"Supralimus"


				"Supralimus"



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The Supralimus™ Stent is designed to prevent in-stent restenosis. Supralimus™ Stent consists of CE approved metallic stent platform (Matrix™) with versatile combination of biocompatible/biodegradable polymer and clinically proven sirolimus drug.

The Supralimus™ Sirolimus Eluting Coronary Stent provides excellent scaffolding to the artery wall which prevents re-blockage; while the drug is released in a programmable pattern. The Drug/Polymer coating is adhered to the entire stent surface. Supralimus™ stent has been widely accepted by the interventional cardiologist for the treatment of patients with complex coronary artery disease.

The delivery vehicle used in Supralimus™ is biodegradable / biocompatible polymers that fulfil pharmacological, pharmacokinetic, and mechanical requirements. The release of the drug into the vessel take place in a manner that is consistent with the drug's mode of action. Drug release is predictable and in a controlled concentration and time. The delivery vehicle is suitable for sterilization and follows the geometric change of configuration during stent expansion and resists mechanical injury caused by the inflation of the balloon.

Supralimus Sirolimus Eluting Stent utilizes our proven The Millennium Matrix™ Coronary Stent System for uniform drug delivery and exhibited following characteristics :

Insignificant action against fibrinogen content in the plasma
The shortening of PTT was minimum.
Rare leukocytes adhesion.
Insignificant Platelet adhesion on surface.
Reduction in the platelet response during the 1hr exposure.
Insignificant elevation of platelet granule protein PF4.
Insignificant difference in platelet width.
Insignificant reduction in RBC, WBC.
No cytotoxic response.
Comparable EC attachment and proliferation.
Safe in humans at blood concentrations far exceeding dose delivered from stents

Mechanism of Action

Although the pre-drug sirolimus (SRL) binds to FKBP-12, the complex that is formed between SRL and FKBP binds to the mammalian target of rapamycin (mTOR). The SRL-FKBP-mTOR complex inhibits biochemical pathways that are required for cell progression through the late G1 phase or entry into the S phase of the cell cycle. Thus, unlike cyclosporine (CsA), SRL blocks cytokine signal transduction. SRL is thought to target:

(1)The 70-kD S6 protein kinase p70S6K

(2)The eukaryotic initiation factor eIF-4F

Sirolimus-Eluting Coronary Stent