| Question | Answer | |----------|--------| | | Not yet. It is a disease‑modifying therapy that aims to extend survival and improve quality of life. | | Who can enroll in the trial? | Adults (≥ 18 y) with confirmed KRAS‑G12D mutation and a RAF‑DimerScore ≥ 2, who have progressed after standard therapy. | | What are the most common side effects observed so far? | Mild nausea, transient fatigue, and occasional Grade 1–2 elevation of alkaline phosphatase—all manageable with standard supportive care. | | When will the drug be available? | If Phase 3 confirms efficacy, we anticipate a 2029 US launch (subject to regulatory approval). | | How does the companion diagnostic work? | A single‑plex NGS assay for KRAS‑G12D plus a validated IHC stain for RAF‑dimer activity; results are returned within 7 days. |
| Model | Outcome | Notes | |-------|---------|-------| | | > 10 µM off‑target activity (clean) | Confirms selectivity | | Mouse AML xenograft (NSG, MOLM‑13) | Tumor regression (complete remission in 4/8 mice) | Oral dosing, BID, 25 mg/kg | | Syngeneic pancreatic cancer (KPC) + anti‑PD‑1 | 78 % TGI, increased CD8⁺ infiltration | Demonstrates immune‑modulating potential | | Rat toxicology (28‑day repeat dose) | NOAEL = 100 mg/kg/day | No observable cardiac, hepatic, or CNS toxicity | | Pharmacokinetics (PK) | Oral bioavailability ≈ 55 % in dogs; half‑life ≈ 12 h | Supports BID oral regimen | MEYD-873
MEYD‑873 is a next‑generation, orally bioavailable inhibitor that shuts down an overactive MYD signaling hub, a driver of both cancer cell survival and pathological inflammation. | Question | Answer | |----------|--------| | | Not yet