InsuranceTom said:The phase 2 numbers were about 24% mean weight loss at 48 weeks on the top dose, with the curve still descending at the end of the study.
Careful with treating an unchanged LDL-C as a failure. If ApoB and triglycerides both fell, the particle picture improved regardless of what the calculated LDL says.
If somebody has the primary source to hand I would rather cite it than paraphrase it.
One concrete data point for the thread. For anyone tracking the class: GLP-1 alone gets you appetite, GLP-1 plus GIP adds tolerability and lipid handling, and adding glucagon adds expenditure and liver-fat reduction. Each addition also adds a receptor system that can generate side effects.
Dr.LipidDallas said:Careful with treating an unchanged LDL-C as a failure.
Before/after bloodwork compilation for the lipid panel — everything in one place for those who want comprehensive data:
| Category | Marker | Before | After 8mo | Change |
|---|---|---|---|---|
| Metabolic | A1C | 7.8% | 5.4% | ⬇️ 2.0% |
| Metabolic | Fasting Glucose | 129 | 85 | ⬇️ 29 |
| Lipids | LDL | 152 | 96 | ⬇️ 44 |
| Lipids | Triglycerides | 224 | 119 | ⬇️ 114 |
| Inflammation | hsCRP | 5.5 | 1.2 | ⬇️ 5.0 |
Every single metabolic marker improved. This is why I'm a believer in this therapy.
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Browse GL BiochemA narrower follow-up, since the general answer is now clear:
Why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose?
Closing the loop on my own question.
Rereading it with the dropout table open changed my view. I still think it is the most interesting molecule in the pipeline; I no longer think the 24% is the number that will end up on a label.