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Cytochroma Announces Positive Comparative Data on CTA018 in Chronic Kidney Disease Model
Date:11/6/2008

replacement therapies (paricalcitol, doxercalciferol and calcitriol) can over-stimulate intestinal absorption of dietary calcium and phosphate, leading to excessive calcium and phosphorus in the blood. These toxicities severely limit the ability of physicians to fully control SHPT with such therapies. Data presented today demonstrate that CTA018 has significantly reduced activity and half-life in human enterocytes (intestinal cells), making CTA018 Injection far less likely to cause hypercalcemia (excessive blood calcium) or hyperphosphatemia (excessive blood phosphorus).

(3) CTA018 Preserves Vitamin D Status

Currently available vitamin D hormone replacement therapies exacerbate vitamin D insufficiency, which is widespread in CKD patients. Repeated administration of these therapies induces CYP24, and consequently depletes blood levels of calcifediol, a condition known as vitamin D insufficiency. Vitamin D insufficiency has been linked to increased mortality in CKD patients. In a preclinical study of adenine-induced CKD, repeated dosing with CTA018 did not decrease blood levels of calcifediol, possibly due to its potent CYP24 inhibitory activity.

(4) CTA018 Has Constant Potency and a Wider Therapeutic Window than Paricalcitol

Current vitamin D hormone replacement therapies can induce treatment resistance in CKD patients over time. Prolonged dosing often induces CYP24 to levels that create a barrier to administered therapy, limiting effectiveness. In a preclinical study of adenine-induced CKD, CTA018 was found to have consistent effectiveness in lowering parathyroid hormone (PTH) throughout a 4-week treatment period. In contrast, paricalcitol became progressively less effective. Additionally, CTA018 exhibited a wider therapeutic window than paricalcitol, having no significant impact on serum calcium or phosphorus at doses which fully controlled SHPT.

Current Status of CTA018 Injection

CTA018 Injection is in Phase II clinical de
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SOURCE Cytochroma
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