Tag: Lp(a)

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Evidence-first notes on bioscience and deep tech, at the edge of the lab and the market. Information only — not investment advice, not medical advice. The 30-second version What. Lipoprotein(a) lowering is already a mature commercial field: three injectable siRNA/ASO agents are in large cardiovascular-outcome Phase 3 trials at roughly 90%+ Lp(a) reduction, an oral…

Oral muvalaplin and the measurement problem — why half of Lp(a)’s “efficacy gap” may be the ruler, not the drug

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Evidence-first notes on bioscience and deep tech, at the edge of the lab and the market. Information only — not investment advice, not medical advice. The 30-second version What. Muvalaplin (Eli Lilly, LY3473329) is the first oral, once-daily small molecule that lowers lipoprotein(a) — it blocks assembly of the Lp(a) particle rather than shutting off…

Lp(a) is causal — so how much do you have to lower it? Mendelian randomization, epidemiology and the 2026 guideline turn

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Evidence-first notes on bioscience and deep tech, at the edge of the lab and the market. Information only — not investment advice, and not medical advice. The 30-second version What. The causal case for lipoprotein(a), Lp(a), as a driver of atherosclerotic cardiovascular disease is one of the strongest genetic cases in cardiology — Mendelian randomization…

The Lp(a) landscape — a genetically fixed axis of residual cardiovascular risk, and the first drugs that lower it 90%+ (while the outcome question stays open)

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Evidence-first notes on bioscience and deep tech, at the edge of the lab and the market. Information only — not investment advice, not medical advice. The 30-second version What. Lipoprotein(a), or Lp(a), is a largely genetically fixed particle that Mendelian randomization (MR) has established as a causal axis of residual cardiovascular risk — the part…

In-vivo gene editing of the lipid axis — PCSK9, ANGPTL3 and Lp(a), and what a “one-shot, lifelong” lowering does and does not yet prove

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