50+ Regulatory-Grade
ADMET Predictions

Predicts mutagenic potential via bacterial reverse mutation assay in Salmonella typhimurium and E. coli strains. A core regulatory genotoxicity test required in early non-clinical safety studies.

Detects micronuclei in the cytoplasm of cells — fragments produced by DNA breakage (clastogens) or whole chromosomes displaced by disruption of the mitotic apparatus (aneugens).

Predicts clastogenic and aneugenic effects in mouse bone marrow and/or blood erythrocytes — the in vivo complement to the in vitro assay.

Predicts structural chromosomal aberrations in mammalian cells — breaks, gaps, and rearrangements observed in metaphase cells. A standard component of the ICH core genotoxicity battery.

Rodent carcinogenicity prediction based on two-year bioassay data. Separate models for rat/mouse, both sexes, plus a general cross-species model.

Predicts inhibition of three major cardiac ion channels. NaV1.5 governs rapid depolarization, CaV1.2 contributes to the plateau phase, and hERG mediates repolarization. Inhibition may lead to QT prolongation and proarrhythmic effects.

Drug-Induced Liver Injury prediction based on human hepatotoxicity data annotated from FDA drug labels, covering serum enzyme elevations, jaundice, and hepatic failure.

Predicts renal damage potential. Nephrotoxicity contributes to 2% of drug failures in pre-clinical studies and 19% in phase 3 — early in silico flagging saves significant time and cost.

Predicts inhibition of AChE, leading to acetylcholine accumulation and disruption of normal neurotransmission — relevant for pesticide and drug candidates.

Predicts nervous system damage or dysfunction caused by drugs or chemicals. Neurotoxicity is a leading cause of post-market drug withdrawals; training data covers clinical cases of neurotoxic effects.

Predicts binding to estrogen receptors — key for endocrine disruption assessment. Disruption can lead to reproductive issues, cancer, and cognitive impairments; required under REACH and EPA regulations.

Predicts androgen receptor activity. AR disruption by exogenous compounds can cause reproductive disorders and various cancers — essential for endocrine disruptor screening in regulatory submissions.

Predicts inhibition of TPO, a crucial enzyme in thyroid hormone synthesis. THs regulate neurodevelopment, metabolism, and cardiac activity; TPO inhibition is a high-priority safety endpoint.

Predicts LD50 after single oral administration in rodents. Compounds are classified per CPSC and DoD guidelines based on toxic reactions within 24–48 hours post-exposure.

Predicts the potential to cause allergic contact dermatitis. Of high regulatory relevance for pharmaceuticals, cosmetics, and industrial chemicals; aligned with OECD TG 429 and the adverse outcome pathway for skin sensitization.

Predicts cytotoxic effects in human hepatocellular carcinoma cells. Cytotoxicity may underlie organ toxicity, genotoxicity artefacts, or carcinogenic responses — a key in vitro safety model.

Predicts compound interference with G0/G1, S, G2, and M cell-cycle phases. Alterations are closely linked to genotoxicity, carcinogenicity, and cytotoxicity and are of high relevance for safety assessment.

Predicts activation of AhR, a ligand-activated transcription factor that triggers CYP enzyme induction and downstream toxicity pathways including immunotoxicity, developmental toxicity, and cancer. Widely used in regulatory and mechanistic hazard screening.

Predicts adverse effects in the respiratory tract — airway irritation, bronchoconstriction, impaired gas exchange, or structural lung damage. Relevant for occupational, environmental, and pharmaceutical safety assessment.

Predicts activation of the tumor suppressor p53, a key stress-responsive indicator of DNA damage and potential genotoxicity. Widely used in regulatory screening and mechanistic hazard assessment.

Predicts compound-induced effects on human hematopoietic cell lines (RPMI-8226, MOLT-4) and the pro-inflammatory cytokine IL-1B — relevant for immunosuppressive, immunostimulatory, or pro-inflammatory hazard assessment.

Predicts inhibition of hepatic uptake transporters OATP1B1 and OATP1B3 — key determinants of hepatic drug disposition and a major factor in transporter-mediated drug–drug interactions. Widely used in regulatory safety assessment.

Predicts logBB (concentration ratio brain/blood). Neuroactive drugs must cross BBB; peripherally-acting drugs should not, to avoid psychotropic side effects.

Predicts reversible drug binding to plasma proteins (albumin, alpha-1 acid glycoprotein). Only the unbound fraction is pharmacologically active.

Predicts apparent permeability across Caco-2 monolayer — the standard in vitro reference for oral absorption and intestinal permeability screening.

Predicts the fraction of orally administered compound absorbed from the gastrointestinal tract into the bloodstream.

Predicts inhibitory potential against the five major CYP450 isoforms responsible for ~90% of drug metabolism. Critical for drug-drug interaction assessment.

Predicts whether the compound is a substrate of major CYP450 enzymes — informing metabolic liability and potential for drug-drug interactions.

Predicts intrinsic hepatic clearance from microsomal stability data — key input for pharmacokinetic modelling and dose prediction.

Predicted at 25°C in mol/L (log scale). Poor aqueous solubility is a major cause of low bioavailability and formulation failure in drug development.

HBA, HBD, molecular weight, LogP, TPSA, Fsp³, rotatable bonds, aromatic rings — the full descriptor set for drug-likeness assessment.

Lipinski Rule of Five, QED score, Drug-likeness, SA Score, PAINS alerts, GSK 4/400 Rule, Pfizer 3/75 Rule — multiple filters in a single computation.

Composite score (0–1) ranking compounds by their likelihood of pharmaceutical acceptance. Derived from: Ames mutagenicity, genotoxicity (in vitro & in vivo micronucleus), carcinogenicity, hERG cardiotoxicity, DILI, DIN, AChE inhibition, estrogen & androgen receptor binding, BBB permeability, PPB, Caco-2, HIA, metabolic stability, and aqueous solubility.

Composite score (0–1) estimated from predicted mutagenicity, genotoxicity, rodent carcinogenicity, and key physicochemical properties. Lower score = lower carcinogenic risk.