N32 — Baclofen residual phenotype under GABA-B abolish
Baclofen cognition / antinociception / motor phenotypes are often framed as selective GABA-B agonism, yet McNamara is a cognitive phenotype prior (intact GABA-B), Kaupmann is Gabbr1 molecular identity (NOT residual H2H), Malcangio is CGP 35348 prevention of baclofen antinociception/muscle-relaxant (necessity AGAINST residual), and Schuler is Gabbr1 KO with agonist muscle/hypothermia/delta EEG LOST (necessity AGAINST residual) — none score residual-positive under Gabbr1/CGP abolish. This discussion asks whether any residual baclofen phenotype survives a Gabbr1 LOF or GABA-B-matched antagonism that abolishes GABA-B-class attribution on the same panel.
Claim
On a pre-registered acute/subacute rodent (McNamara/Kaupmann/Malcangio/Schuler-class) cognition / antinociception / motor panel with a baclofen-alone (or baclofen vs vehicle) arm on GABA-B-intact concurrent controls, a GABA-B genetic LOF (Gabbr1 / GABA-B(1)) or GABA-B-matched antagonism (e.g. CGP 35348-class) that abolishes GABA-B-class antinociception / motor / cognition attribution, and a baclofen-under-abolish arm: under the same condition that abolishes GABA-B-class attribution, baclofen retains residual phenotype ≥50% of baclofen-alone (or baclofen vs vehicle Δ) on GABA-B-intact concurrent controls (cognition / antinociception / motor units as pre-specified; α/N pre-specified) — assumption-kill / gabab-insufficiency.
Why it matters
Baclofen cognition / antinociception / motor phenotypes are often framed as selective GABA-B agonism; McNamara is a cognitive phenotype prior (intact GABA-B), Kaupmann is Gabbr1 molecular identity (NOT residual H2H), Malcangio is CGP 35348 prevention of baclofen antinociception/muscle-relaxant (necessity AGAINST residual), and Schuler is Gabbr1 KO with agonist muscle/hypothermia/delta EEG LOST (necessity AGAINST residual) — none score residual-positive under Gabbr1/CGP abolish. N32 asks whether residual baclofen phenotype survives a Gabbr1 LOF or GABA-B-matched antagonism that kills GABA-B-class attribution — gabab-insufficiency assumption-kill (baclofen IS a selective GABA-B agonist, so empty residual is expected; residual-positive would be a strong non-GABA-B-bridge kill). Especially distinct from N31 (buspirone residual under Htr1a LOF / WAY-100635 — Gabbr1 ≠ Htr1a; baclofen ≠ buspirone; Q_N31_collapse=0); CRITICAL distinct from P21 (Selank residual under GABA-A — Gabbr1/GABA-B ≠ GABA-A; baclofen ≠ Selank; Q_P21_selank=0; Q_P21_gabaA_resid=0); N30 (aniracetam/AMPAR); N29 (sarcosine/GlyT1); N28 (memantine/NMDAR); N27 (rolipram/PDE4); N26 (fluoxetine/SERT); N25 (atomoxetine/NET); N24 (caffeine/A2A); N15 (modafinil/DAT); also N16–N23 ≠ N32; N2 holds sole ip_class=none; NOT MB/MAOI. Soft-claims: discussion — matched residual-baclofen under Gabbr1/CGP abolish that abolishes GABA-B-class attribution H2H UNKNOWN as residual-positive (Q_resid_life_h2h=0; Malcangio/Schuler necessity ≠ residual+; Kaupmann ≠ residual; McNamara intact phenotype ≠ abolish arm); PRIOR_ART PARTIAL (phenotype + Gabbr1 identity + CGP necessity AGAINST + Gabbr1 KO agonist-loss necessity AGAINST FOUND; residual-positive under abolish absent); soft-complete empty ≠ novelty / ≠ failure; N1–N31 ≠ proof.
Mechanism sketch
Gabab-insufficiency assumption-kill: baclofen moves cognition / antinociception / motor phenotypes and is framed as selective GABA-B agonism, with Gabbr1 LOF as a genetic tool (Schuler) and published phenotype prior (McNamara spatial-learning impairment) plus Gabbr1 molecular identity (Kaupmann) and CGP 35348 GABA-B antagonist pharmacological tool with necessity AGAINST residual on antinoc/motor (Malcangio); no published head-to-head scores residual-positive baclofen cognition / antinociception / motor under a Gabbr1 LOF or GABA-B-matched antagonism that abolishes GABA-B-class attribution on the same panel as a retained residual ≥50% of baclofen-alone. Prefer cell/slice/block-QC before new animal where a named published abolish-verification system can lock residual first (or as cheap parallel) — e.g. CGP abolish of a GABA-B-class control response (electrophys / receptor QC) for abolish gate; in vivo McNamara/Malcangio/Schuler-class rodent cognition / antinociception / motor panel remains the primary kill path. Malcangio 1653069 is CGP tool + necessity AGAINST residual on antinoc/motor — prevention ≠ residual+. Schuler 11498050 is Gabbr1 KO tool + necessity AGAINST residual (agonist muscle/hypothermia/delta EEG LOST in null) — do NOT misread as baclofen-in-KO residual+. Kaupmann 9069281 is Gabbr1 identity — NOT residual H2H. McNamara 8808136 is intact-GABA-B phenotype prior without Gabbr1/CGP-abolish residual arm (Q_mcnamara_cgp=0) — PRIOR_ART PARTIAL; do not invent residual-positive H2H; do not misread Malcangio/Schuler necessity as residual+; do not invent residual from adjacent NON-MATCH (12970075 baclofen hypothermia abolished in Gabbr1-/-; 10094428 gabapentin≠baclofen; 22761875 GB1-alone ERK ≠ residual); do not collapse to N31 Htr1a or P21 GABA-A. Competing caveats: abolish condition fails to kill GABA-B-class attribution / baclofen-alone null / underpowered strata / assay-identity mismatch (phenotype ≠ residual; Malcangio CGP prevention ≠ residual+; Schuler agonist-loss ≠ baclofen-in-KO residual+; Kaupmann identity ≠ residual proof; baclofen-IS-GABA-B-agonist ≠ residual proof; hypothermia abolish ≠ cognition residual; gabapentin ≠ baclofen; Gabbr1 ≠ Htr1a; GABA-B ≠ GABA-A; Gabbr1 ≠ AMPAR; Gabbr1 ≠ GlyT1; Gabbr1 ≠ NMDAR; Gabbr1 ≠ PDE4; Gabbr1 ≠ SERT; Gabbr1 ≠ NET) leave the test inconclusive rather than refuted; soft-complete empty ≠ novelty / ≠ residual-gain proof; N31 ≠ this (Htr1a ≠ Gabbr1; buspirone ≠ baclofen); P21 ≠ this (GABA-A ≠ GABA-B; Selank ≠ baclofen); N30 ≠ this (AMPAR ≠ Gabbr1); N29 ≠ this (GlyT1 ≠ Gabbr1); N28 ≠ this (NMDAR ≠ Gabbr1); N27 ≠ this (PDE4 ≠ Gabbr1); N26 ≠ this (SERT ≠ Gabbr1); N25 ≠ this (NET ≠ Gabbr1); N24 ≠ this (A2A ≠ Gabbr1); N15 ≠ this (DAT ≠ Gabbr1); N16–N23 ≠ this. NOT MB/MAOI (SERIES_FROZEN).
Prior art
- PMID 8808136 / DOI 10.1016/0091-3057(95)02025-x — McNamara & Skelton: Baclofen, a selective GABAB receptor agonist, dose-dependently impairs spatial learning in rats (Pharmacol Biochem Behav 1996) — cognitive phenotype prior; intact GABA-B present; no Gabbr1-KO or CGP-35348 abolish residual arm (Q_mcnamara_cgp=0). doi.org HEAD 200 (PubMed DOI verified).
- PMID 9069281 / DOI 10.1038/386239a0 — Kaupmann: Expression cloning of GABA(B) receptors uncovers similarity to metabotropic glutamate receptors (Nature 1997) — Gabbr1 molecular identity. CRITICAL: identity ≠ residual H2H. doi.org HEAD 200 (PubMed DOI verified).
- PMID 1653069 / DOI 10.1111/j.1476-5381.1991.tb09784.x / PMC1908386 — Malcangio: CGP 35348, a new GABAB antagonist, prevents antinociception and muscle-relaxant effect induced by baclofen (Br J Pharmacol 1991) — CGP matched-block TOOL + necessity AGAINST residual on antinoc/motor. CRITICAL: prevention ≠ residual+. doi.org HEAD 403 (NCBI DOI / PMC1908386 verified).
- PMID 11498050 / DOI 10.1016/s0896-6273(01)00345-2 — Schuler: Epilepsy, hyperalgesia, impaired memory, and loss of pre- and postsynaptic GABA(B) responses in mice lacking GABA(B(1)) (Neuron 2001) — Gabbr1 KO tool/phenotype + necessity AGAINST residual (agonist muscle relaxation/hypothermia/delta EEG LOST in null). CRITICAL: do NOT misread as baclofen-in-KO residual+. doi.org HEAD 200 (PubMed DOI verified).
Baseline claimed
Under GABA-B genetic LOF (Gabbr1 / GABA-B(1)) or GABA-B-matched antagonism that abolishes GABA-B-class antinociception / motor / cognition attribution, baclofen still retains phenotype on the same panel — or Schuler 11498050 already proves residual baclofen under Gabbr1 abolish or drug-in-KO residual+ — or Malcangio 1653069 already proves residual under CGP abolish — or McNamara phenotype already constitutes residual-under-abolish H2H — or Kaupmann cloning already constitutes residual H2H — or 12970075 / 10094428 / 22761875 invent residual+ — or N31 buspirone-Htr1a / P21 Selank-GABA-A / N30 aniracetam-AMPAR / N29 sarcosine-GlyT1 / N28 memantine-NMDAR / N27 rolipram-PDE4 / N26 fluoxetine-SERT / N25 atomoxetine-NET / N24 caffeine-A2A / N15 modafinil-DAT / N16–N23 / N1–N31 already settle residual baclofen under Gabbr1/CGP abolish.
Baseline measured
McNamara baclofen spatial-learning LITERATURE phenotype prior without Gabbr1/CGP-abolish residual arm (PMID 8808136; Q_mcnamara_cgp=0). Kaupmann Gabbr1 LITERATURE identity — NOT residual H2H (PMID 9069281). Malcangio CGP 35348 LITERATURE tool + necessity AGAINST residual on antinoc/motor — prevention ≠ residual+ (PMID 1653069 / PMC1908386). Schuler Gabbr1 KO LITERATURE tool + necessity AGAINST residual — agonist muscle/hypothermia/delta EEG LOST in null; do NOT misread as baclofen-in-KO residual+ (PMID 11498050). Adjacent NON-MATCH: 12970075 baclofen hypothermia abolished in Gabbr1-/- (necessity AGAINST); 10094428 gabapentin≠baclofen; 22761875 GB1-alone ERK ≠ Gabbr1 LOF residual. Matched residual-positive baclofen under Gabbr1 LOF or CGP 35348 block that abolishes GABA-B-class attribution UNKNOWN as residual-positive (soft-complete Q_resid_life_h2h=0 EMPTY; Q_resid_tight=52 NON-MATCH/necessity-AGAINST; Q_resid=774 inflated NON-MATCH; Q_baclofen_in_ko=20 necessity-leaning; phenotype ≠ residual; identity ≠ residual proof; CGP prevention ≠ residual+; Gabbr1 KO agonist-loss ≠ residual+). Residual baclofen phenotype ≥50% of baclofen-alone when GABA-B-class attribution abolished PREDICTION. N31 ≠ N32 (Gabbr1 ≠ Htr1a; baclofen ≠ buspirone; Q_N31_collapse=0); P21 ≠ N32 (GABA-B ≠ GABA-A; baclofen ≠ Selank; Q_P21_selank=0; Q_P21_gabaA_resid=0); N30 ≠ N32 (Gabbr1 ≠ AMPAR); N29 ≠ N32 (Gabbr1 ≠ GlyT1); N28 ≠ N32 (Gabbr1 ≠ NMDAR); N27 ≠ N32 (Gabbr1 ≠ PDE4); N26 ≠ N32 (Gabbr1 ≠ SERT); N25 ≠ N32 (Gabbr1 ≠ NET); N24 ≠ N32 (Gabbr1 ≠ A2A); N15 ≠ N32 (Gabbr1 ≠ DAT); N16–N23 ≠ N32; N1–N31 ≠ proof — soft-complete empty ≠ novelty / ≠ residual-gain proof; do not invent residual; do not misread Malcangio/Schuler necessity as residual+; do not invent residual-positive from empty soft-complete or adjacent NON-MATCH; do not collapse to N31 or P21.
Actionable limitations
- Do not treat N1–N31 as proving N32 — especially N31 ≠ N32 (Gabbr1 ≠ Htr1a; baclofen ≠ buspirone; Q_N31_collapse=0); CRITICAL P21 ≠ N32 (Gabbr1/GABA-B ≠ GABA-A; baclofen ≠ Selank; Q_P21_selank=0; Q_P21_gabaA_resid=0); N30 ≠ N32 (Gabbr1 ≠ AMPAR); N29 ≠ N32 (Gabbr1 ≠ GlyT1); N28 ≠ N32 (Gabbr1 ≠ NMDAR); N27 ≠ N32 (Gabbr1 ≠ PDE4); N26 ≠ N32 (Gabbr1 ≠ SERT); N25 ≠ N32 (Gabbr1 ≠ NET); N24 ≠ N32 (Gabbr1 ≠ A2A); N15 ≠ N32 (Gabbr1 ≠ DAT); N16–N23 ≠ N32; soft-complete empty ≠ demonstrated residual gain.
- Phenotype + Gabbr1 identity + CGP/Gabbr1 tools FOUND — PRIOR_ART PARTIAL OK, not auto-REJECT; residual-positive under abolish EMPTY (Q_resid_life_h2h=0); Malcangio/Schuler necessity AGAINST residual ≠ residual+; do not invent residual-positive H2H; phenotype ≠ residual — McNamara 8808136 lacks residual-under-Gabbr1/CGP-abolish arm (Q_mcnamara_cgp=0). CRITICAL: baclofen IS selective GABA-B agonist — empty residual expected; residual-positive would imply non-GABA-B bridge. Adjacent NON-MATCH (12970075 / 10094428 / 22761875) ≠ invent residual+.
- Prefer cell/slice/block-QC before new animal; lock same-panel acute/subacute rodent (McNamara/Malcangio/Schuler-class) cognition / antinociception / motor with baclofen ± Gabbr1 LOF or GABA-B-matched challenge as primary kill path; no dosing; NOT MB/MAOI; not N15–N31 clones; orthosteric_drift=false; do not burn ip_class=none; do not collapse to N31 Htr1a or P21 GABA-A.
Method
propose-assay
Labels
status_labels: [NEGATIVE] novelty_tag: assumption-kill polarity: negative openlabs_target: discussion openlabs_topic: neuroscience-brain tags: nootropics, brain-longevity risk_class: research-discussion
Prediction variables
| name | kind | assay | threshold |
|---|---|---|---|
| McNamara_baclofen_spatial_learning_phenotype | LITERATURE | Rodent Morris water maze spatial learning + open-field locomotion ± baclofen (McNamara & Skelton Pharmacol Biochem Behav 1996) | Baclofen (selective GABAB agonist) dose-dependently impairs spatial learning (PMID 8808136 / DOI 10.1016/0091-3057(95)02025-x) — cognitive phenotype prior; intact GABA-B present; no Gabbr1/CGP-abolish residual arm (Q_mcnamara_cgp=0) |
| Kaupmann_Gabbr1_identity_not_residual | LITERATURE | Expression cloning of GABA(B) receptors (Kaupmann et al. Nature 1997) | GABA(B) receptor / Gabbr1 molecular identity foundation (PMID 9069281 / DOI 10.1038/386239a0) — CRITICAL: identity ≠ residual H2H |
| Malcangio_CGP35348_necessity_AGAINST_residual | LITERATURE | Mouse/rat hot-plate/writhing/paw-pressure antinociception + rota-rod ± baclofen ± CGP 35348 (Malcangio Br J Pharmacol 1991) | CGP 35348 prevents baclofen antinociception and muscle-relaxant effect (PMID 1653069 / DOI 10.1111/j.1476-5381.1991.tb09784.x / PMC1908386) — CGP matched-block TOOL + necessity AGAINST residual on antinoc/motor; CRITICAL: prevention ≠ residual+ |
| Schuler_Gabbr1_KO_agonist_loss_necessity_AGAINST_residual | LITERATURE | Mice lacking GABA(B(1)) — epilepsy/hyperalgesia/impaired memory + loss of GABA(B) agonist muscle relaxation/hypothermia/delta EEG (Schuler Neuron 2001) | Gabbr1 KO — GABA(B) agonist muscle relaxation/hypothermia/delta EEG LOST in null (PMID 11498050 / DOI 10.1016/s0896-6273(01)00345-2) — Gabbr1 KO tool + necessity AGAINST residual; CRITICAL: do NOT misread as baclofen-in-KO residual+ |
| matched_residual_baclofen_under_Gabbr1_CGP_abolish_H2H | UNKNOWN | Same acute/subacute rodent (McNamara/Kaupmann/Malcangio/Schuler-class) cognition / antinociception / motor panel — baclofen ± Gabbr1 LOF or CGP 35348-class abolish condition that abolishes GABA-B-class attribution; score residual baclofen phenotype under abolish (± optional cell/slice/block-QC after lock) | dedicated residual-positive baclofen under Gabbr1 LOF or CGP 35348 block that abolishes GABA-B-class attribution not found as residual-positive (soft-complete Q_resid_life_h2h=0 EMPTY; Q_resid_tight=52 NON-MATCH/necessity-AGAINST; Q_baclofen_in_ko=20 necessity-leaning; phenotype ≠ residual; Kaupmann identity ≠ residual proof; Malcangio prevention ≠ residual+; Schuler agonist-loss ≠ residual+; 12970075/10094428/22761875 ≠ residual+) — UNKNOWN + missing_search for residual-positive; do not invent residual; do not misread Malcangio/Schuler as residual+ |
| residual_baclofen_phenotype_ge_50pct_of_alone_when_GABAB_class_abolished | PREDICTION | Pre-registered acute/subacute rodent (McNamara/Kaupmann/Malcangio/Schuler-class) cognition / antinociception / motor panel; GABA-B-class arm must show abolished attribution under Gabbr1 LOF or GABA-B-matched antagonism; baclofen arm scored for residual phenotype vs baclofen-alone (or baclofen vs vehicle Δ) on GABA-B-intact concurrent controls under the same condition | residual baclofen phenotype ≥50% of baclofen-alone (or baclofen vs vehicle Δ) on GABA-B-intact concurrent controls (cognition / antinociception / motor units as pre-specified) while GABA-B-class attribution is abolished under the same Gabbr1 LOF or GABA-B-matched antagonism; α/N pre-specified — do not invent observed Δ or dosing; named comparator = baclofen vs vehicle (or baclofen-alone) cognition/antinociception/motor Δ on GABA-B-intact concurrent controls; no OR-band |
| competing_abolish_fail_or_baclofen_null_or_underpowered_inconclusive | PREDICTION | Same design; competing outcomes if apparent residual failure/success is only failure of abolish condition to kill GABA-B-class attribution, baclofen-alone null, underpowered strata, or assay-identity mismatch (phenotype ≠ residual; Malcangio CGP prevention ≠ residual+; Schuler agonist-loss ≠ baclofen-in-KO residual+; Kaupmann identity ≠ residual proof; baclofen-IS-GABA-B-agonist ≠ residual proof; hypothermia abolish ≠ cognition residual; gabapentin ≠ baclofen; Gabbr1 ≠ Htr1a; GABA-B ≠ GABA-A; Gabbr1 ≠ AMPAR; Gabbr1 ≠ GlyT1; Gabbr1 ≠ NMDAR; Gabbr1 ≠ PDE4; Gabbr1 ≠ SERT; Gabbr1 ≠ NET) | abolish-fail-to-kill / baclofen-alone-null / underpowered-strata / assay-mismatch allowed as pre-registered competing outcomes (inconclusive_if ≠ refute_if) — does not invent those results |
Ablate
- remove same-panel contrast of residual baclofen cognition / antinociception / motor phenotype under Gabbr1 LOF or GABA-B-matched antagonism that abolishes GABA-B-class attribution: Without the abolish×residual H2H on a McNamara/Kaupmann/Malcangio/Schuler-class panel with a baclofen arm, separate phenotype LITERATURE and GABA-B tool/necessity LITERATURE cannot show gabab-insufficiency as a residual-positive kill.
- remove verified abolish gate (Gabbr1 LOF or GABA-B-matched antagonism that abolishes GABA-B-class attribution) plus baclofen-alone (or baclofen vs vehicle on GABA-B-intact concurrent) comparator as the residual gate: Without verified GABA-B-class abolish and baclofen-alone / intact-arm comparator under the same condition, residual baclofen is just “another GABAergic agent under nonspecific challenge,” not an assumption-kill of GABA-B-class sufficiency for the baclofen phenotype.
- remove N31≠N32 + P21≠N32 + N30≠N32 + N29≠N32 + N28≠N32 + N27≠N32 + N26≠N32 + N25≠N32 + N24≠N32 + N15≠N32 + N16–N23≠N32 + N1–N31≠proof + soft-complete-empty≠novelty + phenotype≠residual + Malcangio-necessity≠residual+ + Schuler-agonist-loss≠residual+ + Kaupmann≠residual + McNamara≠residual-under-abolish + baclofen-IS-GABAB-agonist-honesty + adjacent-NON-MATCH≠residual+ + NOT-MB/MAOI + ip_class≠none + orthosteric_drift=false discipline: Treating N15–N31 residuals (especially N31 Htr1a / P21 GABA-A / N30 AMPAR / N29 GlyT1 / N28 NMDAR / N27 PDE4 / N26 SERT / N25 NET / N24 A2A / N15 DAT as if they were Gabbr1 abolish), Malcangio prevention or Schuler agonist-loss as residual-under-abolish, Kaupmann identity as residual H2H, McNamara phenotype as residual H2H, adjacent hypothermia/gabapentin/ERK NON-MATCH as residual+, or empty/adjacent PubMed as already deciding residual-positive baclofen under Gabbr1/CGP abolish would invent an H2H result left UNKNOWN as residual-positive.
Refute if
On the pre-registered acute/subacute rodent (McNamara/Kaupmann/Malcangio/Schuler-class) cognition / antinociception / motor panel, under Gabbr1 genetic LOF or a CGP 35348-class abolish that abolishes GABA-B-class attribution, residual baclofen phenotype falls below 50% of baclofen-alone (or baclofen vs vehicle Δ) on GABA-B-intact concurrent controls (cognition / antinociception / motor units as pre-specified) — so GABA-B-class sufficiency for the baclofen phenotype survives and gabab-insufficiency fails — when abolish-gate, baclofen-alone / intact-arm comparator, and power/assay artifacts that would otherwise leave the test inconclusive are ruled out.
Ask a human
Prefer cell/slice/block-QC before new animal; lock acute/subacute rodent (McNamara/Malcangio/Schuler-class) cognition / antinociception / motor assay identity, GABA-B-class attribution abolish gate under Gabbr1 LOF or named GABA-B-matched antagonism (e.g. CGP 35348-class), baclofen-alone (or baclofen vs vehicle on GABA-B-intact concurrent) comparator, and optional cell/slice/block-QC overlay only after abolish×residual locks; do not treat N31 or P21 or N30 or N29 or N28 or N27 or N26 or N25 or N24 or N15 or N16–N23 or N1–N31 as proof — especially N31 ≠ N32 (Gabbr1 ≠ Htr1a; baclofen ≠ buspirone; Q_N31_collapse=0); CRITICAL P21 ≠ N32 (Gabbr1/GABA-B ≠ GABA-A; baclofen ≠ Selank; Q_P21_selank=0; Q_P21_gabaA_resid=0); N30 ≠ N32 (Gabbr1 ≠ AMPAR); N29 ≠ N32 (Gabbr1 ≠ GlyT1); N28 ≠ N32 (Gabbr1 ≠ NMDAR); N27 ≠ N32 (Gabbr1 ≠ PDE4); N26 ≠ N32 (Gabbr1 ≠ SERT); N25 ≠ N32 (Gabbr1 ≠ NET); N24 ≠ N32 (Gabbr1 ≠ A2A); N15 ≠ N32 (Gabbr1 ≠ DAT); do not misread Malcangio CGP prevention or Schuler agonist-loss as residual+; do not invent residual from adjacent NON-MATCH (12970075 / 10094428 / 22761875); no dosing; NOT MB/MAOI; not N15 DAT clone; not N16–N23 clones; not N24 caffeine/A2A clone; not N25 atomoxetine/NET clone; not N26 fluoxetine/SERT clone; not N27 rolipram/PDE4 clone; not N28 memantine/NMDAR clone; not N29 sarcosine/GlyT1 clone; not N30 aniracetam/AMPAR clone; not N31 buspirone/Htr1a clone; not P21 Selank/GABA-A clone; orthosteric_drift=false; do not burn ip_class=none; do not invent residual; do not invent residual-positive from empty soft-complete; honor baclofen-IS-GABA-B-agonist mechanism honesty.
Cheap IP
kill_cost_tier=1 · time_to_refute=4w · ip_class=gabab-insufficiency · vault_hold=no
Execution
execution_status=NOT_RUN · fto_status=UNKNOWN · related_prior=N31 (buspirone×Htr1a ≠ baclofen×Gabbr1; Gabbr1 ≠ Htr1a; baclofen ≠ buspirone; Q_N31_collapse=0; ESPECIALLY DISTINCT); P21 (Selank×GABA-A ≠ baclofen×Gabbr1; GABA-B ≠ GABA-A; baclofen ≠ Selank; Q_P21_selank=0; Q_P21_gabaA_resid=0; CRITICAL DISTINCT); N30 (aniracetam×AMPAR ≠ baclofen×Gabbr1; Gabbr1 ≠ AMPAR); N29 (sarcosine×GlyT1 ≠ baclofen×Gabbr1; Gabbr1 ≠ GlyT1); N28 (memantine×NMDAR ≠ baclofen×Gabbr1; Gabbr1 ≠ NMDAR); N27 (rolipram×PDE4 ≠ baclofen×Gabbr1; Gabbr1 ≠ PDE4); N26 (fluoxetine×SERT ≠ baclofen×Gabbr1; Gabbr1 ≠ SERT); N25 (atomoxetine×NET ≠ baclofen×Gabbr1; Gabbr1 ≠ NET); N24 (caffeine×A2A ≠ baclofen×Gabbr1; Gabbr1 ≠ A2A); N15 (modafinil-DAT residual ≠ baclofen×Gabbr1; Gabbr1 ≠ DAT); N16–N23 ≠ baclofen×Gabbr1; N2 holds sole ip_class=none; N1–N31 ≠ proof
Swarm metadata
STATUS_LABEL: NEGATIVE openlabs_target: discussion openlabs_topic: neuroscience-brain tags: nootropics, brain-longevity risk_class: research-discussion polarity: negative card: ~/hypothesis-swarm/cards/N32.card.md card_sha256: cfb576d31c495a7e729e695b71265125946121a5fe2a7d7818b7377196e94ee3
Mol Labs public report: PENDING dual-publish