Biotech Values

[masterlongevity]

"Plus, I think Gotleib was fear mongering and overstating the value of lucentis over avastin (does he consult for dna?).

I don't know what design flaws he was referencing but I'm looking forward to the outcome to see whether there is any relevant clinical difference avastin vs lucentis (I predict not). "


There have been some evidence show that lucentis may be mroe effective. Two DME studies published by DRCRN ahve shown Avastin not to be very effective and Lucnetis to be effective.

These are clearly phase II non comparative trials, but you can't help but compare..


Lucantis and Avastin are clearly very different products, with a much diffent molecuilar design. PFroma preclinical perspective there is evey reasont o beleive that Lucnetis will be superior and less toxic; However, as we know, preclinical results do not always translate. DNA clearly made the right decision in developing Lucentis and IMHO deserve to reap the rewards for their innovative work. Lucentis is still very cost effective in QALY terms, (more so than macugen or Visudyne) and well with ithe threshhold of 50,000 per QALY, but it is impossible to compete with aliquotted avastin in term of cost-effectiveness.


IF the NIH trial ever starts and finishes ( was orignally supposed to start in Q3 06), i don't think the results will eb conclusive. DNA has argued that the trial is not large enough to detect statistical differences in safety. Not sure what will happen here. Lucentis is currently the market share leader, but how that will change is anyone's guess

see DME abstracts below...

: Ophthalmology. 2007 Aug 13; [Epub ahead of print] Links
A Phase II Randomized Clinical Trial of Intravitreal Bevacizumab for Diabetic Macular Edema.Diabetic Retinopathy Clinical Research Network.
OBJECTIVE: To provide data on the short-term effect of intravitreal bevacizumab for diabetic macular edema (DME). DESIGN: Randomized phase II clinical trial. PARTICIPANTS: One hundred twenty-one eyes of 121 subjects (109 eligible for analysis) with DME and Snellen acuity equivalent ranging from 20/32 to 20/320. INTERVENTIONS: Random assignment to 1 of 5 groups: (A) focal photocoagulation at baseline (n = 19), (B) intravitreal injection of 1.25 mg of bevacizumab at baseline and 6 weeks (n = 22), (C) intravitreal injection of 2.5 mg of bevacizumab at baseline and 6 weeks (n = 24), (D) intravitreal injection of 1.25 mg of bevacizumab at baseline and sham injection at 6 weeks (n = 22), or (E) intravitreal injection of 1.25 mg of bevacizumab at baseline and 6 weeks with photocoagulation at 3 weeks (n = 22). MAIN OUTCOME MEASURES: Central subfield thickness (CST) on optical coherence tomography and best-corrected visual acuity (VA) were measured at baseline and after 3, 6, 9, 12, 18, and 24 weeks. RESULTS: At baseline, median CST was 411 mum and median Snellen VA equivalent was 20/50. Compared with group A, groups B and C had a greater reduction in CST at 3 weeks and about 1 line better median VA over 12 weeks. There were no meaningful differences between groups B and C in CST reduction or VA improvement. A CST reduction > 11% (reliability limit) was present at 3 weeks in 36 of 84 (43%) bevacizumab-treated eyes and 5 of 18 (28%) eyes treated with laser alone, and at 6 weeks in 31 of 84 (37%) and 9 of 18 (50%) eyes, respectively. Combining focal photocoagulation with bevacizumab resulted in no apparent short-term benefit or adverse outcomes. Endophthalmitis developed in 1 eye. The following events occurred during the first 24 weeks in subjects treated with bevacizumab without attributing cause to the drug: myocardial infarction (n = 2), congestive heart failure (n = 1), elevated blood pressure (n = 3), and worsened renal function (n = 3). CONCLUSION: These results demonstrate that intravitreal bevacizumab can reduce DME in some eyes, but the study was not designed to determine whether treatment is beneficial. A phase III trial would be needed for that purpose.


Am J Ophthalmol. 2006 Dec;142(6):961-9. Epub 2006 Aug 2. Links
Vascular endothelial growth factor is a critical stimulus for diabetic macular edema.Nguyen QD, Tatlipinar S, Shah SM, Haller JA, Quinlan E, Sung J, Zimmer-Galler I, Do DV, Campochiaro PA.
The Wilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-9277, USA.

PURPOSE: The role of vascular endothelial growth factor (VEGF) in diabetic macular edema (DME) was tested with ranibizumab, a specific antagonist of VEGF. DESIGN: A nonrandomized clinical trial. METHODS: Ten patients with chronic DME received intraocular injections of 0.5 mg of ranibizumab at baseline and at one, two, four, and six months. The primary outcome was change in foveal thickness between baseline and seven months, and the secondary outcome measures were changes from baseline in visual acuity and macular volume. RESULTS: Mean values at baseline were 503 microm for foveal thickness, 9.22 mm3 for macular volume, and 28.1 letters (20/80) read on an Early Treatment Diabetic Retinopathy Study (ETDRS) visual acuity chart. At seven months (one month after the fifth injection), the mean foveal thickness was 257 microm, which was a reduction of 246 microm (85% of the excess foveal thickness present at baseline; P = .005 by Wilcoxon signed-rank test for likelihood that this change is due to ranibizumab rather than chance). The macular volume was 7.47 mm3, which was a reduction of 1.75 mm3 (77% of the excess macular volume at baseline; P = .009). Mean visual acuity was 40.4 letters (20/40), which was an improvement of 12.3 letters (P = .005). The injections were well-tolerated with no ocular or systemic adverse events. CONCLUSION: Intraocular injections of ranibizumab significantly reduced foveal thickness and improved visual acuity in 10 patients with DME, which demonstrated that VEGF is an important therapeutic target for DME. A randomized, controlled, double-masked trial is needed to test whether intraocular injections of ranibizumab provide long-term benefit to patients with DME.