.

Abstract

Objectives: Although methotrexate (MTX) is the anchor drug in the treatment of rheumatoid arthritis (RA), patients experience clinical resistance to MTX upon prolonged treatment. We explored whether new-generation antifolates elicit superior anti-inflammatory properties when compared to MTX, based on their capacity to inhibit tumour necrosis factor (TNF)-α production.

Method: T cells in whole blood from 18 RA patients (including MTX-naïve, MTX- responsive, and MTX non-responsive patients) and seven healthy volunteers were stimulated with αCD3/αCD28 antibodies and incubated ex vivo for 72 h with MTX and eight novel antifolate drugs with potentially favourable biochemical and pharmacological properties. Drug concentrations exerting 50% inhibition (IC-50) of TNF-α production (by enzyme-linked immunosorbent assay, ELISA) were determined as an estimate for their anti-inflammatory capacity. In addition, induction of T-cell apoptosis was evaluated by flow cytometry.

Results: The new-generation antifolates PT523, PT644, raltitrexed, and GW1843 proved to be potent inhibitors of TNF-α production in activated T cells from all three groups of RA patients and from healthy volunteers. Based on IC-50 values, these antifolates were up to 10.3 times more potent than MTX. The anti-inflammatory effects were observed at drug concentrations that provoked suppression of T-cell activation and induction of apoptosis in 20-40% of activated T cells.

Conclusion: In an ex-vivo setting, novel antifolates elicited marked inhibition of TNF-α production in activated T cells from RA patients. Further clinical evaluation is warranted to investigate whether a low dosage of these antifolates can elicit immunosuppressive effects equivalent to MTX, and whether they are superior to MTX in patients who fail to respond to MTX.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antirheumatic Agents / pharmacology*
  • Antirheumatic Agents / therapeutic use
  • Arthritis, Rheumatoid / drug therapy*
  • Arthritis, Rheumatoid / immunology
  • Arthritis, Rheumatoid / metabolism
  • Female
  • Folic Acid Antagonists / pharmacology
  • Humans
  • Male
  • Methotrexate / analogs & derivatives*
  • Methotrexate / pharmacology
  • Methotrexate / therapeutic use
  • Middle Aged
  • Ornithine / analogs & derivatives
  • Ornithine / pharmacology
  • Pterins / pharmacology
  • Quinazolines / pharmacology
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / metabolism
  • Thiophenes / pharmacology
  • Trimetrexate / pharmacology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Antirheumatic Agents
  • Folic Acid Antagonists
  • Pterins
  • Quinazolines
  • Thiophenes
  • Tumor Necrosis Factor-alpha
  • N(alpha)-(4-amino-4-deoxypteroyl)-N(delta)-hemiphthaloyl-L-ornithine
  • Ornithine
  • raltitrexed
  • Trimetrexate
  • Methotrexate