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This is the English list. Each article is also available in Japanese; the link under each entry opens the other language.
Tools, glossary and model catalog
Public mouse-kidney metadata reproduces heterotypic Frequency scores while separating co-clump counts, cell pairs and random-label enrichment. Rare-pair denominators, replicate structure and recovered clump sizes define what proximity evidence can support.
Observed aggregate PK fitting and a public PopPK reconstruction compare equal-average schedules. Hypothetical delayed filters show why tumor enrichment alone does not identify interval-dependent target effects.
A Japanese note re-reading a reported reversion of colorectal cancer cells after triple knockdown of three genes chosen by a Boolean network model, using the public RNA-seq data and a pre-fixed analysis plan. It checks whether the targets were expressed and knocked down, how specific the enterocyte program was, and how consistent the lines were. It does not evaluate the paper's other experiments or any therapy.
An aggregate PK surrogate is fitted and checked against unused repeated-dose summaries. Conditional virtual patients compare equal-average-dose schedules without claiming heart-rate benefit or preserved efficacy.
A Japanese technical note that rebuilds 'doses from measured in vitro ADME' for the 325 OpenADMET-ExpansionRx compounds with transparent PK equations, showing that dose ranks are driven mainly by HLM CLint, that a constant-dose baseline already reaches a 2.4-2.8-fold error, and that the benchmark excludes potency and clinical doses.
A semi-synthetic experiment on public measurements from two healthy bone-marrow donors contrasts crossed and confounded artificial batches. Fixed CytoVI runs separate coarse cell-label readability from within-type reference contrasts; this is not a disease-preservation validation.
An evidence audit and reversible-inhibition counterexample demonstrate that a scalar coadministration ratio does not identify post-cessation behavior. This is not a reconstruction of published PBPK models, a prediction of patient exposure, or a dose-restoration recommendation.
Public PopPK and FDA model-derived ratios compare fixed, weight-band and theoretical continuous dosing. Conditional simulations separate boundary discontinuities from residual variability without predicting clinical benefit.
An audit of AVI rank units and 12 reported DNM1 splice variants, contrasted with PCSK9 evidence. Published aggregates are recalculated; no model inference or API queries were performed.
Published FVC summaries from the rentosertib phase 2a trial are examined under missing-data assumptions, without determining efficacy, dose or safety.
An audit of 10,335 released evaluation rows joins processed DEG labels to average-precision scores. Context-dependent prevalence and paired perturbations clarify what aggregate performance can establish about a limited follow-up budget.
Aggregate AUC ratios estimate relative bioavailability. Public PopPK coefficients compare paired schedules in 4096 conditional virtual patients. Unresolved peak reconstruction and the limits of AUC-only E-R are explicit.
An audit of two public examples, seven original metadata fixtures and a hypothetical value-of-information calculation distinguish evidence scope from project decisions.
An independent audit of five metrics on three public Perturb-seq datasets, comparing technical duplicates with a mean baseline without evaluating predictive models.
A Japanese research note auditing what published phase 1-2 pharmacokinetics, PD-1 receptor occupancy and dose-level response rates can say about 20 versus 10 mg/kg Q3W of ivonescimab, with the analysis plan fixed before computing. The answer is inconclusive. It makes no claim about efficacy ranking, recommended dose or any regulatory decision.
Observed aggregate PK supports a dose-exposure fit. A reconstructed parent PopPK model compares paired regimens in4096 conditional virtual patients. Clinical cohort differences, absorption assumptions and limits of split-dose predictions are explicit.
A Japanese guide comparing purposes, input data, model development, diagnostics and limits of PK/PD, population PK, PBPK and QSP. Three original figures include hypothetical PK/PD dynamics and analytical conditional population distributions. No empirical model estimation or real-drug validation is claimed.
Conditional simulations compare ADC and unconjugated DXd under equal total input. Finite-horizon AUC, late-window exposure and unvalidated formation-clock extrapolation are distinguished; clinical benefit is not inferred.
A known-motif audit of two public phage genomes separates sequence-pattern verification from autonomous discovery. Reported campaign counts, identifier-limited zero recoveries in ten reruns and fixed-input recognition are kept distinct from molecular function.
A one-marker, known-condition diagnostic on public 4i data compares mean-based predictions and a quantile map. Distributional agreement is separated from lineage identification, biological replication and resistance. No CellOT or CMonge model was trained.
A source-typed audit of revumenib and ziftomenib separates calibration, prediction and clinical evidence. Reduced-model calculations examine joint endpoint tolerances, cross-drug borrowing and mechanistic ambiguity without claiming independent clinical validation.
Hill fits, conditional profiles and technical redo comparisons distinguish usable transitions from unidentified EC50 values in a selected three-drug, six-cell-line dataset. Technical precision is not biological reproducibility.
A fixed-effect plasma/PBMC subsystem from a published clinical model is implemented independently. Equal doses give equal plasma AUC, while PBMC AUC differences are determined by a categorical formation-clearance assumption. Constant-formation and tail scenarios clarify limits; no tumor, clinical benefit, safety or regimen recommendation is inferred.
A source-based examination of catalytic motifs, structural metrics, sequence ensembles and denominators in enzyme design. Reported counts are recalculated; no model inference or enzyme experiments were performed.
Two-timepoint lesion volumes from 276 patients reveal heterogeneous changes hidden by aggregation. This analysis examines measurement selection and within-patient organ contrasts, not causal drug effects or RECIST progression.
A descriptive audit of published MAP scores for 16 held-out drugs and four knowledge-pretraining stages, distinguishing unprofiled compounds from unseen structural or mechanistic groups. No model training or inference was performed.
A Japanese essay on the difference between edges inferred from observed variables and the molecular interactions behind them. It links the mathematics of eliminating a mediator, a reproducible synthetic example, chemical-mediated microbial interactions, single-cell gene regulatory networks and mechanism assessment in drug discovery. It makes no claim about any real organism or drug.
An audit of sacituzumab govitecan and datopotamab deruxtecan distinguishes measured and derived analytes, label versions, exposure windows and response endpoints. The public summaries do not establish a shared payload target.
Three equal-dose weekly schedules are compared with an independent implementation of published PK equations. Weekly AUC is nearly unchanged, while minima and cutoff-dependent low-concentration times differ. Conditional sensitivity simulations do not establish clinical equivalence or predict efficacy, toxicity, or recovery.
An independent Python implementation of published structural equations compares 7-, 14- and 21-day lead-ins. Conditional paired simulations and sensitivity analyses separate cumulative exposure, peak-window effects and late troughs. No patient refitting, NONMEM equivalence or efficacy/safety prediction is claimed.
An independent aggregation of released predictions for eight MF-PCBA targets examines affinity-head adaptation, top-100 hit recovery, rescoring budgets and a nearest-active comparison. No model inference, retraining or prospective experiments were performed; scaffold annotations are author supplied.
A Japanese essay on separating limitations of data, models and evaluation in perturbation prediction. Original analytical examples illustrate sampling-time identifiability and signal dilution; recent studies inform a practical measurement audit. This is not a reanalysis of empirical cell data.
A Japanese essay distinguishing observational prediction, prediction under intervention and mechanistic claims, drawing on recent perturbation-prediction benchmarks and ICH M15. A reproducible synthetic indirect-response example shows that parameter sets compatible with the same data agree on a slowly varying regimen but diverge in the unobserved early hours, and that early sampling resolves the practical non-identifiability. It makes no claim about any real drug.
A public clinical PSA dataset used to compare landmark prediction, uncertainty calibration and decline/regrowth identifiability against simple benchmarks.
Public randomized B7-H3 ADC dose-cohort counts used to quantify conditional information value, decision uncertainty and sensitivity to unreported joint outcomes and follow-up.
SCOT trial efficacy and neuropathy compared with endpoint-specific denominators, uncertainty, missingness bounds and limits of joint benefit–risk inference.
Re-implemented population PK models for pembrolizumab and nivolumab were applied to a public adult weight distribution. Fixed doses let trough exposure fall below the trial-tested range most often in heavy patients, weight-based doses in the first interval of light patients; the verdict on extended intervals depends on how the range is defined. No dose is recommended.
Public blood–tumor–DUSP6 reconstruction and hypothetical QD/BID comparisons with target turnover, variability and exposure costs.
Fixed immune scores in 43 public RNA pairs, with paired change, normalization sensitivity and patient-separated response-association diagnostics.
Existing-drug dose comparisons inform priors for hypothetical new drugs. Under the defined utility and deterioration tolerance, weight 0.5 was acceptable in the main condition and 0.25 across all sensitivity conditions; these are not general borrowing rules.
Most tumor-scan dropout was death. A mixed model removed most of the survivor bias in 48-week shrinkage; a joint model and delta adjustment showed the 24-week arm difference was robust but the 48-week difference was fragile.
Public PopPK and efficacy reconstruction, Bayesian CRS sensitivity, and hypothetical measurement value and sampling design.
Published arm-level data from a randomized dose comparison are used to show the decision regions as the weights on benefit and harm change. The difference in severe toxicity is robust, but differences in response rate and OS are uncertain, and the conclusion depends on how harm is defined. No clinical dose is recommended.
Fixed Teff and stromal features evaluated across public urothelial cancer cohorts, with discrimination, calibration, missingness and transport limits.
A review of public ER-PROTAC data and a minimal model of how assumptions about site-of-action exposure and target recovery change comparisons of dosing frequency and PD metrics. The model is not fitted to the actual drug, and no clinical dose is proposed.
A Japanese review of perturbation forecasting, target-gene masking and recent benchmarks, with a reproducible synthetic example distinguishing evaluation shortcuts from downstream prediction. The example does not establish real-data performance or the superiority of pairwise masking.
Three population PK structures estimated from individual PK data, with internal validation, convergence and exposure differences across dosing conditions used to examine the limits of model selection.
At 16, 24 and 32 weeks, a mixed-effects tumor-kinetic estimate added no held-out survival discrimination beyond the observed one-point change, and carrying the last value forward predicted the next measurement best.
A two-compartment model estimated from published aggregate PK values, comparing Q2W, Q3W and Q4W exposure in light of identifiability and uncertainty.
A Japanese essay reviewing experimental workflows, industry disclosures and clinical progress. It distinguishes experimental throughput from evidence useful for development decisions; revenue growth and individual clinical advances do not establish an AI-driven supply shortage or a causal improvement in clinical success.
Between-subject variability simulated from a published population PK model, with efficacy exposure–response, period-specific CRS and maintenance exposure examined separately. Matching average exposure does not preserve peaks and troughs, and the analysis shows the limits of deciding from public information.
A reanalysis of warfarin PK/PCA data, revised with an absorption lag and a Hill exponent: effect delay, held-out prediction and the limits of extra PK.
A patient-separated landmark analysis of public colorectal cancer data, including calibration, censoring, uncertainty and temporal-integrity sensitivity.
Mosunetuzumab PK recalculated from the published paper and its supplement. A paired analysis of 2,000 virtual patients examines the effects of dose and interval and how far exposure can be translated to CD20 occupancy and CRS. Figures, Python code and CSV files included.