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Pharmacology · Agents Regulating Immune Processes

Cycloferon

Meglumini acridonacetas

Cycloferon is a low-molecular-weight inducer of endogenous interferon production. The drug exhibits pronounced antiviral activity, which is realized both by stimulating the immune response and by directly suppressing viral replication inside the infected cell.

GroupLow-molecular-weight interferon (IFN) inducer
TargetsImmunocompetent cells: monocytes, macrophages, lymphocytes
PharmacokineticsFreely crosses the blood-brain barrier (BBB)
SpectrumInfluenza, herpes, hepatitis B and C, HIV, HPV, tick-borne encephalitis
3 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Chemical nature and classification

The active pharmaceutical ingredient is Meglumini acridonacetas. Pharmacologically, it is a low-molecular-weight interferon (IFN) inducer.

When studying antiviral agents, it is important to clearly differentiate their mechanisms of action. You must remember what this drug is not:

  • It is not an M2 channel blocker.
  • It is not a neuraminidase inhibitor.
  • It is not an HIV protease inhibitor.

Its primary pharmacological objective is to prompt the body's own cells to synthesize protective proteins, rather than simply attacking specific viral enzymes.

Main pharmacological effects

The action of Meglumini acridonacetas is complex. Clinical pharmacology distinguishes four key effects of the drug:

  1. Antiviral — the baseline function aimed at eliminating the pathogen from the body.
  2. Immunomodulatory — correction of immune system function and activation of its cellular link.
  3. Anti-inflammatory — limitation of pathological inflammatory reactions in affected tissues.
  4. Radioprotective — increasing cellular resistance to the damaging effects of ionizing radiation.
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Dual mechanism of antiviral action

The drug is unique in that it fights viral infection in two directions simultaneously: indirectly (via the immune system) and directly (by acting on the virus itself).

1. Indirect action Implemented by stimulating the production of own (endogenous) interferon. The main targets for the drug are immunocompetent cells:

  • Monocytes (circulating in the blood).
  • Macrophages (tissue phagocytes).
  • Lymphocytes (adaptive immunity cells).

2. Direct action In addition to stimulating immunity, the molecule can directly disrupt viral replication inside the infected cell. This occurs through three mechanisms:

  • Reduction of specific viral protein synthesis.
  • Blocking the integration of viral nucleic acids (DNA or RNA) into forming capsids.
  • A sharp increase in the proportion of defective viral particles that are unable to infect new cells.

Pharmacokinetics and spectrum of activity

A key pharmacokinetic characteristic of the drug is its ability to cross the blood-brain barrier (BBB). This property is critically important for treating infections affecting the central nervous system.

The spectrum of antiviral activity covers a wide range of pathogens:

  • Respiratory infections: influenza A and B viruses.
  • Herpesviruses: causative agents of herpes simplex and cytomegalovirus (CMV).
  • Hepatotropic viruses: causative agents of viral hepatitis B and C.
  • Retroviruses: human immunodeficiency virus (HIV).
  • Neurotropic viruses: tick-borne encephalitis virus (here, BBB permeability is especially important).
  • Oncogenic viruses: human papillomavirus (HPV).
How to memorize

To remember the direct mechanism of action, use the 'Three NOTs' rule: does NOT allow protein synthesis, does NOT allow DNA/RNA integration into the capsid, does NOT allow the creation of a complete virus (defective particles proliferate).

Class and exam questions

Which pharmacological group does Cycloferon belong to?

This is a low-molecular-weight interferon inducer. It is not an M2 channel blocker, an HIV protease inhibitor, or a neuraminidase inhibitor.

What is the direct antiviral effect of meglumine acridonacetate?

The drug directly interferes with the viral replication cycle: it suppresses the synthesis of viral proteins and blocks the packaging of viral DNA/RNA into capsids. This leads to the mass production of defective, non-viable viral particles.

Why is the drug effective in tick-borne encephalitis?

Tick-borne encephalitis virus affects the tissues of the central nervous system. The drug's efficacy is due to its ability to freely cross the blood-brain barrier (BBB) and act at the site of neuroinfection.

Which cells are the main targets for the drug?

The drug acts predominantly on immunocompetent cells: lymphocytes, monocytes, and macrophages, stimulating them to produce endogenous interferon.

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What else to study on this topic

  • Mechanisms of endogenous interferon induction: receptor apparatus of monocytes and macrophages.
  • Comparative characteristics of interferon inducers and exogenous (recombinant) interferon preparations.
  • Stages of viral replication: protein synthesis, capsid assembly, and formation of defective particles.
  • Pharmacokinetics of antiviral agents: clinical significance of blood-brain barrier (BBB) permeability.
  • Features of the immune response in hepatitis B and C, HIV, and cytomegalovirus infections.

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