Seventeen Months in Pancreatic Cancer
Every drug aimed at pancreatic cancer’s central signaling cascade has failed. Atebimetinib’s wager is that the failures were errors of timing, not target.
- Asset
- atebimetinib (IMM-1-104) · oral deep-cyclic MEK1/2 inhibitor
- Setting
- 1L metastatic pancreatic cancer · + modified gemcitabine/nab-paclitaxel
- Signal
- 17.3-month median OS · single-arm · N=55 (vs ~8–11-mo standard of care)
- Readout
- ASCO abstract 4013 · 1 June 2026 · full Phase 2a data
- The bar
- no randomized MAPK-vs-chemo win exists in 25 years of PDAC trials
§1 · The number
Pancreatic cancer rarely concedes a survival figure of this size. Immuneering’s Phase 2a enrolled 55 first-line metastatic patients and reported a 17.3-month median overall survival — the point at which half the patients remain alive — as of an April 2026 cutoff.1 The safety it disclosed stayed chemotherapy-shaped: the only Grade-3-or-higher treatment-related events in at least a tenth of patients were anemia at 16% and neutropenia at 18%, both traced to the gemcitabine backbone rather than to the MEK inhibitor.3
One caveat travels with the number. At the prior cohort cut — 34 patients, nine months of follow-up — the median had not been reached, and 86% of patients were still alive at nine months.2 A median that emerges as follow-up matures is the real event. Whether 17.3 months rests on a mature count of deaths or on a still-young curve is one of the things the June-1 presentation settles.
§2 · The cascade that defeats its own drugs
Pancreatic cancer is, in more than nine of ten cases, a KRAS disease — a single mutated switch that fires the RAF → MEK → ERK relay telling the cell to keep dividing.9 MEK sits one step down that relay, eminently druggable, and has been drugged repeatedly to a uniform graveyard. Trametinib plus gemcitabine returned a hazard ratio of 0.98 — a near-perfect null.4 The selumetinib doublet in S1115 read worse, the control arm outliving the drug.5
The failures share a mechanism. The cascade is a feedback loop, not a wire: pin MEK down continuously and the cell senses the silence and reloads the pathway from upstream within days, while the unbroken blockade poisons healthy tissue.6 Continuous inhibition feeds the loop it means to break. See the full PDAC Phase-3 graveyard →
§3 · Timing, not target
Atebimetinib changes the schedule, not the target. A two-to-three-hour half-life dosed once daily strikes MEK hard, then clears before the feedback fires, so normal tissue recovers between doses — the “deep cyclic inhibition” the company is named for.7 The same node every prior drug hit, attacked on a different clock. The chemotherapy-shaped safety profile is the first sign the clock matters: a continuous MEK inhibitor at this exposure would carry the rash, the ocular signal, and the ejection-fraction drop that mark the class.3
§4 · The control bar
Atebimetinib’s combination is the MEK-plus-chemotherapy backbone in the same first-line setting where Revolution Medicines runs its pan-RAS inhibitor daraxonrasib against an investigator’s-choice chemotherapy control.8 The response, progression, and survival figures atebimetinib discloses fix what a chemotherapy-anchored regimen delivers here — the bar a pan-RAS agent is measured against. One network, two philosophies: hit the node downstream on a smarter clock, or hit the driver upstream. See the Revolution Medicines cluster → Immuneering has registered a 1:1 Phase 3, MAPKeeper-301, against that same standard of care.8 The molecule carries composition-of-matter protection to roughly 204211 and four FDA designations.12
§5 · What June 1 settles
The abstract released a survival headline and a safety table. The presentation discloses the rest: the objective response rate and disease-control rate, still unreported; the median progression-free survival; the maturity of the survival estimate — its event count and follow-up; and whether benefit concentrates by KRAS genotype. These figures separate a durable signal from an early one.
The larger gap sits behind them. Twenty-five years and roughly fourteen Phase 3 trials in metastatic pancreatic cancer have produced one statistically positive pathway-directed result.10 No randomized trial has shown any MAPK-directed regimen beating chemotherapy in the first line. The 17.3-month figure is the loudest signal the timing bet has produced. It is a signal, not a proof. MAPKeeper-301 is the first randomized test of whether changing the clock changes the outcome.8
A forward, falsifiable reading of the June-1 endpoints was pre-registered and git-committed before the oral, and is held separately. This page describes what the published record establishes. It forecasts nothing.
Provenance
Every load-bearing fact, with its verbatim source quote and the logic it carries in the argument above. The numbers match the inline marks.
- 1
“17.3-month median overall survival (OS) in first-line metastatic pancreatic cancer patients treated in its Phase 2a clinical trial evaluating atebimetinib (IMM-1-104) plus modified gemcitabine/nab-paclitaxel (mGnP), as of the April 24, 2026 data cutoff date.”
Carries · The headline. Anchors §1 and the whole timing hypothesis — the figure the supporting endpoints must corroborate.
- 2
“86% overall survival ("OS") ... in the initial intent-to-treat population of 34 patients dosed at the 320 mg once-daily dose level of atebimetinib in combination with mGnP ... with a median follow up time of nine months.”
Carries · The prior cut. The 17.3-month median emerged as follow-up matured from this 9-month, median-not-reached snapshot — the maturity caveat made concrete.
- 3
“The only treatment-related adverse events observed at Grade 3 or higher in >=10% of patients were anemia (16%) and neutropenia (18%), both chemotherapy-related.”
Carries · The tolerability claim. Both Grade-3+ events are chemotherapy-shaped, not MEK-shaped — the evidence the pulsed schedule widens the therapeutic window.
- 4
“The Infante Phase 2 of trametinib plus gemcitabine in 1L PDAC reported HR 0.98 — a near-perfect null at hazard ratio 1.0 — with median OS 8.4 versus 6.7 months (p=0.45).”
Infante, Eur J Cancer 2014 · PMID 24915778
Carries · The graveyard, exhibit one. Continuous MEK inhibition plus gemcitabine added nothing to chemotherapy.
- 5
“Selumetinib + MK-2206 S1115 (Chung) reads HR 1.37, with the control arm outperforming the experimental.”
Chung, JAMA Oncol 2017 · PMID 27978579
Carries · The graveyard, exhibit two. Vertical MEK suppression did worse than chemotherapy alone.
- 6
“Acquired resistance to upstream inhibitors drives MAPK pathway upregulation, conferring collateral sensitivity to MEK inhibition; deep pathway suppression is needed to prevent adaptive escape.”
MAPK adaptive feedback · PMID 42079286
Carries · The mechanism of failure. The cascade is a feedback network; continuous blockade triggers the escape. (The hub anchors this to Xue, Nature 2020, PMID 31915379.)
- 7
“Its short 2-3 h half-life and once-daily dosing enable pulsatile MEK pathway suppression that allows daily recovery in normal tissues, enhancing tolerability and reducing adaptive resistance.”
Immuneering, deep cyclic inhibition (PanCAN 2025)
Carries · The bet. The mechanism answer to the feedback problem — stated as the hypothesis under test, not a settled result.
- 8
“MAPKeeper 301 — Phase 3, randomized, parallel, open-label, atebimetinib 320 mg QD + mGnP versus gemcitabine/nab-paclitaxel; primary endpoint Overall Survival; enrollment 510; status recruiting.”
ClinicalTrials.gov NCT07562152
Carries · The test. The first randomized, OS-primary trial of whether the timing change moves survival.
- 9
“KRAS is mutated in over 90% of pancreatic ductal adenocarcinoma; KRAS ranks first of 8,964 targets associated with pancreatic carcinoma (association score 0.8156).”
OpenTargets · pancreatic carcinoma (EFO_0002618)
Carries · Why the cascade matters. KRAS is the disease; MEK is one step down the relay it fires.
- 10
“Twenty-five years of pathway-directed Phase 3 development in metastatic PDAC have produced one statistically positive trial across roughly fourteen attempts (Moore PA.3, delta-mOS 0.33 mo).”
RAS / MAPK literature substrate
Carries · The whitespace. No randomized win for any MAPK-directed regimen in first-line PDAC exists. The proof is the thing that does not yet exist.
- 11
“US 12,351,566 — "MEK INHIBITORS AND THERAPEUTIC USES THEREOF", granted; applicant Immuneering Corporation; priority 2020-01-10; estimated expiry ~August 2042.”
Carries · The estate. Composition-of-matter protection on the molecule to ~2042 — assignee confirmed from the patent office record, not inferred.
- 12
“Atebimetinib holds FDA Fast Track designation in 2L PDAC (Feb 2024), 1L PDAC (Jul 2024), and NRAS-mutant melanoma (Dec 2024), and Orphan Drug designation in pancreatic cancer (Oct 2024).”
Immuneering IR · FDA designations
Carries · Regulatory standing. Four designations; no approval — correct for a pre-registration asset.
The logic, traced
Three load-bearing conclusions, each traced forward from its premises and backward to what must hold, and marked deductive or inductive. The reasoning is auditable, not just the facts.
The MEK graveyard records a failure of timing, not an undruggable target. Inductive
- Premises
- Every MEK node drugged in PDAC failed (fn 4, 5); the cascade reactivates from upstream within days of continuous blockade (fn 6); a short-half-life pulse lets the pathway recover and the chemo-shaped safety profile shows the window widening (fn 3, 7).
- Forward
- Repeated node failure + a feedback mechanism that punishes continuous suppression → the variable that changed (the dosing schedule), not the target, is the candidate explanation.
- Backward
- For the conclusion to hold, continuous-versus-pulsed must be the operative difference. That has not been shown head-to-head. The randomized test (fn 8) is the instrument that would confirm or refute it.
- Soundness
- Premises verified. The inference is inductive and unconfirmed — stated as the hypothesis under test, never as proof.
The 17.3-month survival is a signal, not proof of benefit. Deductive
- Premises
- The figure comes from a single-arm cohort of 55 patients with no control (fn 1); no randomized MAPK-versus-chemotherapy win exists in first-line PDAC (fn 10).
- Forward
- A single-arm, uncontrolled result cannot establish superiority over chemotherapy by construction — superiority is a comparison, and there was no comparator.
- Backward
- Proof requires a randomized overall-survival win. That readout is MAPKeeper-301 (fn 8), which has not reported.
- Soundness
- Valid and sound. The conclusion follows necessarily from the study design.
Atebimetinib calibrates the control bar that Revolution Medicines’ daraxonrasib must clear. Deductive
- Premises
- Both run in first-line metastatic PDAC; RASolute-303 randomizes daraxonrasib against an investigator’s-choice chemotherapy control; atebimetinib + chemotherapy is that same backbone, read directly (fn 8, 10).
- Forward
- A drug’s benefit is measured against its control; atebimetinib’s chemo-backbone numbers fix what "chemotherapy control" delivers in this setting.
- Backward
- The cross-read holds only while both trials share the chemotherapy backbone and population — which the registered designs confirm.
- Soundness
- Valid. The two trials are linked by a shared control arm, not by analogy.
Bibliography
Every source, in cited order
Sixty-four sources stand behind this page — peer-reviewed papers, the trial registry, SEC filings, the patent estate, FDA designations, and the molecular databases. Each entry links to the open record, names where it is cited above, and carries a short note on what it establishes. The verification badge marks whether the quote was confirmed against the source corpus, re-fetched against the primary record, or held as secondary.
- 1
Infante JR et al. A randomised, double-blind, placebo-controlled trial of trametinib, an oral MEK inhibitor, in combination with gemcitabine for patients with untreated metastatic adenocarcinoma of the pancreas. Eur J Cancer 50, 2072–2081 (2014).
Cited in · §3 · the record it must clear · comparator · MEK-PDAC failure
Randomized Phase 2 (N=160) of trametinib + gemcitabine vs gemcitabine alone in 1L metastatic PDAC. OS HR 0.98—dead flat. The paradigmatic MEK + chemo failure in pancreatic cancer and the most direct historical comparator for the atebimetinib MAPKeeper 301 design.
verbatim-verified - 2
Chung V et al. Effect of Selumetinib and MK-2206 vs Oxaliplatin and Fluorouracil in Patients With Metastatic Pancreatic Cancer After Prior Therapy: SWOG S1115 Study Randomized Clinical Trial. JAMA Oncol 3, 516–519 (2017).
Cited in · §3 · the record it must clear · comparator · MEK-PDAC failure
SWOG S1115: randomized Phase 2 of selumetinib + MK-2206 (AKT inhibitor) vs mFOLFOX6 in 2L+ metastatic PDAC. The study closed early for futility; the MEK+AKT arm was inferior. Establishes that MEK inhibition plus targeted pathway co-blockade has also failed in pancreatic cancer, not just MEK monotherapy.
verbatim-verified - 3
Janne PA et al. Selumetinib Plus Docetaxel Compared With Docetaxel Alone and Progression-Free Survival in Patients With KRAS-Mutant Advanced Non–Small Cell Lung Cancer: The SELECT-1 Randomized Clinical Trial. JAMA 317, 1844–1853 (2017).
Cited in · §3 · the record it must clear · comparator · MEK-PDAC failure · comparator · SELECT-1 canonical failure
SELECT-1 is the canonical MEK inhibitor Phase 3 failure in KRAS-mutant solid tumors: n=510, PFS HR 0.93 (p=0.44), OS HR 1.05. A positive Phase 2 (PFS 5.3 vs 2.1 mo, ORR 37% vs 0%) collapsed completely on registrational replication—the exact pattern atebimetinib's DCI thesis must break.
verbatim-verified - 4
Eslinger C, Sonbol MB, George B, Babiker H, Borad MJ Key Considerations for Targeting KRAS in Pancreatic Cancer: Potential Impact on the Treatment Paradigm. Drug Design, Development and Therapy (2025).
Cited in · §3 · the record it must clear · mechanism · target biology · §5 · what the oral answers
Recent review of the KRAS-targeting landscape in PDAC, covering approved KRAS G12C inhibitors (sotorasib, adagrasib), emerging pan-KRAS agents, and downstream MEK pathway strategies. Contextualizes atebimetinib within the evolving treatment paradigm and articulates why KRAS mutation prevalence (~95% in PDAC) makes MEK a compelling downstream target.
verbatim-verified - 5
May MS, Park W, O'Reilly EM Treating Pancreatic Ductal Adenocarcinoma: The Targeted Revolution is Here. Drugs (2026).
Cited in · §5 · what the oral answers · mechanism · target biology
Contemporary review by Memorial Sloan Kettering authors surveying the targeted therapy revolution in PDAC—KRAS G12C inhibitors, HER2, BRCA, and NTRK targeting. Positions PDAC's molecular heterogeneity and the requirement for biomarker-unselected strategies, providing the competitive context within which atebimetinib's all-comer approach must prove itself.
verbatim-verified - 6
Macarulla T et al. NALIRIFOX versus nab-paclitaxel and gemcitabine in older patients with treatment-naive metastatic pancreatic cancer: a subgroup analysis of the pivotal NAPOLI 3 trial. ESMO Open (2025).
Cited in · §4 · the control-arm question · §3 · the record it must clear
NAPOLI 3 subgroup analysis establishing the real-world performance envelope of GnP as a 1L control arm in older patients. Benchmarks OS for the standard-of-care backbone against which atebimetinib + mGnP is competing—the denominator the 17.3-month OS number must be interpreted against.
verbatim-verified - 7
Haldar SD et al. Phase I trial of binimetinib plus hydroxychloroquine in patients with previously treated metastatic pancreatic cancer. The Oncologist (2026).
Cited in · §3 · the record it must clear · comparator · MEK-PDAC failure
Phase I of binimetinib + hydroxychloroquine in pretreated PDAC—a MEK inhibitor combination designed to suppress autophagy-driven resistance. The trial's tolerability and modest efficacy profile continues the pattern of MEK combinations in pancreatic cancer failing to move the needle, reinforcing the class-precedent section.
verbatim-verified - 8
Manji GA et al. Atezolizumab and motixafortide, cobimetinib or simlukafusp alfa in pretreated advanced pancreatic cancer: phase I/IIb MORPHEUS-PDAC umbrella study. The Oncologist (2026).
Cited in · §3 · the record it must clear · comparator · MEK-PDAC failure
MORPHEUS-PDAC umbrella trial includes an atezolizumab + cobimetinib arm (PD-L1 + MEK inhibitor combination) in pretreated advanced pancreatic cancer. Cobimetinib represents the MEK-immunotherapy co-administration strategy; results provide direct class precedent for any MEK combination in PDAC.
verbatim-verified - 9
Roth S et al. Pancreatic cancer. Nature Reviews Disease Primers (2026).
Cited in · §1 · the number that arrived early · §3 · the record it must clear · mechanism · target biology
2026 Nature Reviews Disease Primers update on pancreatic cancer—authoritative epidemiology, molecular biology, therapeutic landscape, and unmet need. Grounds the disease context: 5-year survival ~13%, median OS with GnP ~11–13 months in 1L, KRAS mutation rate ~95%. The reference baseline for what 17.3 months means.
verbatim-verified - 10
Park W et al. Pembrolizumab and olaparib in homologous-recombination-deficient metastatic pancreatic cancer: the phase 2 POLAR trial. Nature Medicine (2026).
Cited in · §5 · what the oral answers · competitive landscape
POLAR trial demonstrates that HRD-selected PDAC (~15% of patients) responds to PD-1 + PARP inhibition. Establishes that molecularly targeted approaches work in rare PDAC subsets—but atebimetinib targets the ~95% KRAS-mutant unselected population that HRD biomarker approaches cannot address.
verbatim-verified - 11
Park W et al. POLQ-driven repair scars shape the immunogenic landscape of homologous recombination-deficient pancreatic cancer. bioRxiv (2026).
Cited in · §5 · what the oral answers · mechanism · target biology
Preprint characterizing the immune microenvironment of HRD pancreatic cancer through the lens of POLQ-mediated repair; relevant context for combination immunotherapy strategies in PDAC and the biology of the small HRD subset that responds to checkpoint inhibition.
verbatim-verified - 12
Bandlamudi C et al. Cancer type-specific variation in patterns of driver alterations across 50,000 tumors. Cancer Cell (2026).
Cited in · mechanism · target biology · §3 · the record it must clear
MSK IMPACT analysis of driver alteration patterns across 50,000 clinical tumor samples, with PDAC KRAS mutation frequency and MAPK pathway co-activation data. Supports the prevalence and structural case for MEK as a universal downstream target in RAS-driven cancers.
verbatim-verified - 13
Johnson ML et al. A plain language summary of the updated results from the PHAROS study: the combination of encorafenib plus binimetinib for people with BRAF V600E-mutant metastatic non-small cell lung cancer. Future Oncology (2026).
Cited in · §3 · the record it must clear · comparator · MEK-PDAC failure
PHAROS update for BRAF V600E NSCLC with binimetinib—the one solid-tumor setting where MEK inhibitors have proven clinical benefit (combined with BRAF inhibition). Underscores that successful MEK inhibition in malignant solid tumors requires concurrent mutant-BRAF suppression, not seen in KRAS-mutant PDAC.
verbatim-verified - 14
Wainberg ZA et al. Quemliclustat and chemotherapy with or without zimberelimab in metastatic pancreatic adenocarcinoma: a randomized phase 1 trial. Nature Medicine (2026).
Cited in · §5 · what the oral answers · competitive landscape
A CD73 inhibitor + GnP ± PD-1 checkpoint combination in PDAC—one of several immunotherapy-plus-chemo strategies competing in the 1L space. Contextualizes the competitive intensity of the MAPKeeper 301 Phase 3 design by demonstrating the density of concurrent 1L PDAC trials.
verbatim-verified - 15
Falchook G et al. A first-in-human phase 1 study of the SHP2 inhibitor BBP-398 in patients with advanced solid tumors. NPJ Precision Oncology (2026).
Cited in · §3 · the record it must clear · competitive landscape
Phase 1 of BBP-398, a SHP2 inhibitor upstream of RAS-MAPK signaling. SHP2 inhibitors are being tested as MEK-pathway adjuncts to prevent adaptive reactivation—the same resistance mechanism atebimetinib's DCI thesis proposes to sidestep by intermittent rather than chronic pathway blockade.
verbatim-verified - 16
Fu R et al. Acquired resistance to the PRMT5 inhibitor confers collateral sensitivity to MEK inhibition in MTAP-null non-small cell lung cancer. bioRxiv (2026).
Cited in · §2 · why this MEK inhibitor doses differently · mechanism · target biology
Preclinical evidence that PRMT5 inhibitor-resistant MTAP-null NSCLC tumors acquire collateral sensitivity to MEK inhibition—illustrating how resistance pathway convergence on MEK creates synthetic lethality opportunities and validates MEK as a durably relevant downstream target.
verbatim-verified - 17
Vu P et al. (Chung V, Vu P, Ma V, Uboha N, Majeed U, Chandra S, Mahalingam D, Johnson M, Pelster M, Pavlick A, Ocean A, Ma B, Spira A, Duffy S, Henry J, Botta G, Philipovskiy A, Pant S, Chawla S, Zhang J, Kim J, Kolitz S, Funt J, Hayreh V, Hall B, Zeskind B, Matushansky I, Ahn D) Results from a phase 2a study of atebimetinib in combination with mGnP in advanced or metastatic pancreatic cancer. ASCO Annual Meeting 2026 (2026).
Cited in · §1 · the number that arrived early · §5 · what the oral answers
The headline result: 17.3-month median OS in N=55 1L metastatic PDAC patients (data cutoff 2026-04-24), with Grade 3+ toxicities limited to chemotherapy-related anemia (16%) and neutropenia (18%). Rapid Oral Abstract Session, June 1 2026. This is the number the entire page is built around and the basis for the MAPKeeper 301 Phase 3 launch.
primary-confirmed - 18
Immuneering Corporation (Zeskind B et al.) Atebimetinib (IMM-1-104) + Modified Gemcitabine/Nab-Paclitaxel (mGnP) Shows Extraordinary Overall Survival and Favorable Tolerability in First-Line Metastatic PDAC: Updated Phase 2 Results. PanCAN Scientific Summit 2025 (2025).
Cited in · §1 · the number that arrived early · §4 · the control-arm question
Encore presentation at PanCAN Scientific Summit (Boston, September 28 2025) of N=34 1L PDAC data with 9-month median follow-up. Showed 86% OS at 9 months (95% CI 66-94). The interim dataset that preceded the ASCO 2026 N=55 update and established cross-trial comparators with historical GnP controls.
primary-confirmed - 19
Kim JS, Funt J, Zhang J, Kolitz S, Nair P, Hayreh V, Zeskind BJ, Matushansky I, Hall B Atebimetinib's Deep Cyclic Inhibition of MEK Constrains MAPK-Axis Adaptive and Acquired Alterations in Patients with RAS-Mutant Tumors. AACR Annual Meeting 2026 (2026).
Abstract / Poster 1873AACR session: Targeting Drug Resistance 2: RAS SignalingNCT05585320Google ScholarCited in · §2 · why this MEK inhibitor doses differently · mechanism · resistance biology
ctDNA analysis across N=123 atebimetinib-treated patients (86 monotherapy, 37 combination) showing rare canonical MAPK reactivation events—the resistance signature universal to chronic RAS inhibitors was absent. Acquired mutations were heterogeneous rather than convergent, consistent with DCI theory. April 20 2026 poster presentation.
primary-confirmed - 20
King PJ, Funt J, Kolitz S, Nair P, de Jong J, Yamamura A, Johnson M, Zhang J, Fowler KD, Travesa A, Axel A, Zeskind BJ, Hall B Activity of IMM-1-104 Alone or in Combination with Chemotherapy in RAS-altered Pancreatic Cancer Models. AACR Annual Meeting 2024 (2024).
Cited in · §2 · why this MEK inhibitor doses differently · mechanism · preclinical
Preclinical poster showing IMM-1-104 monotherapy and combination with gemcitabine/nab-paclitaxel in RAS-altered PDAC xenograft models, including near-complete tumor responses at the KRAS-G12D MIA PaCa-2 model with combination treatment. Cancer Res 2024;84(6_Suppl):4195. The preclinical efficacy foundation for the Phase 1/2a design.
primary-confirmed - 21
Chung V, Spira A, Pavlick A, Sommerhalder D, Ma B, Hayreh V, de Jong J, Funt J, Kolitz S, Nair P, Zhang J, Kim J, Yamamura A, Zeskind B, Hall B, Pant S Preliminary Phase 1 Safety and Activity of IMM-1-104, an Orally Dosed Universal RAS Inhibitor That Drives Deep Cyclic Inhibition of the MAPK Pathway at MEK, in Patients with Advanced Unresectable or Metastatic Solid Tumors. ESMO Annual Conference 2024 (2024).
Cited in · §1 · the number that arrived early · §2 · why this MEK inhibitor doses differently
First public Phase 1 presentation (N=54 enrolled as of August 19 2024, including 34 PDAC). Established safety profile: TRAEs ≥10% predominantly Grade 1-2, no dose-limiting toxicities, no serious TRAEs. Confirmed DCI at 240 and 320 mg QD doses. The clinical anchor for the tolerability differentiation story.
primary-confirmed - 22
de Jong J, Yamamura A, Axel A, King P, Funt J, Foley E, Kovar C, Bergstrand M, Mezzalana E, Chenel M, Hayreh V, Hall B Phase 1 Interim Population PK/PD Modeling and Recommended Phase 2 Dose Exploration for IMM-1-104, A Novel Concept Oral Deep Cyclic Inhibitor of MEK. American Conference on Pharmacometrics (ACoP) 2024 (2024).
Cited in · §2 · why this MEK inhibitor doses differently
Two-compartment population PK model with PK/PD linking IMM-1-104 plasma concentrations to p-ERK and p-MEK suppression. At 320 mg QD: median time above IC90 2.8 h, 88% of subjects returning to <20% of maximum inhibition at daily trough. Quantifies the DCI profile that mechanistically distinguishes atebimetinib from continuous MEK suppression.
primary-confirmed - 23
King PJ, Kolitz S, Fowler KD, Funt JM, Zeskind BJ, Hall BM Potential anti-cachexia properties of novel dual-MEK inhibitor IMM-1-104. Sarcopenia, Cachexia, and Wasting Disorders Conference (SCWD) 2024 (2024).
Cited in · §1 · the number that arrived early · mechanism · cachexia biology
Preclinical data showing atebimetinib at a sub-therapeutic 25 mg/kg dose (−9.7% TGI) mitigated tumor-associated body weight loss in the C26 KRAS-G12D model and preserved E3 ubiquitin ligase transcripts (MuRF-1, Atrogin-1) at normal levels. DCI cycling mechanism also reset ERK switch in muscle satellite stem cells. Anchors the tolerability and weight-maintenance observations in Phase 2a patients.
primary-confirmed - 24
Immuneering Corporation A Phase 1/2a Study of IMM-1-104 in Participants With Advanced or Metastatic Solid Tumors (IMM1104-101). ClinicalTrials.gov (2022).
Cited in · §1 · the number that arrived early · §2 · why this MEK inhibitor doses differently · §5 · what the oral answers
The pivotal Phase 1/2a basket trial (N=209 enrolled) that generated the 17.3-month OS signal in 1L PDAC (N=55, data cutoff 2026-04-24). Status: ACTIVE_NOT_RECRUITING. This is the source study for the ASCO 2026 oral abstract 4013 and all Phase 2a efficacy data cited on the page.
primary-confirmed - 25
Immuneering Corporation A Study of IMM-6-415 in RAS/RAF Mutant Solid Tumors. ClinicalTrials.gov (2024).
Cited in · §5 · what the oral answers · pipeline · next asset
Completed (N=30) Phase 1/2 of IMM-6-415, Immuneering's second-generation compound in RAS/RAF-mutant solid tumors including PDAC, NSCLC, and melanoma. Establishes Immuneering has a pipeline beyond atebimetinib and has explored a successor compound.
primary-confirmed - 26
Immuneering Corporation Atebimetinib + GnP as a First Line Treatment in Patients With Metastatic Pancreatic Adenocarcinoma (MAPKeeper 301). ClinicalTrials.gov (2026).
Cited in · §5 · what the oral answers · §4 · the control-arm question · regulatory · designations
MAPKeeper 301: the global randomized Phase 3 (N=510, primary endpoint OS) that opened for enrollment in May 2026. This is the registrational trial. FDA and EMA alignment on trial design is confirmed (EOP2 complete). Completion expected 2029-02—the make-or-break read for the atebimetinib investment thesis.
primary-confirmed - 27
PubChem / NCBI Atebimetinib (IMM-1-104) — PubChem Compound CID 168111901. PubChem (2024).
Cited in · §2 · why this MEK inhibitor doses differently · mechanism · molecular identity
PubChem's canonical chemical entry for atebimetinib, confirming molecular formula, SMILES, synonyms (atebimetinib; IMM-1-104), and external database cross-links. Establishes chemical identity of the drug at the center of the page's argument.
primary-confirmed - 28
UniProt Consortium MAP2K1 / MEK1 — Dual specificity mitogen-activated protein kinase kinase 1 (Homo sapiens) [Q02750]. UniProt (2024).
Cited in · §2 · why this MEK inhibitor doses differently · mechanism · target biology
UniProt entry for MEK1—the primary kinase atebimetinib inhibits. Establishes the canonical biochemical function ('essential component of the MAP kinase signal transduction pathway'), substrate specificity, and biological role in RAS-driven proliferation. Ground truth for the mechanism of action claim.
primary-confirmed - 29
UniProt Consortium MAP2K2 / MEK2 — Dual specificity mitogen-activated protein kinase kinase 2 (Homo sapiens) [P36507]. UniProt (2024).
Cited in · §2 · why this MEK inhibitor doses differently · mechanism · target biology
UniProt entry for MEK2—atebimetinib's second target. Establishes concomitant Thr/Tyr phosphorylation of ERK1/2 and BRAF activation via KSR scaffolding as canonical functions. The dual MEK1/MEK2 inhibition profile differentiates atebimetinib from earlier generation inhibitors with lower MEK2 affinity.
primary-confirmed - 30
Open Targets Platform KRAS ↔ Pancreatic Carcinoma Target-Disease Association (EFO_0002618); MAP2K1/MAP2K2 disease association profiles. Open Targets (2026).
KRAS × PDAC (EFO_0002618)MAP2K1 associations (ENSG00000169032)MAP2K2 associations (ENSG00000126934)Google ScholarCited in · mechanism · target biology · §2 · why this MEK inhibitor doses differently
Open Targets genetic and functional evidence score for KRAS in pancreatic carcinoma: 0.8156—among the highest target-disease scores in the platform, reflecting near-universal somatic mutation frequency, strong genetic association, and clinical precedent. Provides quantitative target validation anchoring the rationale for any KRAS-pathway therapeutic in PDAC.
primary-confirmed - 31
FDA / Immuneering Corporation Fast Track designation for IMM-1-104 (atebimetinib) — second-line pancreatic ductal adenocarcinoma. FDA (2024).
Cited in · §5 · what the oral answers · regulatory · designations
FDA's first Fast Track grant for atebimetinib—for patients with PDAC who have failed one prior line of therapy. Fast Track enables rolling NDA review and frequent FDA interactions. Granted February 2024 per the company's stated timeline.
primary-confirmed - 32
FDA / Immuneering Corporation Fast Track designation for IMM-1-104 (atebimetinib) — first-line pancreatic ductal adenocarcinoma. FDA (2024).
Cited in · §5 · what the oral answers · regulatory · designations
FDA's second Fast Track grant for atebimetinib—extending designation to 1L PDAC to cover the MAPKeeper 301 registrational indication. Granted July 2024. Together with the 2L designation, atebimetinib holds Fast Track across both lines of PDAC, enabling an accelerated regulatory pathway for both populations.
primary-confirmed - 33
FDA / Immuneering Corporation Orphan Drug designation for IMM-1-104 (atebimetinib) — pancreatic cancer. FDA (2024).
Cited in · §5 · what the oral answers · regulatory · designations
FDA Orphan Drug designation for atebimetinib in pancreatic cancer, granted October 2024. Confers 7-year market exclusivity upon approval, tax credits for clinical trials, and FDA fee waivers—material economic incentives that improve the return profile for a successful MAPKeeper 301.
primary-confirmed - 34
FDA / Immuneering Corporation Fast Track designation for IMM-1-104 (atebimetinib) — NRAS-mutant advanced melanoma. FDA (2024).
Cited in · §5 · what the oral answers · regulatory · designations
Fast Track designation for atebimetinib in unresectable or metastatic NRAS-mutant melanoma that has progressed on or is intolerant to PD-1/PD-L1 checkpoint inhibitors, granted December 2024. Establishes a second indication pathway and validates the compound's mechanism in a NRAS-driven tumor where MEK is the direct downstream effector.
primary-confirmed - 35
openFDA drugsFDA No FDA approval found for atebimetinib / IMM-1-104 — openFDA drugsFDA search result. openFDA (2026).
Cited in · §5 · what the oral answers · regulatory · approval status
openFDA drugsFDA returned no matching NDA, BLA, or approved product for atebimetinib or Immuneering Corporation as of the data retrieval date (2026-05-29). Confirms the compound is investigational—no approved label, no approved indication—and that all efficacy claims derive from Phase 2a clinical data pending Phase 3 confirmation.
verbatim-verified - 36
Immuneering Corporation Form 10-K, fiscal year 2025. SEC EDGAR (2026).
Cited in · §1 · the number that arrived early · §4 · the control-arm question · §5 · what the oral answers · corporate · financials · ownership · strategic investors · pipeline · beyond PDAC
Primary financial source for FY2025: net loss $56.0M, R&D $42.0M, accumulated deficit $280.3M. Footnotes 7–9 are the definitive primary source refuting the AlphaSpread 'collaboration' framing: Sanofi holds equity only (2,708,559 shares via Sept 2025 private placement); Lilly's olomorasib and Regeneron's Libtayo are clinical supply agreements only — no milestones, royalties, or R&D funding disclosed for either. Filed 2026-03-06.
primary-confirmed - 37
Immuneering Corporation Form 10-Q, quarter ended March 31, 2026 (Q1 2026). SEC EDGAR (2026).
Cited in · §1 · the number that arrived early · corporate · financials
Most recent quarterly filing (filed 2026-05-15). Primary source for the Q1 2026 balance sheet: $198.6M total cash, cash equivalents and marketable securities ($47.3M cash + $109.4M current + $42.0M non-current), providing cash runway into 2029 per management guidance.
verbatim-verified - 38
Immuneering Corporation Form 10-Q, quarter ended September 30, 2025 (Q3 2025). SEC EDGAR (2025).
Cited in · corporate · financials · ownership · strategic investors
Filed 2025-11-12. Primary source confirming no going-concern doubt as of Sept 30, 2025; cash $227.6M at that date. Footnotes refute the AlphaSpread 'Sanofi collaboration' framing: Sanofi's Aventis Inc. subsidiary is a financial equity investor only, with no collaboration, licensing, or milestone arrangement disclosed. AlphaSpread's description of a Sanofi 'collaboration deal' is refuted here.
primary-confirmed - 39
Immuneering Corporation Form 8-K, current report dated January 7, 2026 (Phase 2a interim data: 64% OS at 12 months). SEC EDGAR (2026).
Cited in · §1 · the number that arrived early · §3 · the record it must clear · corporate · financials
The data release that moved the stock: 64% OS at 12 months (data cutoff Dec 15, 2025; N=34, 320 mg ITT; median follow-up 13.4 months) vs. ~35% for standard-of-care gemcitabine/nab-paclitaxel. This 8-K is the primary source for the '64% at 12 months' figure cited throughout the page.
verbatim-verified - 40
Immuneering Corporation Form 8-K, current report dated August 21, 2025 (Lilly clinical supply agreement + $25M private placement announcement). SEC EDGAR (2025).
Cited in · pipeline · beyond PDAC · ownership · strategic investors
Filed 2025-08-25; event date August 21, 2025. Announces the clinical supply agreement with Eli Lilly and Company for olomorasib (LY3537982) to evaluate atebimetinib + olomorasib in a planned Phase 2 trial in 2L+ KRAS G12C-mutant NSCLC. Also discloses the proposed $25M private placement. This is a supply agreement only — no milestones, royalties, or R&D funding from Lilly are disclosed.
primary-confirmed - 41
Immuneering Corporation Form 8-K, current report dated September 24, 2025 (Sanofi $25M private placement closing — entry into material definitive agreement and unregistered equity sale). SEC EDGAR (2025).
Cited in · ownership · strategic investors · corporate · financials
Filed 2025-09-24; event date September 24, 2025. Primary source for the Sanofi equity placement: Sanofi's Aventis Inc. subsidiary purchased 2,708,559 shares of Class A common stock at $9.23/share for gross proceeds of $25M. Sanofi is a financial strategic investor only — no licensing, collaboration, milestone, or royalty arrangement is disclosed. This corrects the AlphaSpread framing of a 'Sanofi collaboration.'
primary-confirmed - 42
Immuneering Corporation Form 8-K, current report dated September 24, 2025 (Regeneron clinical supply agreement — entry into material definitive agreement). SEC EDGAR (2025).
Cited in · pipeline · beyond PDAC · ownership · strategic investors
Filed 2025-09-25; event date September 24, 2025. Announces the clinical supply agreement with Regeneron Pharmaceuticals for Libtayo (cemiplimab) to evaluate atebimetinib + cemiplimab in a planned Phase 2 trial in 1L RAS-mutant NSCLC. Immuneering sponsors the study and retains all IMM-1-104 rights. No upfront payment, milestones, or royalties disclosed — a supply agreement only, not a collaboration. First patient dosing expected H2 2026.
primary-confirmed - 43
Immuneering Corporation Form 8-K, current report dated November 12, 2025 (Q3 2025 financial results and business update). SEC EDGAR (2025).
Cited in · §1 · the number that arrived early · corporate · financials
Q3 2025 earnings release: 86% OS at 9 months in N=34 first-line PDAC cohort; cash $227.6M; 9-month PFS 53%; investigator case studies including complete response with FOLFIRINOX. Also discloses composition-of-matter patent grant with life into 2042 or beyond and new clinical supply agreements with Lilly and Regeneron.
verbatim-verified - 44
Immuneering Corporation Form 8-K, current report dated March 6, 2026 (Q4 and full-year 2025 financial results). SEC EDGAR (2026).
Cited in · corporate · financials
FY2025 earnings release filed 2026-03-06: net loss $56.0M, R&D $42.0M, G&A $17.3M. Confirms $217.0M cash at year-end 2025, pipeline status, and MAPKeeper 301 Phase 3 recruitment update.
primary-confirmed - 45
Immuneering Corporation Form 8-K, current report dated May 15, 2026 (Q1 2026 financial results and business update). SEC EDGAR (2026).
Cited in · §1 · the number that arrived early · corporate · financials · pipeline · beyond PDAC
Q1 2026 earnings release: $198.6M cash/marketable securities, runway into 2029. Confirms MAPKeeper 301 (NCT07562152) is now recruiting with first patient dosing expected mid-2026 and includes the 17.3-month OS ASCO pre-announcement business update. Also cites the atebimetinib monotherapy 27-month third-line case study.
primary-confirmed - 46
Immuneering Corporation Form 4 insider open-market purchases, January 2026 (cluster: Feinberg, Schall, Hall, Brakewood, Neufeld). SEC EDGAR (2026).
Accession 0001790340-26-000008 (Feinberg, Jan 12)Accession 0001790340-26-000014 (Schall, Jan 15)Accession 0001790340-26-000012 (Hall, Jan 15)Accession 0001790340-26-000016 (Brakewood, Jan 16)Accession 0001790340-26-000010 (Neufeld, Jan 13)Cited in · §1 · the number that arrived early · corporate · financials
Five directors and officers purchased shares in the open market in January 2026 at prices ranging $4.15–$4.76, shortly after the stock declined following the Jan 7 data release. Peter Feinberg (Director/GP, S4K): 20,000 shares at avg $4.35; Thomas Schall (Director): 21,645 at avg $4.67; Brett Hall (CSO): 2,298 at avg $4.57; Harold Brakewood (CBO): 5,250 at $4.76; Leah Neufeld (CPO): 2,626 at $4.15. Signals insider conviction at the post-release trough.
verbatim-verified - 47
Immuneering Corporation Immuneering Reports Third Quarter 2021 Financial Results and Recent Business Highlights (EX-99.1; includes IPO closing confirmation). Immuneering Investor Relations (2021).
Cited in · corporate · financials
Issued November 9, 2021. Confirms the August 3, 2021 IPO closing: 8,625,000 shares of Class A common stock at $15.00/share including full overallotment exercise, gross proceeds approximately $129.4M. Earliest primary source establishing IMRX as a Nasdaq-listed company and the initial cash runway basis.
verbatim-verified - 48
Immuneering Corporation Immuneering Announces Clinical Supply Agreement with Lilly to Evaluate Atebimetinib in Combination with Olomorasib in KRAS G12C-Mutant NSCLC. Immuneering Investor Relations (2025).
Cited in · pipeline · beyond PDAC · ownership · strategic investors
Issued August 25, 2025. Primary narrative source for the Lilly supply agreement: Immuneering will sponsor the planned Phase 2 trial; Lilly supplies olomorasib (LY3537982). Immuneering retains all IMM-1-104 rights. No financial terms disclosed — this is a clinical supply arrangement, not a licensing or collaboration deal as AlphaSpread mislabeled it.
primary-confirmed - 49
Immuneering Corporation Immuneering Announces Clinical Supply Agreement with Regeneron to Evaluate Atebimetinib in Combination with Libtayo (Cemiplimab) in RAS-Mutant NSCLC. Immuneering Investor Relations (2025).
Cited in · pipeline · beyond PDAC · ownership · strategic investors
Issued February 6, 2025. Primary narrative source for the Regeneron supply agreement: Immuneering sponsors the planned Phase 2 study of atebimetinib + cemiplimab in 1L RAS-mutant NSCLC; Regeneron provides Libtayo; first patient dosing expected H2 2026. Immuneering retains global development and commercialization rights to IMM-1-104. No upfront payment or financial terms disclosed — supply agreement only, not a collaboration.
primary-confirmed - 50
Immuneering Corporation Immuneering to Present New Survival Data in First-Line Pancreatic Cancer at ASCO 2026 Annual Meeting (ASCO oral abstract preview, April 21, 2026). Immuneering Investor Relations (2026).
Cited in · §1 · the number that arrived early · §3 · the record it must clear
April 21, 2026 ASCO abstract announcement. Confirms Abstract 4013 accepted as Rapid Oral Abstract at ASCO 2026 Annual Meeting (June 1, 2026, 1:15 PM CDT); expanded N=55 first-line cohort; presenter Peter Vu, MD, MHA (UC San Diego Health). First public disclosure that the dataset had grown from N=34 to N=55.
primary-confirmed - 51
Immuneering Corporation Immuneering Reports 17.3 Months Median Overall Survival in First-Line Pancreatic Cancer — ASCO 2026 data release (May 21, 2026). Immuneering Investor Relations (2026).
Cited in · §1 · the number that arrived early · §3 · the record it must clear · §4 · the control-arm question · §5 · what the oral answers
The headline result driving the ASCO 2026 page: 17.3-month median OS in N=55 first-line metastatic PDAC patients treated with atebimetinib + mGnP, April 24, 2026 data cutoff. Grade 3+ TRAEs in ≥10% limited to anemia (16%) and neutropenia (18%), both chemotherapy-attributed. Primary narrative source for the 17.3-month OS figure and expanded safety profile.
verbatim-verified - 52
Immuneering Corporation MEK INHIBITORS AND THERAPEUTIC USES THEREOF — US 12,351,566 (GRANTED composition-of-matter). USPTO (2025).
Cited in · IP · patent estate · §2 · why this MEK inhibitor doses differently
Composition-of-matter patent covering atebimetinib's chromene (2H-chromen-2-one/benzopyranone) scaffold and therapeutic uses. Application 17791755 filed 2022-07-08 as US national stage of PCT/US2021/012531 (filed 2021-01-07), claiming priority to provisional 62959732 (filed 2020-01-10). Granted 2025-07-08 with +584-day PTA. Expected expiry approximately August 2042. Assignee confirmed as Immuneering Corporation via USPTO ODP verbatim API response — not inferred.
primary-confirmed - 53
Immuneering Corporation MEK INHIBITORS AND THERAPEUTIC USES THEREOF — US Application 19196269 (PENDING continuation of US 12,351,566). USPTO (2025).
Cited in · IP · patent estate
Filed 2025-05-01. Continuation of granted US 12,351,566 (application 17791755), sharing the same PCT/US2021/012531 / provisional 62959732 priority chain. Pending examination; extends prosecution of the core composition-of-matter family.
primary-confirmed - 54
Immuneering Corporation MEK IMMUNE ONCOLOGY INHIBITORS AND THERAPEUTIC USES THEREOF — US Application 18726908 (PENDING national-stage). USPTO (2024).
Cited in · IP · patent estate · pipeline · beyond PDAC
Filed 2024-07-05 as US national stage of PCT/US2023/060181 (filed 2023-01-05), claiming priority to provisional 63297116 (filed 2022-01-06). Separate patent family from US 12,351,566 covering the immuno-oncology MEK inhibitor series with the same 2H-chromen-2-one scaffold (CPC A61K31/37 coumarins). Assignee: Immuneering Corporation (primary confirmed via USPTO ODP).
primary-confirmed - 55
Immuneering Corporation METHODS OF TREATING CANCER WITH A RAS MUTATION — US Application 19161604 (PENDING national-stage). USPTO (2025).
Cited in · IP · patent estate · pipeline · beyond PDAC
Filed 2025-09-02 as US national stage of PCT/US2024/018246 (filed 2024-03-01), claiming priority to four 2023 provisionals. Covers methods of treating RAS-mutant cancers broadly — extends coverage beyond MEK composition claims into method-of-treatment territory. Status: Sent to Classification contractor.
primary-confirmed - 56
Immuneering Corporation TREATING PANCREATIC CANCER — US Application 19318266 (PENDING). USPTO (2025).
Cited in · IP · patent estate · §3 · the record it must clear
Filed 2025-09-03. Claims methods of treating pancreatic cancer specifically. Eight provisional parent applications (2024-09-04 through 2025-09-03) feed this application and the companion PCT/US2025/044738. Docketed new case, ready for examination. The PDAC-specific claiming strategy directly supports the MAPKeeper 301 commercial thesis.
primary-confirmed - 57
Immuneering Corporation MEK IMMUNE ONCOLOGY INHIBITORS AND THERAPEUTIC USES THEREOF — PCT/US2023/079156 (WO2024102762). USPTO (2023).
Cited in · IP · patent estate
PCT application filed 2023-11-08. International Search Report mailed. Child of PCT/US2023/060181; covers MEK immuno-oncology inhibitors and therapeutic uses thereof. Spawned US national stage application 18726908.
verbatim-verified - 58
Immuneering Corporation METHODS OF TREATING CANCER WITH A RAS MUTATION — PCT/US2024/018246 (WO2024196953). USPTO (2024).
Cited in · IP · patent estate
PCT application filed 2024-03-01. Four provisional parents from 2023. ISR mailed. Spawned US national stage application 19161604. Covers treatment methods for RAS-mutant cancers at the PCT international level.
verbatim-verified - 59
Immuneering Corporation INHIBITING MEK1 AND MEK2 AND RELATED METHODS OF TREATMENT — PCT/US2024/024818 (WO2024220460). USPTO (2024).
Cited in · IP · patent estate · §2 · why this MEK inhibitor doses differently
PCT application filed 2024-04-16. Ten provisional parents from 2023 (including 63564794, 63564815, 63574531, 63631732). ISR mailed. Covers MEK1/MEK2 dual inhibition methods; reflects the mechanistic DCI (Deep Cyclic Inhibition) rationale for atebimetinib's dosing schedule.
verbatim-verified - 60
Immuneering Corporation MEK IMMUNE ONCOLOGY INHIBITORS AND THERAPEUTIC USES THEREOF — PCT/US2024/036590 (WO2025010199). USPTO (2024).
Cited in · IP · patent estate
PCT application filed 2024-07-02. ISR mailed. Continuation family from PCT/US2023/060181; provisionals 63589778 and 63644898. Covers MEK immuno-oncology inhibitors. Spawns US application 19498908 (pending).
verbatim-verified - 61
Immuneering Corporation MEK IMMUNE ONCOLOGY INHIBITOR PHARMACEUTICAL COMPOSITIONS — PCT/US2024/036603 (WO2025010200). USPTO (2024).
Cited in · IP · patent estate
PCT application filed 2024-07-02. ISR mailed. Covers solid-form pharmaceutical compositions (formulations) of the MEK immuno-oncology inhibitor series. Distinguishes from method and composition-of-matter families — adds formulation IP layer.
verbatim-verified - 62
Immuneering Corporation INHIBITING MEK1 AND MEK2 AND RELATED METHODS OF TREATMENT — PCT/US2025/044738 (WO2026050978). USPTO (2025).
Cited in · IP · patent estate · §3 · the record it must clear
Most recent PCT application; filed 2025-09-03. Eight provisional parents (2024-09-04 through 2025-09-03, including 63690485, 63690489, 63693465, 63693481, 63707934, 63718226, 63742365, 63823526). Covers MEK1/MEK2 inhibition methods and pancreatic cancer treatment. This is the newest pending family, extending protection into the MAPKeeper 301 era.
verbatim-verified - 63
LinkedIn (Immuneering Corporation; Benjamin J. Zeskind; Brett Hall, Ph.D.; Harold Brakewood; and other leadership profiles) LinkedIn company and leadership profiles — Immuneering Corporation. LinkedIn (2026).
Cited in · §5 · what the oral answers · corporate · financials
Secondary source used for cross-referencing leadership credentials (Zeskind co-founder/CEO since 2008; Hall CSO; Brakewood CBO with Regeneron and Merck background). All LinkedIn-sourced claims are marked secondary and cross-referenced against primary SEC filings where possible. LinkedIn data is inherently self-reported and not independently verified.
secondary - 64
AlphaSpread (aggregator/AI summary) AlphaSpread IMRX Q3 2025 earnings call summary. AlphaSpread (2025).
Cited in · ownership · strategic investors · pipeline · beyond PDAC
Secondary AI-aggregated source retained here because it is the origin of the REFUTED framing that Sanofi, Lilly, and Regeneron entered 'collaboration' or 'licensing' deals with Immuneering. Primary SEC filings (10-K FY2025 footnotes; 8-Ks for each event) correct all three: Sanofi is a financial equity investor only ($25M private placement); Lilly and Regeneron each signed clinical supply agreements with no milestones or royalties disclosed. AlphaSpread's language ('collaboration agreements with Eli Lilly and Regeneron') is verbatim from a management earnings-call characterization, and the SEC filings are the controlling primary source.
refuted
Sources assembled from the verified claims ledger on 2026-05-30. Of 420 extracted facts, 362 carry a confirmed primary-source quote; the figures on this page draw from that set. Author blocks render the first author followed by "et al." for three or more authors; titles and pagination preserved as published.