Ketonal Sprint Max

CHARACTERISTICS OF THE MEDICINAL PRODUCT

1. NAME OF THE MEDICINAL PRODUCT

Ketonal Sprint, 25 mg, granules for oral solution, in sachet
Ketonal Sprint Max, 50 mg, granules for oral solution, in sachet

2. QUALITATIVE AND QUANTITATIVE COMPOSITION

Ketonal Sprint, 25 mg
One sachet contains 25 mg of ketoprofen (Ketoprofenum) in the form of ketoprofen lysinate (40 mg).
Ketonal Sprint Max, 50 mg
One divisible sachet contains 50 mg of ketoprofen (Ketoprofenum) in the form of ketoprofen lysinate (80 mg).
Full list of excipients: see section 6.1.

3. PHARMACEUTICAL FORM

Granules for oral solution, in sachet.
Granules are white or yellowish in color.

4. CLINICAL PARTICULARS

4.1 Therapeutic Indications

Ketonal Sprint is indicated for short-term symptomatic treatment of acute pain of mild or moderate intensity, such as:
headache
toothache
menstrual cramps
pain caused by minor sprains and strains
Ketonal Sprint is indicated for use in adults and adolescents from 16 years of age.

4.2 Posology and Method of Administration

Dosage
Taking the medicinal product in the smallest effective dose for the shortest duration necessary to relieve symptoms reduces the risk of adverse reactions (see section 4.4).
Adults and adolescents from 16 years of age

• 25 mg of ketoprofen up to three times a day or
• 50 mg of ketoprofen up to two times a day (which corresponds to 40 mg of ketoprofen lysinate up to three times a day or 80 mg of ketoprofen lysinate up to two times a day).

There should be at least an 8-hour interval between doses.
Elderly patients
In elderly patients, the dose should be determined by the doctor and, if necessary, a lower dose than the one mentioned above should be recommended (see section 4.4).
Children and adolescents
Ketonal Sprint is not intended for use in children and adolescents under 16 years of age.
The medicinal product is intended for short-term use only.
If adolescents from 16 years of age need to use this medicinal product for more than 3 days or if symptoms worsen, they should consult a doctor.
If adults need to use this medicinal product for more than 5 days or if symptoms worsen, they should consult a doctor.
Liver function disorders
In patients with mild or moderate liver function disorders, it is recommended to reduce the initial dose and continue treatment with the smallest effective dose (see section 4.4).
In patients with severe liver function disorders, the use of ketoprofen is contraindicated (see section 4.3).
Kidney function disorders
In patients with mild or moderate kidney function disorders, it is recommended to reduce the initial dose and continue therapy with the smallest effective dose. Individual dose adjustment should be considered only after good tolerance of the initial dose has been established.
Kidney function should be monitored (see section 4.4).
In patients with severe kidney function disorders, the use of ketoprofen is contraindicated (see section 4.3).
Method of administration
Oral administration.
Ketonal Sprint, 25 mg
The sachet contains granules with 25 mg of ketoprofen (which corresponds to 40 mg of ketoprofen lysinate).
Preparation of the oral solution, see section 6.6.
The solution should be taken during meals.
Ketonal Sprint Max, 50 mg
After opening the sachet along the line marked "half dose", granules with 25 mg of ketoprofen are obtained (which corresponds to 40 mg of ketoprofen lysinate).
After opening the sachet along the line marked "full dose", granules with 50 mg of ketoprofen are obtained (which corresponds to 80 mg of ketoprofen lysinate).
Preparation of the oral solution, see section 6.6.
The solution should be taken during meals.

4.3 Contraindications

Ketonal Sprint and Ketonal Sprint Max medicinal products should not be administered in the following cases:
hypersensitivity to the active substance, to acetylsalicylic acid (ASA) or to other nonsteroidal anti-inflammatory drugs (NSAIDs), or to any of the excipients listed in section 6.1;
in patients with a history of hypersensitivity reactions, such as bronchospasm, asthma attack, acute rhinitis, urticaria, nasal polyps, angioedema, or other types of allergic reactions caused by the administration of ketoprofen or other substances with a similar mechanism of action (e.g., acetylsalicylic acid or other NSAIDs). In such patients, severe, sometimes fatal, anaphylactic reactions have been reported (see section 4.8).
in patients with a history of asthma;
active peptic ulcer and/or gastrointestinal bleeding or recurrent bleeding and/or ulceration in the gastrointestinal tract in history (two or more confirmed, separate episodes of bleeding or ulceration);
gastrointestinal bleeding, ulceration, or perforation in history or chronic dyspepsia;
gastrointestinal bleeding or perforation after previous NSAID treatment in history;
leukopenia or thrombocytopenia;
Crohn's disease or ulcerative colitis;
gastritis;
severe heart failure;
severe liver failure (liver cirrhosis, severe hepatitis);
severe kidney failure.
bleeding disorders and other coagulation disorders, patients with hemostasis disorders;
patients undergoing intensive diuretic treatment;
third trimester of pregnancy.

4.4 Special Warnings and Precautions for Use

Warnings
Taking the medicinal product in the smallest effective dose for the shortest duration necessary to relieve symptoms reduces the risk of adverse reactions (see section 4.2 and below: risk of gastrointestinal complications and cardiovascular).
Concomitant use of ketoprofen with other nonsteroidal anti-inflammatory drugs (NSAIDs), including selective cyclooxygenase-2 inhibitors, is not recommended.
Gastrointestinal bleeding, ulceration, and perforation
All NSAIDs have been associated with gastrointestinal bleeding, ulceration, and perforation (with possible fatal outcome), which may occur at any time during treatment, even without warning symptoms or a history of serious gastrointestinal events.
Some epidemiological data suggest that the use of ketoprofen (especially high doses) may be associated with a higher risk of severe gastrointestinal toxicity compared to some other NSAIDs (see also sections 4.2 and 4.3).
Care should be taken in patients receiving concomitant medications that may increase the risk of gastrointestinal ulceration or bleeding, such as oral corticosteroids, anticoagulants (e.g., warfarin), selective serotonin reuptake inhibitors, antiplatelet agents (e.g., acetylsalicylic acid), or nicorandil (see section 4.5).
The risk of gastrointestinal bleeding, ulceration, or perforation is higher during the use of higher doses of NSAIDs, in patients with a history of peptic ulcer disease of the stomach and/or duodenum, especially if complicated by bleeding or perforation (see section 4.3), and in elderly patients. In these patients, treatment should be initiated with the lowest available dose.
In these patients, as well as in patients who require concomitant use of low-dose acetylsalicylic acid or other medications that may increase the risk of gastrointestinal complications, consideration should be given to the concurrent use of medications with a protective effect, such as misoprostol or proton pump inhibitors (see below and section 4.5).

• 4.5).

Patient monitoring
Patient with a history of gastrointestinal complications, especially the elderly, should report any unusual abdominal symptoms (especially gastrointestinal bleeding), especially during the initial treatment period.
Elderly patients: the frequency of adverse reactions associated with NSAID use increases in elderly patients, especially gastrointestinal bleeding and perforation, which can be fatal (see section 4.2).
If gastrointestinal bleeding or peptic ulcer disease occurs in patients taking ketoprofen, treatment should be discontinued.
Skin reactions:
Severe skin reactions (some with a fatal outcome), including exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis, have been very rarely reported in association with NSAID use (see section 4.8). The risk of such reactions is likely to be higher in the initial treatment period – in most cases, they occurred within the first month of treatment. Upon the appearance of the first signs of a rash, mucosal lesions, or any other symptoms of hypersensitivity, ketoprofen should be discontinued.
Ketonal Sprint and Ketonal Sprint Max do not affect low-calorie diets or controlled diets and may be administered to patients with diabetes.
Ketonal Sprint and Ketonal Sprint Max do not contain gluten, so the medicinal product is not contraindicated in patients with celiac disease.
From clinical trials and epidemiological data, it appears that the use of some nonsteroidal anti-inflammatory drugs (especially in high doses and long-term) may be associated with an increased risk of arterial thrombotic events (e.g., myocardial infarction or stroke). These data are insufficient to exclude such a risk for ketoprofen.
There have also been reports of an increased risk of arterial thrombotic events in patients treated with NSAIDs (excluding acetylsalicylic acid) in postoperative pain after coronary artery bypass grafting (CABG).
Children and adolescents
In some children and adolescents taking ketoprofen lysinate, gastrointestinal bleeding (sometimes severe) and ulceration have been reported (see section 4.8). For this reason, the medicinal product should be used in these patients under close medical supervision, and the doctor should assess the treatment regimen individually for each patient.
This medicinal product is not intended for children and adolescents under 16 years of age.
Patient with a history of gastrointestinal disease should be carefully monitored for signs of gastrointestinal disorders, especially gastrointestinal bleeding.
Patient with active or history of peptic ulcer disease:
NSAIDs should be used with caution in patients with a history of gastrointestinal diseases (ulcerative colitis, Crohn's disease), as these conditions may worsen (see section 4.8 - Adverse Reactions).
Precautions
Disorders of the cardiovascular, renal, and hepatic systems:
In patients with renal function disorders, ketoprofen should be administered with caution due to the fact that the drug is primarily eliminated by the kidneys.
In patients with heart failure, cirrhosis, and nephrotic syndrome, patients taking diuretics, patients with chronic renal failure, especially the elderly, it is necessary to carefully monitor renal function at the beginning of treatment. Administration of ketoprofen to these patients may cause a decrease in renal perfusion due to inhibition of prostaglandin synthesis and lead to decompensation of renal function (see section 4.3 – Contraindications).
Care should also be taken in patients taking diuretics or in patients who may develop hypovolemia, as the risk of nephrotoxicity is increased.
As with all NSAIDs, the medicinal product may increase the levels of urea and creatinine in the blood.
As with other prostaglandin synthesis inhibitors, the medicinal product may be associated with adverse renal effects, which can lead to interstitial nephritis, renal papillary necrosis, nephrotic syndrome, and acute renal failure.
In patients with abnormal liver function test results or a history of liver disease, liver enzymes should be periodically monitored, especially during long-term treatment. As with other NSAIDs, the medicinal product may cause minor, transient increases in some liver parameters, as well as significant increases in aspartate aminotransferase (SGOT) and alanine aminotransferase (SGPT) activity. If significant increases in these parameters are observed, treatment should be discontinued.
There have been rare reports of jaundice and hepatitis during ketoprofen use.
During long-term treatment, liver and kidney function tests and blood morphology should be performed.
Elderly patients are more susceptible to worsening of renal, cardiovascular, or hepatic function.
Effect on circulation and cerebrovascular system:
As with all NSAIDs, caution should be exercised when treating patients with uncontrolled hypertension, congestive heart failure, established ischemic heart disease, peripheral artery disease, and/or cerebrovascular disease, as well as before starting long-term treatment in patients with risk factors for cardiovascular disease (e.g., hypertension, hyperlipidemia, diabetes, smoking).
In patients with a history of hypertension and/or mild to moderate congestive heart failure, careful monitoring and appropriate recommendations are necessary, as NSAID treatment has been associated with fluid retention and edema.
Data from clinical trials and epidemiological data indicate that the use of some nonsteroidal anti-inflammatory drugs (especially in high doses and long-term) may be associated with an increased risk of arterial thrombotic events (e.g., myocardial infarction or stroke). There is insufficient data to exclude such a risk for ketoprofen.
There have been reports of an increased risk of atrial fibrillation associated with NSAID use.
Hyperkalemia is possible, especially in patients with diabetes, renal failure, and/or taking concomitant medications that promote hyperkalemia (see section 4.5). In such cases, regular monitoring of potassium levels is necessary.
Masking of infection symptoms:
Ketoprofen may mask the symptoms of infection, leading to delayed initiation of appropriate treatment and worsening of infection outcomes. This phenomenon has been observed in cases of community-acquired bacterial pneumonia and bacterial complications of chickenpox.
If ketoprofen is used for fever or pain associated with infection, it is recommended to monitor the course of the infection. In outpatient settings, the patient should consult a doctor if symptoms persist or worsen.
The medicinal product should be administered with caution in patients with a history of allergy or allergic reactions.
NSAIDs may impair female fertility (see section 4.6).
Respiratory diseases:
As with all NSAIDs, ketoprofen use in patients with asthma or allergic rhinitis may trigger an asthma attack.
In patients with asthma associated with chronic rhinitis, chronic sinusitis, and/or nasal polyps, allergic reactions to acetylsalicylic acid and/or NSAIDs are more common than in other individuals. Administration of Ketonal Sprint may trigger an asthma attack or bronchospasm, especially in individuals allergic to acetylsalicylic acid or NSAIDs (see section 4.3). Due to the interaction of the medicinal product with arachidonic acid metabolism, patients with asthma and those prone to it may experience bronchospasm, and even anaphylaxis and other allergic conditions.
Visual disturbances:
In case of visual disturbances (such as blurred vision), treatment should be discontinued.
Ketonal Sprint and Ketonal Sprint Max should be administered with caution in patients with hematopoietic disorders, systemic lupus erythematosus, or mixed connective tissue disease.
Ketonal Sprint and Ketonal Sprint Max contain less than 1 mmol (23 mg) of sodium per sachet, which means the medicinal product is considered "sodium-free".

4.5 Interaction with Other Medicinal Products and Other Forms of Interaction

Concomitant use is not recommended
Other NSAIDs (including selective cyclooxygenase-2 inhibitors) and high-dose salicylates (>3 g/day):
concomitant use of different NSAIDs, due to a synergistic effect, may increase the risk of gastrointestinal ulceration and bleeding.
Anticoagulants (heparin and vitamin K antagonists [e.g., warfarin]):
NSAIDs may enhance the effect of anticoagulants, such as warfarin (see section 4.4). Increased risk of bleeding due to inhibition of platelet function and gastrointestinal mucosal damage (see section 4.4). If concomitant use cannot be avoided, patients should be closely monitored.

• 4.4). Increased risk of bleeding due to inhibition of platelet function and gastrointestinal mucosal damage (see section 4.4). If concomitant use cannot be avoided, patients should be closely monitored

Platelet aggregation inhibitors (e.g., ticlopidine and clopidogrel):
increased risk of bleeding due to inhibition of platelet function and gastrointestinal mucosal damage (see section 4.4). If concomitant use cannot be avoided, patients should be closely monitored.
Lithium (interactions have been reported with various NSAIDs):
risk of increased lithium levels in the blood (sometimes to toxic values) due to decreased renal excretion. If necessary, careful monitoring of lithium levels in the blood and adjustment of the dose at the start and end of ketoprofen treatment and other NSAIDs is recommended.
Methotrexate at a dose of 15 mg/week or higher:
increased risk of methotrexate hematologic toxicity, especially when used in high doses (≥15 mg/week), likely due to displacement of methotrexate from protein binding sites and decreased renal clearance by anti-inflammatory drugs in general.
A minimum of 12 hours should be allowed between discontinuation or initiation of ketoprofen treatment and methotrexate administration.
Hydantoin derivatives (e.g., phenytoin) and sulfonamides:
ketoprofen may enhance the toxic effects of these substances.
Concomitant use requiring caution
Medicinal products and groups of medicinal products that may promote hyperkalemia (i.e., potassium salts, potassium-sparing diuretics, ACE inhibitors, and angiotensin II receptor antagonists, NSAIDs, heparins [low molecular weight or unfractionated], cyclosporine, tacrolimus, and trimethoprim):
risk of hyperkalemia may be increased when the above-mentioned medicinal products are used concomitantly.
Tenofovir:
concomitant use of tenofovir disoproxil fumarate and NSAIDs may increase the risk of renal failure.
Diuretics:
in patients, especially dehydrated ones, taking diuretics, there is an increased risk of developing secondary renal failure due to decreased perfusion resulting from inhibition of prostaglandin synthesis. These patients should be hydrated before starting concomitant treatment, and their renal function should be closely monitored after starting treatment (see section 4.4). NSAIDs may reduce the effect of diuretics.
ACE inhibitors and angiotensin II receptor antagonists:
in patients with renal function disorders (e.g., dehydrated and elderly patients), concomitant use of an ACE inhibitor or angiotensin II receptor antagonist and a drug that inhibits cyclooxygenase activity may cause further deterioration of renal function, with the possibility of acute renal failure. Therefore, this combination should be used with caution, especially in elderly patients. Patients should be properly hydrated, and renal function should be considered after starting concomitant treatment.
Methotrexate at doses lower than 15 mg/week:
increased risk of methotrexate hematologic toxicity due to decreased renal clearance by anti-inflammatory drugs in general. During the first few weeks of concomitant treatment, weekly monitoring of blood morphology is necessary. Control tests should be performed more frequently in case of any changes in renal function and in elderly patients.
Corticosteroids:
increased risk of gastrointestinal ulceration or bleeding (see section 4.4).
Pentoxifylline:
increased risk of bleeding. More frequent clinical monitoring of the patient's condition and control of bleeding time are necessary.
Zidovudine:
risk of increased toxic effects on red blood cells due to an unfavorable effect on reticulocytes, with the possibility of severe anemia within a week of starting NSAID use. Within 1 to 2 weeks of starting ketoprofen lysinate treatment, complete blood count and reticulocyte count should be monitored.
Sulfonylurea derivatives:
NSAIDs may enhance the hypoglycemic effect of sulfonylurea derivatives by displacing them from protein binding sites in the blood.
Digitalis glycosides:
NSAIDs may worsen heart failure, reduce glomerular filtration, and increase glycoside levels in the blood. However, no pharmacokinetic interaction has been demonstrated between ketoprofen and active glycosides.
Nicorandil:
concomitant use of nicorandil and NSAIDs may increase the risk of severe complications, such as gastrointestinal ulceration, perforation, and bleeding (see section 4.4).
Concomitant use to be considered
Antihypertensive drugs (beta-blockers, ACE inhibitors, diuretics):
NSAIDs may reduce the effect of antihypertensive drugs. NSAID treatment may reduce their antihypertensive effect by inhibiting the synthesis of vasodilatory prostaglandins.
Mifepristone:
the efficacy of the contraceptive method may be theoretically reduced due to the anti-prostaglandin properties of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin (acetylsalicylic acid). There is some evidence to suggest that concomitant use of NSAIDs on the day of prostaglandin administration does not adversely affect the efficacy of mifepristone or prostaglandin on cervical ripening and uterine contractions, and does not reduce the clinical efficacy of medical abortion.
Intrauterine contraceptive devices:
the efficacy of the device may be reduced, which may lead to pregnancy.
Cyclosporine, tacrolimus:
risk of additional nephrotoxic effects, especially in elderly patients.
Thrombolytic agents:
increased risk of bleeding.
Antiplatelet agents (ticlopidine and clopidogrel) and selective serotonin reuptake inhibitors (SSRIs):
increased risk of gastrointestinal bleeding (see section 4.4).
Probenecid:
concomitant use of probenecid may significantly reduce the clearance of ketoprofen from the blood, resulting in increased ketoprofen levels in the blood; this interaction may be due to a mechanism that inhibits renal tubular secretion and glucuronidation, and requires adjustment of the ketoprofen dose.
Quinolone antibiotics:
data from animal studies suggest that NSAIDs may increase the risk of seizures associated with quinolone antibiotic use. Patients taking NSAIDs and quinolones may be at increased risk of seizures.
Diphenylhydantoin and sulfonamides:
since ketoprofen is highly bound to plasma proteins, it may be necessary to reduce the dose of diphenylhydantoin or sulfonamides during treatment.
Gemeprost:
reduced efficacy of gemeprost.
Alcohol consumption should be avoided

4.6 Fertility, Pregnancy, and Lactation

Pregnancy
Ketoprofen should be avoided during the first and second trimesters of pregnancy.
Inhibition of prostaglandin synthesis may have a harmful effect on pregnancy and/or fetal/embryo development. Epidemiological data suggest that the use of a prostaglandin synthesis inhibitor in early pregnancy is associated with an increased risk of miscarriage and fetal heart defects, as well as intestinal malformations. The absolute risk of cardiovascular defects increased from less than 1% to approximately 1.5%. It is believed that the risk increases with the dose and duration of treatment. Animal studies have shown that the administration of a prostaglandin synthesis inhibitor results in increased pre- and post-implantation loss of embryos and increased fetal and embryonic mortality. Additionally, it has been shown that the administration of a prostaglandin synthesis inhibitor to animals during the organogenesis period increases the frequency of various developmental abnormalities, including those affecting the cardiovascular system.
Ketoprofen should not be used during the first and second trimesters of pregnancy, unless absolutely necessary.
From the 20th week of pregnancy, ketoprofen use may cause oligohydramnios due to fetal renal function disorders. This can occur shortly after starting treatment and is usually reversible after discontinuation. Additionally, there have been reports of fetal ductus arteriosus constriction after treatment in the second trimester, which in most cases resolved after treatment discontinuation. Therefore, ketoprofen should not be used during the first and second trimesters of pregnancy, unless absolutely necessary. If ketoprofen is used in women attempting to conceive or in women during the first and second trimesters of pregnancy, it should be administered in the smallest possible dose for the shortest possible time. Consideration should be given to monitoring for oligohydramnios and ductus arteriosus constriction after exposure to ketoprofen for several days from the 20th week of pregnancy. Ketoprofen should be discontinued in case of oligohydramnios or ductus arteriosus constriction.
All prostaglandin synthesis inhibitors:

• when used in the third trimester of pregnancy, may expose the fetus to:
• cardiovascular and pulmonary toxicity (premature constriction/closure of the ductus arteriosus and pulmonary hypertension);
• renal dysfunction, which may lead to renal failure with oligohydramnios (see above);
• when used at the end of pregnancy, may expose the mother and the newborn to:
• prolonged bleeding time, anti-aggregatory effect, which may occur even with low doses of ketoprofen;
• inhibition of uterine contractions, leading to delayed or prolonged labor.

The use of ketoprofen in the third trimester of pregnancy is contraindicated.
Breast-feeding
There are no available data on the excretion of ketoprofen into human milk. The medicinal product is not recommended for use in breast-feeding women.
Fertility
The use of NSAIDs may impair female fertility and is not recommended in women planning to become pregnant. The use of Ketonal Sprint and Ketonal Sprint Max, as well as any drugs that inhibit prostaglandin synthesis and cyclooxygenase inhibitors, is not recommended in women who intend to become pregnant. In women who have difficulty becoming pregnant or who are undergoing fertility testing, consideration should be given to discontinuing NSAIDs.

4.8 Effects on Ability to Drive and Use Machines

Ketonal Sprint has no or negligible influence on the ability to drive and use machines. However, patients should be warned about the possibility of adverse reactions, such as drowsiness, dizziness, seizures, or blurred vision, and advised not to drive or operate machinery in such cases.

4.8 Adverse Reactions

The most commonly observed adverse reactions are related to the gastrointestinal tract. Gastrointestinal ulceration, perforation, or bleeding (sometimes fatal) may occur, especially in elderly patients (see section 4.4). Nausea, vomiting, diarrhea, bloating, constipation, indigestion, abdominal pain, dyspepsia, and stomatitis have also been reported. Less frequently, gastritis has been observed.
In clinical trials in infants and children, vomiting, diarrhea, and hypersensitivity reactions have been reported.
Classification of adverse reaction frequency: very common (≥1/10); common (≥1/100 to <1>The following adverse reactions have been reported during ketoprofen use in adults:

From clinical trials and epidemiological data, it appears that the use of some nonsteroidal anti-inflammatory drugs (especially in high doses and long-term) may be associated with an increased risk of arterial thrombotic events (e.g., myocardial infarction or stroke), see section 4.4.
Reporting of suspected adverse reactions
After the medicinal product has been placed on the market, it is important to report any suspected adverse reactions. This allows for continuous monitoring of the benefit/risk ratio of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Department of Adverse Reaction Monitoring of Medicinal Products, Medical Devices, and Biocides of the Office for Registration of Medicinal Products, Medical Devices, and Biocides: Al. Jerozolimskie 181C, 02-222 Warsaw, tel.: +48 22 49 21 301, fax: +48 22 49 21 309, website: https://smz.ezdrowie.gov.pl
Adverse reactions can also be reported to the marketing authorization holder.

4.9 Overdose

Symptoms
There have been reports of ketoprofen overdose after administration of doses up to 2.5 g. In most cases, the symptoms were mild and limited to lethargy, drowsiness, nausea, vomiting, and abdominal pain, headache, dizziness, and diarrhea.
In cases of severe overdose, hypotension, respiratory depression, and gastrointestinal bleeding have been observed.
Patient should be immediately taken to a specialized center for initiation of symptomatic treatment.
Procedure
There is no specific antidote in case of ketoprofen overdose.
In case of significant overdose, the recommended procedure includes gastric lavage in combination with symptomatic and supportive treatment to correct dehydration, monitor urine output, and correct possible acidosis.
Close monitoring of renal and liver function is necessary. In case of renal failure, hemodialysis may be useful in removing the drug from the body.

5. PHARMACOLOGICAL PROPERTIES

5.1 Pharmacodynamic Properties

Therapeutic group: nonsteroidal anti-inflammatory and anti-rheumatic drugs, propionic acid derivatives.
ATC code: M01AE03
Mechanism of action
The mechanism of action of NSAIDs is associated with a decrease in prostaglandin synthesis due to inhibition of cyclooxygenase enzyme activity.
Particularly, it can be observed that the conversion of arachidonic acid to cyclic endoperoxides prostaglandins G (PGG) and H (PGH), precursors of prostaglandins PGE, PGE, PGF, and PGD, as well as prostacyclin PGI and thromboxanes (TxA and TxB), is inhibited. Additionally, the inhibition of prostaglandin synthesis may disrupt the function of other inflammatory mediators, such as kinins, resulting in indirect effects, in addition to the direct effect.
Pharmacodynamic effects
Ketoprofen lysinate (2-(3-benzoylphenyl) propionic acid) has analgesic, anti-inflammatory, and antipyretic effects. It belongs to the class of nonsteroidal anti-inflammatory drugs (NSAIDs). Ketoprofen lysinate is more soluble than the acid form.
Ketoprofen lysinate has potent analgesic effects, which correlate with both anti-inflammatory and central effects. It has antipyretic effects without disrupting physiological thermoregulatory processes.
It causes the regression or alleviation of painful inflammatory conditions, which promotes joint mobility.

5.2 Pharmacokinetic Properties

Ketoprofen lysinate is more soluble than the acid form.
Absorption
The pharmaceutical form (granules for oral solution) allows the active substance to be taken in an aqueous solution. This leads to a rapid increase in the concentration of the active substance in the blood and a rapid achievement of the maximum concentration. The clinical consequence is a rapid onset of action and enhanced analgesic and anti-inflammatory effects.
The pharmacokinetic profile in children does not differ from that in adults.
Distribution
Multiple administration does not change the kinetics of the drug.
Elimination
Ketoprofen is primarily eliminated by the kidneys.

5.3 Preclinical safety data

After oral administration, the LD value of ketoprofen lysinate in rats and mice was, respectively
102 and 444 mg/kg, which corresponds to 30-120 times the active dose with anti-inflammatory
and analgesic effects in the tested animals. After intraperitoneal administration, the LD value of ketoprofen lysinate
in rats and mice was, respectively, 104 and 610 mg/kg.
In rats, dogs, and monkeys, long-term oral administration of ketoprofen lysinate in doses equal to
or higher than the recommended therapeutic doses did not cause any toxic effects. After administration of high doses, changes related to the gastrointestinal tract
and kidneys associated with the known adverse effects caused by non-steroidal anti-inflammatory drugs in animals were found.
In a long-term toxicity study conducted in rabbits, it was shown that ketoprofen administered rectally is better tolerated than when administered orally. In tolerance studies conducted in rabbits, ketoprofen lysinate administered intramuscularly was well tolerated.
In in vitroand in vivostudies, no mutagenic effect of ketoprofen lysinate was found.
In studies on mice and rats, it was not found that ketoprofen has a carcinogenic effect.
Data on the toxic effects of NSAIDs on the embryo and fetus, as well as on teratogenic effects, see section 4.6.

6. DETAILED PHARMACEUTICAL PARTICULARS

6.1 List of excipients

Mannitol (E 421)
Povidone K30
Peanut flavor (contains maltodextrin and arabic gum)
Sodium chloride
Sodium saccharin
Colloidal anhydrous silica

6.2 Incompatibilities

None known.

6.3 Shelf life

3 years
The solution obtained after dissolving the granulate should be used immediately after preparation.

6.4 Special precautions for storage

No special storage precautions.

6.5 Nature and contents of container

Ketonal Sprint 25 mg
The medicinal product is packaged in paper/Aluminum/PE sachets, in a cardboard box.
Pack sizes: 12, 15, and 18 sachets.
Ketonal Sprint Max 50 mg
The medicinal product is packaged in double sachets paper/Aluminum/PE, in a cardboard box.
Pack sizes: 6, 8, 10, and 12 double sachets.
Not all pack sizes may be marketed.

6.6 Special precautions for disposal and preparation of the medicinal product for

administration
Ketonal Sprint 25 mg
Pour the contents of the sachet into a glass half-filled with water (50 ml) and mix thoroughly
for about 30 seconds, until the granulate is dissolved.
Ketonal Sprint Max 50 mg
Pour the contents of the sachet into a glass of water (100 ml) and mix thoroughly for about 30 seconds,
until the granulate is dissolved.
Any unused medicinal product or waste should be disposed of in accordance with local regulations.

7. MARKETING AUTHORISATION HOLDER

RESPONSIBLE FOR BATCH RELEASE

Sandoz GmbH
Biochemiestrasse 10
6250 Kundl, Austria

8. MARKETING AUTHORISATION NUMBER

Ketonal Sprint 25 mg
Marketing authorisation number: 24985
Ketonal Sprint Max 50 mg
Marketing authorisation number: 24986

9. DATE OF FIRST AUTHORISATION

AND RENEWAL

Date of first authorisation: 15.11.2018

10. DATE OF REVISION OF THE TEXT

OF THE SUMMARY OF PRODUCT CHARACTERISTICS

14.03.2025