ADME Products

Before a drug can do anything therapeutically, it has to get into the bloodstream — for oral compounds, that means crossing the gut wall. Solubility, membrane permeability, efflux transporter activity, and first-pass gut metabolism all play a part, and a weakness in any one of them can sink an otherwise promising molecule. Our Absorption line-up covers that whole workflow: PAMPA screening for a quick first read on passive permeability, Caco-2 and MDCK assays for bidirectional transport and efflux, intestinal microsomes for first-pass clearance, and biorelevant dissolution media for solubility work — with the Vesitra™ transporter cell lines and membrane vesicles available for more mechanistic follow-up.

Once a drug is in the blood, the next question is where it ends up. That depends on how much stays free versus protein-bound (f_u,p), how readily it partitions into fatty or protein-rich tissue, and whether it can cross specialised barriers like the blood–brain barrier. Together these factors set the volume of distribution and how concentrated the drug becomes in different tissues. To study this, we offer plasma protein binding devices, multi-species tissue homogenates, cell-based BBB models, and whole blood / RBC partitioning kits.

Most of a drug's metabolism happens in the liver, and how fast and how thoroughly it gets broken down shapes intrinsic clearance (CL_int), the metabolite profile, and the risk of drug–drug interactions. Phase I enzymes — CYPs, FMOs, MAOs — handle the initial oxidation; Phase II enzymes such as UGTs, SULTs, and NATs take care of conjugation afterward, and between them they decide both the elimination rate and whether any reactive metabolites turn up. For this work we stock liver microsomes, S9 fractions, and cryopreserved hepatocytes, plus the AccuMetab™ recombinant enzyme series, the P450-Metric™ CYP inhibition kits, and eight further specialist assay brands.

Excretion is the last stop — whatever hasn't been broken down or retained eventually has to leave the body. Hydrophilic compounds tend to exit through the kidneys, via filtration and active transport through OAT1/3, OCT2, and MATE1/2-K; bulkier compounds and glucuronide conjugates are more often cleared through bile, via MRP2, BSEP, and BCRP. To model both routes, we provide renal proximal tubule cell models, inside-out membrane vesicles, sandwich-cultured hepatocyte biliary systems, and the BiliTrack™ ELISA kit series for measuring excretory function biomarkers.