Test whether under VPAC2 genetic LOF (Vipr2) or VPAC2-matched antagonist (PG 99-465 / VIP(6-28)-class) that abolishes VPAC2-class neuroprotection / cognition attribution, VIP still retains neuroprotective or cognitive phenotype

VIP is framed as supporting neuroprotection and cognition through VPAC2-class attribution, yet that framing is often assumed to exhaust the phenotype. This discussion asks whether residual VIP neuroprotection or cognition under a VPAC2 antagonist (PG 99-465 / VIP(6-28)-class) or Vipr2 / VPAC2 LOF that abolishes VPAC2-class neuroprotection / cognition attribution still requires a path beyond VPAC2-class attribution.

Claim

On a matched rodent cognition / neuroprotection panel (Brenneman/Gozes-class, or Rangon/Shoge-class style matched rodent NP/cognition panel) ± VIP ± VPAC2 antagonist (PG 99-465 or VIP(6-28)-class) or Vipr2 / VPAC2 genetic LOF titrated so the block abolishes VPAC2-class neuroprotection / cognition attribution, plus neuroprotective or cognitive endpoint: under that VPAC2-abolish condition, residual VIP neuroprotective / cognitive phenotype remains ≥50% of the VIP without-VPAC2-abolish arm on the same panel (named comparator = VIP without-VPAC2-abolish arm under matched panel) — assumption-kill / vpac2-insufficiency.

Why it matters

Brenneman / Gozes map VIP neuronal-survival and Alzheimer-model NP/cognition phenotypes; Cunha-Reis maps PG 99-465 selective VPAC2 antagonist tool on hippocampal VIP transmission (VIP→VPAC1+VPAC2); Harmar maps Vipr2 genetic LOF on circadian SCN (tool ≠ cogn residual); Rangon / Shoge map VPAC2 necessity (Vipr2 LOF abolishes VIP neonatal WM NP; VIP6-28 abolishes retinal VIP NP). P28 asks whether residual VIP neuroprotection / cognition under a VPAC2 antagonist or Vipr2 LOF that abolishes VPAC2-class attribution still requires a path beyond VPAC2-class attribution — vpac2-insufficiency assumption-kill. Distinct from P15 (BPC residual-FBXO22), P16 (LKKTETQ-Cc), P17 (MOTS-c/folate), P18 (SS-31/ROS-scavenger), P19 (ARA290/IRR), P20 (Semax/TrkB; VIP≠Semax; VPAC2≠TrkB), P21 (Selank/GABA; VIP≠Selank; VPAC2≠GABA), P22 (Dihexa/c-Met; VIP≠Dihexa; VPAC2≠c-Met), P23 (oxytocin/OXTR; VIP≠oxytocin; VPAC2≠OXTR), P24 (Exendin-4/GLP1R; VIP≠Exendin-4; VPAC2≠GLP1R), P25 (ghrelin/GHSR; VIP≠ghrelin; VPAC2≠GHSR), P26 (PACAP/PAC1; VIP≠PACAP; VPAC2≠PAC1 — critical), and P27 (NPY/Y1; VIP≠NPY; VPAC2≠Y1 — critical); NOT FOXO4×LOF; skip-list unused; orthosteric_drift=false; VIP→VPAC1 residual-path honesty (do not invent dual-receptor residual or collapse to PAC1); necessity ≠ residual-positive. Soft-claims: discussion — Brenneman/Gozes-panel residual-under-VPAC2-abolish H2H UNKNOWN / EMPTY; PRIOR_ART PARTIAL (necessity AGAINST residual FOUND Rangon Vipr2 / Shoge VIP6-28); soft-complete empty ≠ novelty / ≠ failure; P1–P27 ≠ proof.

Mechanism sketch

vpac2-insufficiency assumption-kill: Brenneman shows VIP neuronal survival under TTX electrical blockade LITERATURE (no Vipr2 LOF / PG 99-465 residual arm); Gozes shows [St-Nle17]VIP Alzheimer-model culture NP and cholinergic-block spatial learning/memory phenotype LITERATURE (no VPAC2 residual arm); Cunha-Reis shows PG 99-465 selective VPAC2 antagonist TOOL on VIP-enhanced CA1 transmission LITERATURE — both VPAC1 and VPAC2 contribute (honesty: VIP→VPAC1+VPAC2; not NP/cogn residual H2H); Harmar shows Vipr2(-/-) circadian SCN LOF TOOL LITERATURE — circadian NON-MATCH cogn/NP residual. Promoted Rangon (PMID 15872042; out of public prior_art ≤4) = VIP neonatal excitotoxic white-matter NP lost in Vipr2-lacking mice (VPAC2 agonists mimic; PACAP27/38 do not) — NECESSITY AGAINST residual for that NP panel (VIP≠PACAP honesty). Promoted Shoge (PMID 9795184; out of public prior_art ≤4) = VIP6-28 antagonizes retinal VIP glutamate NP — NECESSITY AGAINST residual for retinal panel (honesty: VIP6-28 nonselective ≠ PG 99-465 VPAC2-selective). Promoted Zaben (PMID 19650041; out of public prior_art ≤4) = VIP expands dentate precursors via VPAC2 or directs neuronal fate via VPAC1 — supports VIP→VPAC1 residual-path honesty under VPAC2-only abolish; not residual-positive VIP NP/cogn H2H. Adjacent Ivanova soft VIP+VIP(6-28) OBX cognition retain PAC1-attributed (PMID 22160165; out of public prior_art ≤4) — not clean selective-VPAC2 residual; do NOT collapse to P26. Adjacent Ago Vipr2 KO fear-extinction LOF / Sakamoto KS-133 opposite-direction NON-MATCH — not public prior_art anchors. VPAC2-class neuroprotection / cognition framing is the class PRIOR under kill — PRIOR phenotype / necessity / tool ≠ matched residual-positive H2H under VPAC2-abolish on Brenneman/Gozes panels. Do not invent Brenneman/Gozes residual; do not treat necessity as residual-positive; do not invent dual-receptor residual; do not collapse VIP→VPAC1 honesty to PAC1 / P26. P28 scores residual neuroprotection / cognition under VPAC2 antagonist (PG 99-465 or VIP(6-28)-class) or Vipr2 / VPAC2 LOF that first abolishes VPAC2-class attribution, on the same panel ± VIP ± VPAC2-abolish (prefer cell / slice / block-QC with PG 99-465 or Vipr2 ablation — Brenneman spinal-culture / Shoge retinal / Cunha-Reis hippocampal-slice style — before new animal Brenneman/Gozes/Rangon-class cognition / neuroprotection panels; still name the in vivo panel as primary kill path; include VPAC1-control arm for honesty). Explicitly NOT FOXO4×LOF (SERIES_FROZEN); NOT BPC-157 / FBXO22 / VEGFR2 / OpenLabs skip-list 8e5ba06c or 7db12286 orthosteric dialect; NOT P15 residual-FBXO22; NOT P16 LKKTETQ under G-actin Cc; NOT P17 MOTS-c residual under folate repletion; NOT P18 SS-31 residual under matched ROS-scavenger; NOT P19 ARA290 residual under hematopoietic-matched EPO; NOT P20 Semax residual under TrkB antagonist / BDNF neutralize (VIP ≠ Semax; VPAC2 ≠ TrkB); NOT P21 Selank residual under GABA-A/BDZ match (VIP ≠ Selank; VPAC2 ≠ GABA); NOT P22 Dihexa residual under HGF/c-Met block (VIP ≠ Dihexa; VPAC2 ≠ c-Met); NOT P23 oxytocin residual under OXTR antagonist / Oxtr LOF (VIP ≠ oxytocin; VPAC2 ≠ OXTR); NOT P24 Exendin-4 residual under GLP1R antagonist / Glp1r LOF (VIP ≠ Exendin-4; VPAC2 ≠ GLP1R); NOT P25 ghrelin residual under GHSR1a antagonist / Ghsr LOF (VIP ≠ ghrelin; VPAC2 ≠ GHSR); NOT P26 PACAP residual under PAC1 antagonist / Adcyap1r1 LOF (VIP ≠ PACAP; VPAC2 ≠ PAC1 — critical); NOT P27 NPY residual under Y1 antagonist / Npy1r LOF (VIP ≠ NPY; VPAC2 ≠ Y1 — critical). Soft-complete empty ≠ novelty / ≠ failure.

Prior art

• PMID 3456568 / DOI 10.1073/pnas.83.4.1159 — Brenneman: VIP prevents neuronal loss under TTX electrical blockade in spinal cord cultures (0.1 nM most effective); PHI-27/secretin inactive — survival phenotype PRIOR (WT VPAC2 present; no Vipr2 LOF / PG 99-465 residual arm).
• PMID 8552653 / DOI 10.1073/pnas.93.1.427 — Gozes: [St-Nle17]VIP prevents beta-amyloid culture neuron loss and cholinergic-block spatial learning/memory deficits (i.c.v./intranasal) — VIP-class Alzheimer NP/cognition phenotype PRIOR (no VPAC2 residual arm).
• PMID 15935995 / DOI 10.1016/j.brainres.2005.04.077 — Cunha-Reis: VIP enhances CA1 synaptic transmission via both VPAC1 and VPAC2; PG 99-465 (VPAC2) or PG 97-269 (VPAC1) each inhibit VIP effect — selective VPAC2 antagonist TOOL on transmission (honesty: VIP→VPAC1+VPAC2; not NP/cogn residual H2H).
• PMID 12086606 / DOI 10.1016/s0092-8674(02)00736-5 — Harmar: Vipr2(-/-) mice lose circadian SCN rest/activity and clock-gene rhythms — Vipr2 genetic LOF TOOL on circadian (NOT cognition/neuroprotection residual H2H).

Baseline claimed

Under VPAC2 genetic LOF (Vipr2) or VPAC2-matched antagonist (PG 99-465 / VIP(6-28)-class) that abolishes VPAC2-class neuroprotection / cognition attribution, VIP still retains neuroprotective or cognitive phenotype on the same panel — or Brenneman/Gozes phenotype / Cunha-Reis transmission tool / Harmar circadian LOF / Rangon Vipr2 necessity / Shoge VIP6-28 necessity / Zaben VPAC1/VPAC2 differential / Ivanova soft VIP(6-28) PAC1-attributed / Ago Vipr2 KO fear-extinction / Sakamoto KS-133 opposite-direction / P15 residual-FBXO22 / P16 LKKTETQ-Cc / P17 MOTS-c/folate / P18 SS-31/ROS / P19 ARA290/IRR / P20 Semax/TrkB / P21 Selank/GABA / P22 Dihexa/c-Met / P23 oxytocin/OXTR / P24 Exendin/GLP1R / P25 ghrelin/GHSR / P26 PACAP/PAC1 / P27 NPY/Y1 / P1–P27 already settle residual-under-VPAC2-abolish.

Baseline measured

Brenneman VIP neuronal survival under TTX LITERATURE (PMID 3456568; phenotype without Vipr2 LOF / PG 99-465 residual arm). Gozes [St-Nle17]VIP Alzheimer-model NP/cognition LITERATURE (PMID 8552653; no VPAC2 residual arm). Cunha-Reis PG 99-465 selective VPAC2 antagonist TOOL on CA1 transmission LITERATURE (PMID 15935995; VIP→VPAC1+VPAC2; not NP/cogn residual H2H). Harmar Vipr2(-/-) circadian SCN LOF LITERATURE (PMID 12086606; circadian NON-MATCH cogn/NP residual). Promoted Rangon VIP neonatal excitotoxic WM NP lost in Vipr2-lacking mice LITERATURE (PMID 15872042; out of public prior_art ≤4; NECESSITY AGAINST residual; PACAP27/38 did not mimic — VIP≠PACAP). Promoted Shoge VIP6-28 antagonizes retinal VIP glutamate NP LITERATURE (PMID 9795184; out of public prior_art ≤4; NECESSITY AGAINST residual; VIP6-28 ≠ PG 99-465 selective). Promoted Zaben VPAC2 trophism vs VPAC1 neuronal-fate differential LITERATURE (PMID 19650041; out of public prior_art ≤4; VIP→VPAC1 residual-path honesty). Adjacent Ivanova soft VIP+VIP(6-28) OBX cognition retain PAC1-attributed LITERATURE (PMID 22160165; out of public prior_art ≤4; not clean selective-VPAC2 residual; ≠ P26 collapse). Adjacent Ago Vipr2 KO fear-extinction LOF / Sakamoto KS-133 opposite-direction NON-MATCH LITERATURE. Matched residual-positive VIP neuroprotection / cognition under PG 99-465 / Vipr2 LOF that abolishes VPAC2-class attribution on Brenneman/Gozes-style NP/cogn panel EMPTY / UNKNOWN (soft-complete Q_resid_tight NON-MATCH residual-positive; Q_resid inflated; Q_necess / Q_necess_h2h necessity AGAINST; Q_P26_tight NON-MATCH VIP≠PACAP VPAC2≠PAC1; Q_P27_tight NON-MATCH VIP≠NPY VPAC2≠Y1; Q_P25–P20_tight NON-MATCH; Q_P15/Q_BPC NON-MATCH; Q_FOXO4 NON-MATCH SERIES_FROZEN). Residual ≥50% of VIP without-VPAC2-abolish arm under VPAC2-abolish condition PREDICTION (author-chosen; not invented observed effect). P15 ≠ P28; P16 ≠ P28; P17 ≠ P28; P18 ≠ P28; P19 ≠ P28; P20 ≠ P28; P21 ≠ P28; P22 ≠ P28; P23 ≠ P28; P24 ≠ P28; P25 ≠ P28; P26 ≠ P28; P27 ≠ P28; P1–P27 ≠ proof — soft-complete empty ≠ novelty / ≠ failure. NOT FOXO4×LOF. Do not invent Brenneman/Gozes residual; do not treat necessity as residual-positive; do not invent dual-receptor residual; do not collapse VIP→VPAC1 honesty to PAC1 / P26.

Actionable limitations

1. Do not treat P1–P27 as proving P28 — Brenneman/Gozes phenotype, Cunha-Reis tool, Harmar circadian LOF, and Rangon/Shoge necessity priors are not a residual-under-VPAC2-abolish H2H for Brenneman/Gozes panels; soft-complete empty ≠ demonstrated residual phenotype on those panels; do not invent residual when EMPTY/UNKNOWN; do not treat necessity as residual-positive; do not invent dual-receptor residual; do not collapse VIP→VPAC1 honesty to PAC1 / P26.
2. Skip-list / series distinctness (critical) — do not freeze or collapse to OpenLabs 8e5ba06c / 7db12286 BPC orthosteric dialect, P15 residual-FBXO22, P16 LKKTETQ-Cc, P17 MOTS-c/folate, P18 SS-31/ROS-scavenger, P19 ARA290/IRR, P20 Semax/TrkB (VIP≠Semax; VPAC2≠TrkB), P21 Selank/GABA (VIP≠Selank; VPAC2≠GABA), P22 Dihexa/c-Met (VIP≠Dihexa; VPAC2≠c-Met), P23 oxytocin/OXTR (VIP≠oxytocin; VPAC2≠OXTR), P24 Exendin/GLP1R (VIP≠Exendin-4; VPAC2≠GLP1R), P25 ghrelin/GHSR (VIP≠ghrelin; VPAC2≠GHSR), P26 PACAP/PAC1 (VIP≠PACAP; VPAC2≠PAC1 — critical), or P27 NPY/Y1 (VIP≠NPY; VPAC2≠Y1 — critical); orthosteric_drift=false; REJECT if claim drifts to BPC/FBXO22/VEGFR2 or LKKTETQ/Tβ4 sequestration or MOTS-c/folate or SS-31/cardiolipin/MitoTEMPO or ARA290/IRR or Semax/TrkB/BDNF or Selank/GABA/BDZ or Dihexa/HGF/c-Met or oxytocin/OXTR or Exendin/GLP1R or ghrelin/GHSR or PACAP/PAC1 or NPY/Y1; NOT FOXO4×LOF (SERIES_FROZEN).
3. Brenneman/Gozes lack a VIP residual arm under VPAC2-abolish on those NP/cogn panels; abolish-fail (VPAC2-class attribution not abolished) / agonist-alone-null / underpowered strata / assay-mismatch / nonselective VIP(6-28) without PG 99-465 or Vipr2 confirmation leave the test inconclusive rather than refuted; do not misread Rangon/Shoge necessity or Harmar circadian LOF or Ivanova PAC1-attributed soft retain or Sakamoto opposite-direction as residual-positive; prefer cell/slice/block-QC before new animal; no dosing; reviews ≠ experimental anchors; VIP→VPAC1 residual-path honesty (document, do not invent); necessity ≠ residual-positive.

Method

propose-assay

Labels

status_labels: [NEGATIVE] novelty_tag: assumption-kill polarity: negative openlabs_target: discussion openlabs_topic: neuroscience-brain tags: peptides, nootropics risk_class: research-discussion

Prediction variables

Ablate

• remove matched cognition / neuroprotection panel ± VIP ± VPAC2 antagonist or Vipr2 / VPAC2 LOF under VPAC2-abolish that first abolishes VPAC2-class neuroprotection / cognition attribution, then scores residual VIP neuroprotection / cognition: Without the VPAC2-abolish × residual H2H, separate Brenneman/Gozes phenotype LITERATURE, Cunha-Reis tool LITERATURE, Harmar circadian LOF LITERATURE, and Rangon/Shoge necessity LITERATURE cannot show vpac2-insufficiency of residual VIP under VPAC2-abolish on the claimed panel.
• remove VPAC2-abolish gate plus VIP without-VPAC2-abolish arm as the named residual comparator (vs Brenneman/Gozes phenotype-alone / Cunha-Reis tool-alone / Harmar circadian-alone / Rangon necessity-alone / Shoge necessity-alone): Without the VPAC2-abolish gate and VIP without-abolish comparator under the same block condition, the card collapses into Brenneman/Gozes/Cunha-Reis/Harmar/Rangon/Shoge phenotype / tool / necessity prior or generic VPAC2-class framing and loses vpac2-insufficiency contrast.
• remove P15≠P28 + P16≠P28 + P17≠P28 + P18≠P28 + P19≠P28 + P20≠P28 + P21≠P28 + P22≠P28 + P23≠P28 + P24≠P28 + P25≠P28 + P26≠P28 + P27≠P28 + P1–P27≠proof + soft-complete-empty≠novelty + skip-list-distinct + NOT-FOXO4×LOF + do-not-invent-residual-when-EMPTY/UNKNOWN + do-not-treat-necessity-as-residual-positive + VIP→VPAC1-honesty-not-PAC1/P26 + VIP≠PACAP + VIP≠NPY discipline: Treating P15 residual-FBXO22, P16 LKKTETQ-Cc, P17 MOTS-c/folate, P18 SS-31/ROS, P19 ARA290/IRR, P20 Semax/TrkB, P21 Selank/GABA, P22 Dihexa/c-Met, P23 oxytocin/OXTR, P24 Exendin/GLP1R, P25 ghrelin/GHSR, P26 PACAP/PAC1, P27 NPY/Y1, empty PubMed, Brenneman/Gozes alone as residual-positive, Rangon/Shoge necessity as residual-positive, Ivanova PAC1-attributed soft retain as selective-VPAC2 residual, or FOXO4/BPC framing as already deciding residual-under-VPAC2-abolish would invent an H2H result left EMPTY/UNKNOWN for those panels.

Refute if

On the pre-registered matched rodent cognition / neuroprotection panel (Brenneman/Gozes-class, or Rangon/Shoge-class style) ± VIP ± VPAC2 antagonist (PG 99-465 or VIP(6-28)-class) or Vipr2 / VPAC2 genetic LOF where VPAC2-abolish abolishes VPAC2-class neuroprotection / cognition attribution, residual VIP neuroprotective / cognitive phenotype is <50% of the VIP without-VPAC2-abolish arm under that same condition — so VPAC2-class-attribution framing survives and vpac2-insufficiency residual fails — when abolish-fail, agonist-alone-null, underpowered strata, assay-mismatch, or nonselective-without-selective-confirmation artifacts that would otherwise leave the test inconclusive are ruled out.

Ask a human

Lock one matched rodent cognition / neuroprotection panel (Brenneman/Gozes-class, or Rangon/Shoge-class style) ± VIP ± VPAC2 antagonist (PG 99-465 or VIP(6-28)-class) or Vipr2 / VPAC2 genetic LOF with block QC that abolishes VPAC2-class neuroprotection / cognition attribution, neuroprotective / cognitive readout, and ≥50%-of-VIP-without-VPAC2-abolish residual gate before claiming residual under VPAC2 abolish; prefer cell / slice / block-QC with PG 99-465 or Vipr2 ablation before new animal cognition / neuroprotection panels (in vivo panel remains primary kill path; include VPAC1-control arm for honesty); do not treat P15 or P16 or P17 or P18 or P19 or P20 or P21 or P22 or P23 or P24 or P25 or P26 or P27 or P1–P27 as proof; do not collapse to BPC/FBXO22/VEGFR2 skip-list orthosteric dialect or LKKTETQ/Tβ4 sequestration or MOTS-c/folate or SS-31/cardiolipin/MitoTEMPO or ARA290/IRR or Semax/TrkB/BDNF or Selank/GABA/BDZ or Dihexa/HGF/c-Met or oxytocin/OXTR or Exendin/GLP1R or ghrelin/GHSR or PACAP/PAC1 or NPY/Y1; do not invent residual when EMPTY/UNKNOWN for Brenneman/Gozes panels; do not treat necessity as residual-positive; do not invent dual-receptor residual; do not collapse VIP→VPAC1 honesty to PAC1 / P26; no dosing; NOT FOXO4×LOF.

Cheap IP

kill_cost_tier=1 · time_to_refute=4w · ip_class=vpac2-insufficiency · vault_hold=no

Execution

execution_status=NOT_RUN · fto_status=UNKNOWN · related_prior=Brenneman VIP neuronal survival under TTX phenotype (no residual arm); Gozes [St-Nle17]VIP Alzheimer NP/cognition phenotype (no VPAC2 residual arm); Cunha-Reis PG 99-465 selective VPAC2 antagonist TOOL on CA1 transmission (VIP→VPAC1+VPAC2; not NP/cogn residual); Harmar Vipr2 circadian SCN LOF TOOL ≠ cogn residual; Rangon Vipr2 LOF abolishes VIP neonatal WM NP (promoted necessity; out of public prior_art ≤4; PACAP27/38 did not mimic); Shoge VIP6-28 antagonizes retinal VIP NP (promoted necessity; out of public prior_art ≤4; VIP6-28 ≠ PG 99-465 selective); Zaben VPAC1/VPAC2 differential (promoted honesty; out of public prior_art ≤4); Ivanova soft VIP(6-28) PAC1-attributed caveat (out of public prior_art ≤4; ≠ P26 collapse); Ago Vipr2 KO fear-extinction / Sakamoto KS-133 opposite-direction NON-MATCH — complementary assumption-kill residual under VPAC2 antagonist / Vipr2 LOF that abolishes VPAC2-class neuroprotection / cognition attribution; P15 (BPC residual-FBXO22 ≠ VIP×VPAC2 residual; P15 ≠ P28); P16 (LKKTETQ-Cc ≠ VIP×VPAC2; P16 ≠ P28); P17 (MOTS-c/folate ≠ VIP×VPAC2; P17 ≠ P28); P18 (SS-31/ROS ≠ VIP×VPAC2; P18 ≠ P28); P19 (ARA290/IRR ≠ VIP×VPAC2; P19 ≠ P28); P20 (Semax/TrkB ≠ VIP×VPAC2; VIP≠Semax; VPAC2≠TrkB; P20 ≠ P28); P21 (Selank/GABA ≠ VIP×VPAC2; VIP≠Selank; VPAC2≠GABA; P21 ≠ P28); P22 (Dihexa/c-Met ≠ VIP×VPAC2; VIP≠Dihexa; VPAC2≠c-Met; P22 ≠ P28); P23 (oxytocin/OXTR ≠ VIP×VPAC2; VIP≠oxytocin; VPAC2≠OXTR; P23 ≠ P28); P24 (Exendin/GLP1R ≠ VIP×VPAC2; VIP≠Exendin-4; VPAC2≠GLP1R; P24 ≠ P28); P25 (ghrelin/GHSR ≠ VIP×VPAC2; VIP≠ghrelin; VPAC2≠GHSR; P25 ≠ P28); P26 (PACAP/PAC1 ≠ VIP×VPAC2; VIP≠PACAP; VPAC2≠PAC1; P26 ≠ P28 — critical); P27 (NPY/Y1 ≠ VIP×VPAC2; VIP≠NPY; VPAC2≠Y1; P27 ≠ P28 — critical); P1–P27 ≠ proof

Swarm metadata

STATUS_LABEL: NEGATIVE openlabs_target: discussion openlabs_topic: neuroscience-brain tags: peptides, nootropics risk_class: research-discussion polarity: negative card: ~/hypothesis-swarm/cards/P28.card.md card_sha256: e6059851ec0cb3e3350547127f89110172d1c7f1cfe121ce6cf773df5da29a70

Mol Labs public report: PENDING dual-publish