On structure-related properties of synthetic organic clot-dissolving (thrombolytic) compounds

Kaulla, K. N. von; Ens, Gordon

doi:10.1016/0006-2952(67)90275-4

Cited by 15 publications

(8 citation statements)

References 11 publications

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“…He found that a fibrin clot formed from plasma containing various synthetic bulky anionic compounds would spontaneously lyze when it was incubated in vitro . Although the pathway by which this fibrinolysis induction occurs was not fully understood, he postulated that the synthetic fibrinolysis‐inducing compounds evoke fibrinolytic activity indirectly by inactivating inhibitors of fibrinolysis since the compounds did not activate plasminogen directly [7]. I was asked to explore this possibility.…”

Section: Initiation Of the Researchmentioning

confidence: 99%

Discovery of α2‐plasmin inhibitor and its congenital deficiency

Aoki

2005

Journal of Thrombosis and Haemostasis

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Section: Initiation Of the Researchmentioning

confidence: 99%

Discovery of α2‐plasmin inhibitor and its congenital deficiency

Aoki

2005

Journal of Thrombosis and Haemostasis

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“…Compound No. 35724 Our next interest was to look at the possible mechanism of action of those synthetic fibrinolytic agents which are derivatives of salicylic acid and which were studied first by von Kaulla (11). Fig.2 shows t he formula of such a compound which was representative for that group and which was investigated as is demonstrated by Fig.…”

Section: Resultsmentioning

confidence: 99%

A Method to Study Inhibitors of Plasminogen Activation

Hd¹

1971

Thromb Haemost

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SummaryA method to study inhibitors of plasminogen activation is described. It is mainly thought to be a one-stage plasminogenolytic method. The same type of inhibition is found in this one-stage assay system and in a two-stage caseinolytic assay system when epsilon aminocaproic acid and salicylic acid derivatives are investigated in parallel in both assay systems. Epsilon aminocaproic acid and salicylic acid derivatives inhibit the activation of plasminogen by urokinase in a competitive way. Alpha2-macroglobulin and antithrombin III did not inhibit the activation of plasminogen by urokinase.

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“…However, a Type III has also been reported where the molecule is structurally and functionally normal but somehow there is improper interaction between the AT and heparin [5]. Acquired antithrombin deficiency can occur due medication with heparin, disseminated intravascular coagulation, liver disease or nephrotic syndrome [6,7].…”

Section: Discussionmentioning

confidence: 99%

Cortical Venous Thrombosis due to Familial AT-III Deficiency Presenting with Seizures

Purkait¹,

Ghosh²,

Samanta³

et al. 2016

JCR

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Abstract:Cortical venous thrombosis is a rare but treatable condition of the central nervous system which can manifest with bizarre signs and symptoms. However, a prompt clinical suspicion which can be confirmed by a T2 weighted MR image followed by venography is immediately needed to assess the patient and start therapy. We report a case of familial anti-thrombin III deficiency in a young male who presented to us with seizures. Successful treatment of this patient holds promise of an essentially non curable neurological condition.

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On structure-related properties of synthetic organic clot-dissolving (thrombolytic) compounds

Cited by 15 publications

References 11 publications

Discovery of α2‐plasmin inhibitor and its congenital deficiency

Discovery of α2‐plasmin inhibitor and its congenital deficiency

A Method to Study Inhibitors of Plasminogen Activation

Cortical Venous Thrombosis due to Familial AT-III Deficiency Presenting with Seizures

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