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Hyphen BioMed offers a full range of platelet agonists and lyophilised platelets for platelet function analysis and exploration of  von Willebrand disease.

These reagents were specialy developed for the use with the Thrombo-Aggregometer TA~8V and Sysmex CS instruments but can be used on all Light Transmission  or Impedance  Platelet Function analysers.

Reagent Reference Package
ADP AG001K Set of 3×0.5 ml (43 µg)
Epinephrine AG002K Set of 3×0.5 ml (160 µg)
Arachidonic acid AG003K Set of 3×0.5 ml (2.5 mg)
Ristocetin AG004K Set of 3×0.5 ml (7.5 mg)
Collagen AG005K Set of 3×0.5 ml (0.5 mg)
Lyophilised Platelets AG006A 1x 5 ml
Lyophilised Platelets AG006K 3 x 5 ml

ADP

When added to platelet-rich plasma (PRP), adenosine 5′-diphosphate (ADP) binds to P2Y1 and P2Y12 receptors at the platelet surface, inducing a two-phase aggregation process. ADP mediated platelet activation leads to a change in platelet shape and induces an initial wave of aggregation. If the ADP concentration is sufficiently high, a second wave of aggregation occurs, following the release of the contents of platelet granules, consisting amongst others of serotonin, fibrinogen, thromboxane and endogenous ADP. ADP is considered to be a weak agonist as the effects it produces are partial and reversible.

Screening for thrombocytopathy, whether systemic (e.g.: Glanzmann thrombasthenia, Bernard-Soulier syndrome, gray platelet syndrome, etc.) or acquired (myelodysplastic syndrome, myeloproliferative disorder, multiple myeloma, Waldenström disease, liver or kidney failure, etc.).
Biological monitoring of anti-platelet therapy such as aspirin, NSAIDS, thienopyridines, abciximab or other glycoprotein IIb/IIIa (GPIIbIIIa) inhibitors.

Arachidonic acid

Arachidonic acid is converted to thromboxane A2 (TXA2) by the enzyme cyclooxygenase (COX) when added to platelet-rich plasma (PRP). The TXA2 generated induces platelet activation
and granules release, leading to a change in platelet shape, revealed by a decrease in light transmission, followed by a single wave of aggregation. Arachidonic acid is considered to be a
strong agonist1,2.

As ADP it is also used in the screening for thrombocytopathy, whether systemic (e.g.: Glanzmann thrombasthenia, Bernard-Soulier syndrome, gray platelet syndrome, etc.) or acquired (myelodysplastic syndrome, myeloproliferative disorder, multiple myeloma, Waldenström disease, liver or kidney failure, etc.).
Biological monitoring of anti-platelet therapy such as aspirin, NSAIDS, thienopyridines, abciximab or other glycoprotein IIb/IIIa (GPIIbIIIa) inhibitors.

Collagen

If collagen is added to platelet-rich plasma (PRP), it adheres to the platelets via the GPIa/IIa and GPVI receptors. GPVI receptor is responsible for platelet activation, leading to the release of ADP and thomboxane A2 and to intraplatelet calcium mobilisation1, 2, 3. Platelet aggregation in response to collagen typically displays a latency period determined by collagen concentration, followed by a change in platelet shape, revealed by a decrease in light transmission and finally simple wave of aggregation. Collagen is considered to be a strong agonist.

Collagen is used in the detection of constitutional thrombocytopathy (e.g.: Glanzmann thrombasthenia, grey platelet syndrome, empty sack syndrome, etc.) or acquired thrombocytopathy (e.g.: myelodysplastic syndrome, myeloproliferative syndrome, multiple myeloma, Waldenstrom’s disease, etc.).
Biological monitoring of anti-platelet therapy such as aspirin, NSAIDS, thienopyridines, abciximab or other glycoprotein IIb/IIIa (GPIIbIIIa) inhibitors.

Epinephirin

Epinephrine binds to the alpha 2-adrinergic receptors on the platelet surface, inducing an initial wave of reversible aggregation when added to platelet-rich plasma (PRP). This primary aggregation leads to exposure of fibrinogen receptors and inhibition of adenylate cyclase activity. A second wave of aggregation, clearly distinct from the first, is triggered by ADP release from alpha granules and by thromboxane A2 synthesis. Epinephrine is considered to be a weak agonist as the effects it produces are partial and reversible1,2

Ephinephirin can be used in the screening for thrombocytopathy, whether systemic (e.g.: Glanzmann thrombasthenia, Bernard-Soulier syndrome, gray platelet syndrome, etc.) or acquired myelodysplastic syndrome, myeloproliferative disorder, multiple myeloma, Waldenström disease, liver or kidney failure, etc.).
Biological monitoring of anti-platelet therapy such as aspirin, NSAIDS, thienopyridines, abciximab or other glycoprotein IIb/IIIa (GPIIbIIIa) inhibitors.

Ristocetin

When added to platelet-rich plasma (PRP), Ristocetin promotes interaction between von Willebrand factor (vWF) and its platelet receptor, glycoprotein GPIb-V-IX. Ristocetin-induced platelet aggregation (RIPA) is used to measure the patient’s PRP aggregation in the presence of various Ristocetin concentrations. Ristocetin can also be used for the vWF:RCo test, using lyophilized platelets.

Ristocetin reagent is available for use in Ristocetin-induced platelet aggregation (RIPA) tests. It is used to detect von Willebrand disease, more specifically to highlight an increase affinity in von Willebrand factor (vWF) for GPIb in type 2B and to identify Bernard-Soulier syndrome. Ristocetin reagent can also be used with lyophilized platelets (AG006A) for the Ristocetin cofactor activity assay (vWF:RCo), to assist in the diagnosis of von Willebrand disease.