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  "docSlug": "f06b0b5d2079",
  "documentTitle": "Soleno Therapeutics (SLNO)",
  "authorId": "58_Scorpion_Capital",
  "authorName": "Scorpion Capital",
  "documentKindSlug": "activist-deck",
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  "sourceTypeSlug": "short_seller",
  "sourceTypeLabel": "Short seller",
  "presentationDate": "2025-08-15 00:00:00",
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  "pageNumber": 105,
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  "density": "balanced",
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  "notes": "The slide uses a direct comparison of drug mechanisms to challenge the target company's safety claims.",
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      "kind": "callout",
      "text": "Diazoxide mechanism (OPEN KATP channel) vs. sulfonylureas (CLOSE KATP channel)",
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      "text": "Soleno's framing of this risk as “manageable” is clinically irresponsible and unsupported by robust evidence.",
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      "text": "Diazoxide binds SUR1 subunit to open KATP channel → primary effects = vasodilation and ↓ insulin\nForm (route): indication\n- Hyperstat, sodium salt (IV solution): emergency hypertension\n- Proglycem, non-salt base (oral suspension): hyperinsulinemia (congenital & insulinoma) to normalize insulin levels and attenuate hypoglycemia\n- VYKAT XR (DCCR), choline salt (oral tablet 50, 100 and 150 mg): Prader-Willi Syndrome suppress hyperphagia by blocking CNS-mediated starvation response\n- Commonly prescribed T2D medication bind to SUR1 to close KATP channels (opposite of diazoxide). Sulfonylureas: ↑ pancreatic insulin secretion to normalize insulin levels in type 2 diabetes (T2D) → normalize circulating glucose levels\n- First generation sulfonylureas (tolbuteride) bind to a low-affinity site on SUR1 (examples: tolbutamide, chlorpropamide)\n- Second generation sulfonylureas (examples: glipizide and glimepiride) bind with high-affinity to a different SUR1 binding site -greater potency/lower doses.",
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      "text": "Diazoxide and sulfonylureas both interact with the SUR1 subunit of the KATP channel with opposing actions. Sulfonylureas are a class of medications used to treat diabetes by stimulating the pancreas to release more insulin. Diazoxide OPENS the channel while sulfonylureas CLOSES it. Therefore, it is logical to assume that diazoxide may cause diabetes in norm-insulin PWS patients. Soleno's framing of this risk as “manageable” is clinically irresponsible and unsupported by robust evidence.",
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      "kind": "title",
      "text": "Long-term, mechanism-based blockade of insulin-secretion by diazoxide in patients with normal insulin levels is highly likely to promote type 2 diabetes, particularly in PWS with obese phenotype.",
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