Differentiating between the two syndromes can be challenging. Genetics
The WT1 gene exists on chromosome 11 (at 11p13), and codes for a four zinc finger transcription factor. Its role as a transcription factor is related to proper kidney and gonadal development. The link between kidney and gonadal development and WT1 was highlighted in past studies looking at the related Denys-Drash syndrome. Results of various investigations identified the loss of function of WT1 to be a prerequisite of Wilms tumour development, and also a key trait of individuals with genital abnormalities.Mutations responsible for Frasier syndrome predominantly occur in intron 9 of the WT1 gene, specifically nucleotide substitutions that influence an intron splice site. Mutations in this region proved for the absence of three amino acids—K T S—between the third and fourth WT1 zinc fingers. Referring to the autosomal dominant expressive nature of this disease, it is only necessary for an individual to have one complement of the mutated intronic sequence to appear affected. Differing from the similar Denys-Drash syndrome, where a mutated form of the WT1 protein exists, Frasier syndrome expression works solely on the existence of a changed ratio of KTS isoforms: normal WT1 proteins including the KTS site (+KTS), and mutated, shortened proteins lacking the KTS site (–KTS). Through alternative splicing, a specific ratio of the two isoforms normally exists, though the mutation in the intron 9 splice site severely lowers levels of the +KTS isoform; this leads to Frasier syndrome.
Though safety has been established through previous clinical trials, there is ongoing debate about whether this is an effective treatment for ischemic stroke, and significant ongoing discussion between Emergency Physicians, Neurologists and Pharmacists about whether this treatment should be used for that indication. The American Heart Association/American Stroke Association 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke supports considering tenecteplase over alteplase in patients without contraindication to intravenous thrombolytics. Pharmacokinetics
Distribution: approximates plasma volume
Metabolism: Primarily hepatic
Half-life elimination: Biphasic: Initial: 20–24 minutes; Terminal: 90–130 minutes
Excretion: Clearance: Plasma: 99-119 mL/minute

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External links
MedlinePlus DrugInfo uspdi-500145