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Pharmacology · Drugs and Prescriptions

Acidin-pepsin

Acidin-pepsini

Acidin-pepsin is a combination drug from the group of agents affecting the functions of the digestive organs. It provides a pronounced replacement effect, compensating for the deficiency of hydrochloric acid and proteolytic enzymes in the stomach for adequate food digestion.

Dosage form0.25 g tablets
RegimenOrally 0.2–0.5 g 3–4 times a day during or after meals
MediumCreates an acidic environment (source of HCl)
TargetDietary proteins (ensures proteolysis)
How to write a prescription
Rp.: Tab. "Acidin-pepsini" 0,25
D.t.d. N 50
S. Внутрь по 1-2 таблетки 3-4 раза в день во время или сразу после еды, предварительно растворив в 1/4-1/2 стакана воды

Alternative spelling options: Tab. Acidin-pepsini 0.25; Tabulettas "Acidin-pepsinum" 0.25; Tab. "Acidin-pepsinum" 0.25

Dosage form
Tab. 0.25 g
Administration
Orally 0.2–0.5 g 3–4 times a day during or immediately after meals
Group
Drugs Affecting Digestive System Functions
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

Mechanism of action and physiological principles

The action of the drug Acidin-pepsin (Acidin-pepsini) is based on the replacement effect — it artificially compensates for the deficiency of the stomach's own secretion (gaster).

Under physiological norms, parietal cells secrete hydrochloric acid (HCl). The mechanism of proton ($H^+$) transport from the cell cytoplasm across the membrane occurs in exchange for potassium ions ($K^+$). This creates a colossal gradient: inside the cell, the pH is 7.8, while in the gastric lumen, it is 0.8.

This sharply acidic environment is absolutely necessary for the functioning of proteolytic enzymes. The main one is pepsin, which carries out proteolysis (breakdown of protein structures). By taking the drug orally (per os), we deliver the ready-made enzyme and substrate to the stomach to create an acidic environment, triggering the digestive process even in the event of atrophy of the body's own glands.

Pharmacokinetics

The drug exerts its effect prior to absorption. Unlike most medicinal substances, for which the small intestine is the main site of absorption into the venous bed (portal vein for the first-pass effect) or the lymphatic duct, Acidin-pepsin works exclusively in the gastric lumen. It interacts with the food bolus and is subsequently destroyed or inactivated in the alkaline environment of the intestine.

Test your knowledge on the topicTasks from the «Pharmacology» course bank — instant answers and explanations.

Indications and place in combination therapy

The main indication is hypoacid conditions (reduced acidity) and insufficient enzyme production.

Gastric acidity directly affects the efficacy of other drugs. For example, the herbal preparation Nigedaza (a lipolytic from black cumin seeds) is less active at low acidity. In such cases, it is recommended to wash it down with gastric juice. Acidin-pepsin can serve as a pharmacological alternative, creating the required pH background for lipolytics to work.

Also, the drug is conceptually close to agents containing bile (where the gastric mucosa extract contains pepsin and cathepsin), which are prescribed for the comprehensive replenishment of gastric and pancreatic secretion deficiencies.

Mucosal defense factors and adverse effects

The introduction of exogenous acid and pepsin is the delivery of aggressive factors into the stomach. Normally, the epithelium is protected by a powerful gastroprotection system, the regulation of which depends on prostaglandins ($E_2$ and $I_2$):

  • Mucus: Hydrophilic glycoproteins form a physical gel that protects the wall from acid and pepsin.
  • Blood supply: Ensures the "washout" of hydrogen ions (back diffusion).
  • Bicarbonates: Neutralize acid on the cell surface.

If the drug is taken on an empty stomach or the dose is exceeded, the aggressiveness of pepsin and HCl may exceed the protective potential of the mucosa.

Clinical parallel: Excess acid and pepsin lead to mucosal damage. This is clearly manifested during long-term therapy with systemic glucocorticoids, which stimulate the secretion of HCl and pepsin, causing an ulcerogenic effect ("steroid" ulcers).

In hyperacid conditions and peptic ulcer disease, Acidin-pepsin is strictly contraindicated. In such situations, drugs with the opposite effect are used: antacids (magnesium oxide, algeldrate), $H_2$-histamine receptor blockers (reduce basal secretion of acid and pepsin), or gastroprotectors (sucralfate, which locally neutralizes HCl and reduces pepsin activity).

Prescribing and administration rules

The drug is available in 0.25 g tablets.

  • Dosage: Orally 0.2–0.5 g per single dose.
  • Frequency: 3–4 times a day.
  • Relation to food: Strictly during or immediately after meals. This is critically important so that the enzyme breaks down food proteins rather than attacking the gastric mucosa.
How to memorize

ACIDin (acidum — acid) + PEPSIN (enzyme) = artificial gastric juice for protein digestion.

Class and exam questions

Why should Acidin-pepsin be taken strictly during or after meals?

So that exogenous hydrochloric acid and the proteolytic enzyme (pepsin) interact with the food bolus. Taking it on an empty stomach will lead to an aggressive effect on the gastric mucosa.

How does the gastric mucosa normally protect itself against the aggression of pepsin and acid?

The basis of gastroprotection is mucus (hydrophilic glycoproteins), bicarbonate secretion, and adequate blood supply. A key role in stimulating this defense is played by prostaglandins E2 and I2.

In which iatrogenic pathologies is an excess of pepsin and HCl observed?

During long-term therapy with systemic glucocorticoids. They stimulate the secretion of hydrochloric acid and pepsin, which leads to an ulcerogenic effect (formation of ulcers).

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What else to study on this topic

  • Physiology of hydrochloric acid secretion: the work of the proton pump and ion exchange.
  • Aggression and defense factors of the gastric mucosa (the role of prostaglandins).
  • Ulcerogenic effect of medicinal products (using glucocorticoids as an example).
  • Pharmacology of antacids (absorbable and non-absorbable drugs).
  • Mechanism of action of H2-histamine receptor blockers and sucralfate.

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