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€129.00
KLOW 80mg EU – Buy Online | In Stock & Ready to Ship
Buy KLOW 80mg in Europe with fast shipping and guaranteed ≥99% purity — verified with COA and HPLC documentation. A trusted choice for peptides EU research teams rely on, with no customs delays or lengthy international wait times. Whether you’re searching for KLOW 80mg Europe suppliers, looking to buy KLOW 80mg in the EU, or sourcing peptides Europe-wide, we have you covered. Research teams across the EU can count on consistent stock, rapid fulfilment and full batch documentation every time.
For research use only. Not intended for human or veterinary use.



KLOW 80mg is a research-grade oral tablet formulation combining Ketoprofen and Omeprazole, available to buy in Europe for laboratory research into NSAID pharmacology, COX enzyme inhibition, prostaglandin biology, and gastrointestinal protection mechanisms in NSAID co-administration models.
Laboratories and research institutions across the EU can order verified, research-grade KLOW 80mg with fast international dispatch to Europe, full batch documentation, and verified purity confirmed by HPLC and analytical testing.
✅ Verified Purity — Analytically Tested
✅ Batch-Specific Certificate of Analysis (CoA)
✅ Oral Tablet Formulation | GMP Manufactured
✅ Fast Dispatch to EU & Europe | Tracked Shipping
KLOW 80mg is a combination research formulation containing Ketoprofen — a potent, non-selective non-steroidal anti-inflammatory drug (NSAID) — and Omeprazole — a proton pump inhibitor (PPI) — combined in a single oral tablet to enable research into NSAID pharmacology alongside the gastrointestinal protection strategies used to mitigate NSAID-associated gastric injury.
Ketoprofen is a propionic acid class NSAID that inhibits both cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) enzymes — the enzymes responsible for converting arachidonic acid into prostaglandins, thromboxanes, and prostacyclins that mediate inflammation, pain signalling, fever, and platelet aggregation. Its non-selective COX inhibition profile produces potent anti-inflammatory and analgesic effects while also reducing the gastroprotective prostaglandins normally produced by COX-1 activity in gastric mucosa — a mechanistic basis for NSAID-associated gastric injury that makes gastrointestinal protection research directly relevant to ketoprofen pharmacology.
Omeprazole is a benzimidazole PPI that irreversibly inhibits the H+/K+-ATPase proton pump in gastric parietal cells — reducing gastric acid secretion and raising intragastric pH. Its inclusion in the KLOW formulation mirrors the standard clinical and pre-clinical strategy of co-administering a PPI with NSAIDs to reduce gastric acid-mediated mucosal injury in the context of COX-1-mediated gastroprotective prostaglandin suppression.
Together, the KLOW combination provides a research tool for studying NSAID-PPI co-administration pharmacology — an area of significant interest in gastrointestinal protection research, drug interaction biology, and the mechanistic investigation of NSAID-associated gastric injury and its mitigation.
In laboratory settings, KLOW 80mg is studied as a combined NSAID-PPI formulation, with research applications spanning COX enzyme pharmacology, prostaglandin biology, and gastrointestinal protection mechanisms. EU and European researchers working with KLOW typically focus on:
All research applications are for in vitro and pre-clinical use only.
The individual components of KLOW — Ketoprofen and Omeprazole — each have extensive, well-characterised research literatures, with a growing body of combination pharmacology research examining their co-administration profile.
Ketoprofen COX inhibition: Ketoprofen is one of the most extensively studied propionic acid NSAIDs in the pre-clinical and clinical literature — with studies comprehensively characterising its dual COX-1/COX-2 inhibitory activity, its potency relative to other NSAIDs in prostaglandin synthesis inhibition assays, and its anti-inflammatory and analgesic effects in standard pre-clinical inflammatory models including carrageenan paw oedema, adjuvant arthritis, and writhing assays.
Gastrointestinal NSAID injury mechanisms: Research has established that NSAID-associated gastric injury involves two complementary mechanisms — topical irritant effects of acidic NSAID molecules on gastric mucosa, and systemic suppression of COX-1-derived gastroprotective prostaglandins (primarily PGE2 and PGI2) that normally maintain mucosal blood flow, bicarbonate secretion, and epithelial integrity. Studies using ketoprofen as the NSAID model have contributed to characterising both mechanisms and their relative contributions to mucosal injury.
Omeprazole PPI pharmacology: Omeprazole’s irreversible inhibition of the gastric H+/K+-ATPase proton pump is among the most comprehensively characterised drug mechanisms in gastrointestinal pharmacology — with studies documenting its dose-dependent acid suppression profile, the covalent nature of its pump inhibition, and its CYP2C19-mediated hepatic metabolism that produces individual variation in acid suppression responses relevant to pharmacokinetic research designs.
NSAID-PPI combination research: Studies examining PPI co-administration in NSAID users have characterised the degree of gastric mucosal protection conferred by acid suppression against NSAID injury — with research establishing that while PPI co-administration substantially reduces NSAID-associated gastric ulcer risk, it provides incomplete protection against small intestinal NSAID injury where acid suppression is not the primary injury mechanism. This distinction has driven continued research into the limits and mechanisms of PPI gastroprotection in NSAID models.
Ketoprofen central nervous system effects: Research has characterised ketoprofen’s ability to cross the blood-brain barrier and inhibit central COX activity — distinguishing it from NSAIDs with poor CNS penetration and making it relevant to research examining spinal and supraspinal prostaglandin-mediated pain sensitisation and central analgesic mechanisms.
Omeprazole drug interaction research: Studies have characterised omeprazole’s CYP2C19 inhibitory activity and its influence on the pharmacokinetics of co-administered drugs metabolised by this enzyme — a pharmacokinetic interaction relevant to combination formulation research and drug-drug interaction studies using the KLOW model.
| Compound | Type | COX Profile | GI Protection | Key Research Distinction |
|---|---|---|---|---|
| KLOW (Ketoprofen + Omeprazole) | NSAID + PPI combination | Non-selective COX-1/COX-2 | PPI co-administration model | Combined NSAID-GI protection pharmacology research |
| Ketoprofen alone | Propionic acid NSAID | Non-selective | None | Reference non-selective COX inhibitor |
| Ibuprofen | Propionic acid NSAID | Non-selective | None | High-volume reference NSAID, COX pharmacology |
| Celecoxib | Coxib NSAID | COX-2 selective | Reduced GI risk | Selective COX-2 inhibition research |
| Indomethacin | Indole acetic acid NSAID | Non-selective — potent | None | Potent reference NSAID, gastric injury model induction |
| Omeprazole alone | Proton pump inhibitor | None | H+/K+-ATPase inhibition | Reference PPI, acid suppression biology |
| Lansoprazole | Proton pump inhibitor | None | H+/K+-ATPase inhibition | Comparative PPI pharmacology research |
Every order of KLOW 80mg dispatched to EU and European research institutions includes:
Yes. We supply research-grade KLOW 80mg with fast tracked international dispatch to all EU member states and wider European destinations. All orders include full batch documentation and are packaged to maintain formulation integrity throughout transit. KLOW is supplied strictly for laboratory research use only.
Ketoprofen is a propionic acid class non-steroidal anti-inflammatory drug that inhibits both COX-1 and COX-2 isoforms of the cyclooxygenase enzyme — blocking the conversion of arachidonic acid to prostaglandins, thromboxanes, and prostacyclins. Its non-selective inhibition profile produces potent anti-inflammatory and analgesic effects through prostaglandin synthesis suppression in inflamed tissue, while simultaneously reducing the gastroprotective prostaglandins normally produced by constitutive COX-1 activity in gastric mucosa — the mechanistic basis for NSAID-associated gastric injury that makes PPI co-administration research relevant.
Omeprazole is a proton pump inhibitor (PPI) that irreversibly inhibits the H+/K+-ATPase enzyme in gastric parietal cells — the final common pathway of gastric acid secretion. By blocking acid production at its source, omeprazole raises intragastric pH and reduces the acid-mediated component of NSAID-associated gastric mucosal injury. Its inclusion in the KLOW combination reflects the established research and clinical strategy of PPI co-administration to mitigate NSAID gastric injury risk — providing a model for studying the pharmacodynamic interaction between acid suppression and NSAID-mediated prostaglandin depletion in gastrointestinal protection research.
COX-1 is a constitutively expressed isoform present in most tissues — including gastric mucosa, platelets, and kidney — where it produces prostaglandins with homeostatic functions including gastric mucosal protection, platelet aggregation, and renal blood flow regulation. COX-2 is an inducible isoform upregulated at sites of inflammation — producing the prostaglandins that drive inflammatory pain and fever. Non-selective NSAIDs like ketoprofen inhibit both isoforms — producing anti-inflammatory effects through COX-2 inhibition but also gastric and platelet effects through COX-1 inhibition. This distinction is central to NSAID pharmacology research and drives studies examining selective COX-2 inhibitors versus non-selective NSAIDs in gastrointestinal safety research.
NSAID-associated gastrointestinal injury is one of the most studied adverse drug effect mechanisms in pharmacology — with research establishing that COX-1-mediated gastroprotective prostaglandin suppression creates a vulnerability to acid-driven mucosal damage that PPI co-administration partially mitigates. The KLOW combination provides a defined, characterised research model for studying this interaction — enabling investigation of the mechanistic boundaries of PPI gastroprotection, the relative contributions of acid suppression versus prostaglandin replacement strategies, and the pharmacokinetic interactions between NSAID and PPI components in combined administration protocols.
KLOW 80mg is supplied as an oral tablet formulation. For in vitro research applications requiring solution preparation, tablets should be handled according to standard pharmaceutical research protocols — with appropriate solvent selection based on the research application. Store at room temperature in a dry environment protected from light and moisture. Standard laboratory safety protocols for handling pharmaceutical research compounds apply.
Orders are dispatched promptly via tracked international courier. Delivery to EU and European destinations typically takes 3–7 working days depending on location, with packaging designed to maintain formulation integrity throughout transit.
| Parameter | Detail |
|---|---|
| Type | Combination NSAID + PPI Oral Research Tablet |
| Active Components | Ketoprofen (NSAID) + Omeprazole (PPI) |
| Dose | 80mg per tablet |
| COX Profile | Non-selective COX-1 / COX-2 inhibition (Ketoprofen) |
| GI Mechanism | H+/K+-ATPase inhibition — acid suppression (Omeprazole) |
| Primary Research Interest | NSAID-PPI combination pharmacology, GI protection research |
| Form | Oral Tablet |
| Storage | Room temperature, dry, protected from light |
| Intended Use | Research use only |
KLOW 80mg is supplied exclusively for legitimate scientific research conducted within licensed laboratory environments. This product is not approved for human consumption, self-administration, or any therapeutic, clinical, or veterinary application. It must be handled solely by qualified researchers in compliance with applicable EU regulations, national legislation, and institutional ethics guidelines. By purchasing, you confirm this compound will be used exclusively for approved in vitro or pre-clinical research purposes.



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