What is Enzymetherapy?

Most enzymes are proteins that accelerate chemical reactions in living organisms. They work by providing an alternative path of low activation energy for a reaction, thereby dramatically increasing the speed of the reaction. Catalysts have these functions in lifeless systems. Enzymes are therefore also called "biocatalysts". Without enzymes, biological processes might take place, but they would be much slower and life as we know it would not be possible.

The enzymes used in KaRazym® are proteases. They cleave proteins at the peptide bond between the individual amino acids. Modern enzyme therapy goes back to Max Wolf and Helene Benitez, who in the 1940s developed an enzyme mixture which, in similar composition, e.g. in KaRazym® is successfully used today for the treatment of chronic inflammatory conditions (for example rheumatism), swellings, thromboses etc. and also in complementary cancer therapy.

The effect of the enzyme therapy is actually not based on supporting the digestion by the proteases contained. Rather, the tablets provided with a gastric acid-resistant coating are first dissolved in the intestine. From there, the released ingredients pass through the intestinal wall into the blood, where they develop a systemic effect (see below).



Bromelain is the name of two enzymes from the family of cysteine proteases, which are found in the pineapple plant. They are extracted from their fruit (pineapple) and the plant itself (strain) and are generally used as an enzyme complex.


Papain is an enzyme that naturally occurs in relatively high concentrations in the still greenish peel and the kernels of the papaya fruit from which it is derived. The enzyme has a broad protein-splitting effect and belongs to the group of cysteine proteases.


The pancreatin used by Volopharm is derived from the pancreas of the pig. Pancreatin is a mixture of several enzymes and contains amylases, lipases and the proteases trypsin and chymotrypsin.


Rutin is not an enzyme but a flavonoid. Flavonoids are a group of phytochemicals, which include much of the floral colorants. With flavonoids, plants protect themselves against predators, diseases (such as fungal infestation) or even against UV radiation. Flavonoids have antiallergic and antiinflammatory, as well as antioxidant properties.

Mode of action


The vast majority of applications of KaRazym® are directly or indirectly related to inflammation. These are often chronic inflammatory conditions.

The establishment and degradation of inflammation is regulated by cytokines. Cytokines are local messengers, which allow the cells of the immune system to communicate with each other. Proinflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6) or the tumor necrosis factor α (TNF-α) help build an inflammatory response. They cause the migration of immune cells into the affected area to fight the cause of inflammation (such as a bee sting, injury or infection with bacteria). The patient also feels pain.

Normally, the inflammatory response diminishes when the cause has been eliminated. Anti-inflammatory cytokines such as Interleukin-4 (IL-4), Interleukin 10 (IL-10) or Vascular Endothelial Growth Factor (VEGF) stop the inflammatory response and initiate healing processes such as scarring or vascular and tissue remodeling.

In a healthy organism, the concentration of pro- and anti-inflammatory cytokines is small and both groups of cytokines are in equilibrium. During acute inflammation, proinflammatory cytokines and subsequently anti-inflammatory cytokines are overproduced, and after healing, equilibrium is re-established.

Chronic inflammation, on the other hand, leads to the simultaneous release of pro- and anti-inflammatory cytokines. In contrast to acute inflammation, a permanent overproduction of cytokines  is observed in chronic inflammation. Thus, the inflammation cannot subside and is maintained permanently.

Causes of chronic inflammation can be e.g. Bacteria that have survived through inconsistent antibiotic therapy or in anatomical niches (e.g., gallbladder, bowel diverticulum) and repeatedly provoke inflammatory responses. Other causes include the persistent supply of toxins such as alcohol, which can lead to chronic liver inflammation if abused, or the inhalation of asbestos, which can cause chronic pneumonia. Even autoimmune diseases, in which the immune system attacks the body's own structures, can cause chronic inflammatory conditions. Examples are rheumatoid arthritis, fibromyalgia, ankylosing spondylitis, psoriasis or lupus erythematosus.


The enzymes contained in KaRazym® are proteases (protein-splitting enzymes) that can bind to the body's own protein α-2-macroglobulin (a2M). A2M is an antiprotease that has the task of eliminating a broad spectrum of extrinsic proteases (e.g., ingested through food and entering the blood via the intestinal wall) and eliminating excess endogenous proteases (e.g., trypsin, elastase). After binding of the protease, a2M docks to the LRP receptor of the endothelial cells and is taken up into the cell. Subsequently, a2M and the protease are degraded in the vacuole of the cell.

However, this is not the only function of a2M. Upon binding of the protease, the molecule undergoes a conformational change, meaning it changes its structure. This releases binding sites for cytokines; one speaks now of activated a2M. The enzymes supplied with KaRazym® increase the amount of activated a2M and deliver more cytokines (pro- and anti-inflammatory) to the endothelial cells to be degraded (Bonner and Brody 1995, LaMarre et al., 1991).

The effect of Karazym® is thus to reduce the duration of acute inflammation and to curb the progression of chronic inflammation. Both take place by the disposal of excessively produced cytokines via the antiprotease a2M. A study (Wu, Patel and Pizzo 1998) even suggests that the affinity of a2M for proinflammatory cytokines such as TNF-α, IL-2 or IL-6 or for anti-inflammatory cytokines such as TGF-β changes depending on the phase of the inflammatory response.

The binding of proteases causes a conformational change of alpha-2-macroglobulin, thereby activating binding sites for cytokines.