BioBridgeX
Log inCompare quotes
Preclinical / Nonclinical

DMPK / ADME CROs

Free for buyersNeutral marketplace
Quick answer

DMPK / ADME is the preclinical lab work that measures what the body does to your drug: absorption, distribution, metabolism, and excretion. You source it in nonclinical development, after a lead is chosen and before the GLP toxicology program, to pick a dose and catch liabilities early. On BioBridgeX, buyers source and compare qualified DMPK CROs and contract directly with their chosen supplier, free for buyers.

DMPK / ADME CROs on BioBridgeX

We are qualifying and publishing DMPK / ADME CROs now. Tell us what you need and we will match you with vetted vendors, or list your organization to be among the first.

What is DMPK / ADME and when do you need it?

DMPK stands for Drug Metabolism and Pharmacokinetics, and ADME is the four things it measures: Absorption, Distribution, Metabolism, and Excretion. Put plainly, this is the body of work that answers what your body does to the drug, as opposed to pharmacology, which answers what the drug does to the body. You have a molecule that hits its target in a dish. DMPK tells you whether enough of it survives the gut, the liver, and the bloodstream to reach that target at a tolerable dose, and for how long.

You reach for DMPK once you have a credible lead or a short series and you are deciding which compound to carry forward. It runs through the preclinical (nonclinical) stage and feeds directly into the work that follows: the PK/PD model, the human dose projection, and the GLP toxicology package in IND-enabling. Most of these early DMPK studies are non-GLP. Their job is to inform a go/no-go decision and a dose, not to satisfy a reviewer. The definitive, GLP-validated bioanalytical and the toxicokinetics that travel inside the pivotal tox studies come later.

Getting DMPK right early is some of the cheapest insurance in the whole program. A compound that is metabolically unstable, poorly permeable, or a strong CYP inhibitor will fail eventually, and it is far less painful to learn that from a microsomal stability assay and a CYP panel than from a clinical drug-drug interaction surprise or a tox study where exposure was too low to mean anything. Buyers sourcing here are usually choosing between a small molecule with a clean ADME profile and a more potent one that the body chews up too fast to dose.

What does a DMPK / ADME CRO actually do?

A DMPK CRO runs a menu of in vitro and in vivo assays, and most programs buy a panel rather than a single test. The in vitro work is fast and cheap and tends to come first, because it screens out the obvious losers before you spend money on animals. The in vivo work confirms what the in vitro data predicted and gives you the real exposure numbers a dose decision rests on.

The exact assay mix depends on your modality. Classic small-molecule DMPK leans heavily on metabolism and transporters. For peptides, oligonucleotides, antibodies, and other biologics the questions shift toward catabolism, biodistribution, and immunogenicity rather than CYP enzymes, so the assay menu and the right CRO change with the molecule.

  • In vitro metabolism: metabolic stability in liver microsomes and hepatocytes (intrinsic clearance, half-life), plasma stability, and species comparison to pick the right tox species.
  • Drug-drug interaction (DDI) work: CYP inhibition (reversible and time-dependent) and CYP induction panels, plus reaction phenotyping to identify which enzymes clear the compound.
  • Permeability and absorption: Caco-2 or MDCK monolayers, PAMPA, and efflux ratios that flag a P-gp or BCRP substrate likely to have absorption or CNS-penetration problems.
  • Distribution: plasma protein binding (equilibrium dialysis), blood-to-plasma partitioning, and aqueous and biorelevant solubility.
  • Transporters: substrate and inhibitor assays for P-gp, BCRP, OATP, OAT, and OCT, the panel regulators expect for the DDI story.
  • In vivo pharmacokinetics: IV and oral dosing across species, exposure (Cmax, AUC, half-life, clearance, volume of distribution), oral bioavailability (F), and tissue distribution where it matters.
  • Metabolite identification (Met ID): finding major circulating and reactive metabolites by LC-MS/MS so you are not blindsided by a metabolite liability later.
  • Bioanalytical support: fit-for-purpose LC-MS/MS methods to quantify drug and metabolites in plasma and tissue, the step that often gates everything downstream.

How to choose a DMPK / ADME CRO?

Start with fit to your molecule, not the size of the catalog. A site that runs flawless small-molecule CYP and transporter panels may be the wrong choice for an oligonucleotide or an antibody, where the live questions are catabolism, biodistribution, and immunogenicity rather than P450 metabolism. Match the CRO to your modality and your therapeutic area before you compare quotes, because the assay menu changes completely across small molecules, peptides, ADCs, and advanced therapies.

Beyond modality fit, the items below are what actually separate a clean engagement from a frustrating one. The cheapest panel is rarely the cheapest outcome, since a result you cannot trust, or a bioanalytical method that cannot detect your compound at the concentration you care about, forces a repeat that costs you weeks.

  • Quality and GxP status: confirm whether each study is non-GLP exploratory or GLP, and whether their bioanalytical can be validated to GLP later when the same method moves into your tox program. Ask about data integrity and SOPs even for non-GLP work.
  • Capacity and lead time: a great lab booked solid for months can be slower than a good lab with an open slot. Pin down report turnaround, not just bench time, since bioanalytical and in vivo PK are common critical-path items.
  • Modality and indication fit: ask for relevant experience in your exact molecule class, and confirm the specific assay or species you need is already running in-house with reference data, not stood up for the first time on your dollar.
  • Region and regulatory track record: confirm the DDI and transporter panels follow current FDA and EMA DDI guidance, and check the lab has supported submissions in the regions where you plan to file.
  • Data quality: expect clean, auditable reports with the assay controls and acceptance criteria stated, honest flagging of solubility or recovery issues, and a method that detects your compound at a relevant lower limit of quantification.
  • IP and confidentiality: settle ownership of data and any metabolite findings up front, and confirm the CDA covers a structure or target you may not want disclosed.

Frequently asked questions

What is the difference between DMPK and ADME?
They overlap heavily and are often used interchangeably. ADME names the four physiological processes a drug goes through: absorption, distribution, metabolism, and excretion. DMPK (drug metabolism and pharmacokinetics) is the discipline and the set of studies that measure those processes and turn them into numbers like clearance, half-life, and bioavailability. In practice, when a CRO advertises DMPK or ADME services they mean the same panel of in vitro and in vivo assays. Pharmacokinetics specifically refers to the in vivo exposure-over-time part of that work.
When in drug development do I need DMPK / ADME studies?
You start once you have a lead compound or a short series and need to decide which one to advance. DMPK runs through the preclinical (nonclinical) stage, after discovery hands you a potent molecule and before the GLP toxicology program in IND-enabling. Early in vitro screens (metabolic stability, permeability, CYP) help triage compounds; in vivo PK confirms exposure and supports the human dose projection. The toxicokinetics built into your pivotal GLP tox studies comes later and is a separate, regulated workstream.
Do DMPK / ADME studies need to be GLP?
Mostly no. The early DMPK screens (metabolic stability, CYP, permeability, exploratory PK) are typically non-GLP because they inform your decisions rather than support a submission. Non-GLP does not mean low quality; the data still has to be solid enough to bet a program on. The regulated pieces come later: the definitive DDI package supporting your label and the toxicokinetics inside your GLP tox studies need GLP-grade bioanalytical. A practical move is to build a fit-for-purpose bioanalytical method now that can be validated to GLP when the same compound enters the tox program.
What does a CYP inhibition or induction assay tell me, and why does it matter?
Cytochrome P450 (CYP) enzymes clear most small-molecule drugs. A CYP inhibition assay tells you whether your compound blocks those enzymes, which would raise the blood levels of co-administered drugs and create a drug-drug interaction (DDI) risk. A CYP induction assay tells you whether it ramps the enzymes up, which can lower exposure of other drugs or itself. Reaction phenotyping identifies which specific enzyme clears your compound. Regulators expect this DDI characterization before approval, and a strong inhibitor or inducer can limit a drug's commercial use even if it works, so catching it preclinically shapes go/no-go and trial design.
Are DMPK assays different for biologics versus small molecules?
Yes, substantially. Small-molecule DMPK centers on CYP metabolism, transporters, and permeability. Large molecules such as antibodies, peptides, and oligonucleotides are not cleared by CYP enzymes, so the questions shift to catabolism, biodistribution, target-mediated disposition, immunogenicity, and ligand-binding bioanalytical (ELISA or MSD) rather than LC-MS/MS in every case. A CRO that is excellent at small-molecule ADME may not be set up for biologics PK, which is exactly why matching the supplier to your modality matters before you compare prices.
Can I source DMPK and downstream toxicology from different suppliers on BioBridgeX?
Yes. Many sponsors use a specialist DMPK CRO and a separate GLP toxicology lab, since the best provider for each rarely sits under one roof. The friction is normally papering a separate contract, CDA, and PO with every lab. Through BioBridgeX you source and compare qualified suppliers for DMPK / ADME, then contract directly with each chosen supplier, in one place, with BioBridgeX as the neutral marketplace. It is free for buyers, suppliers pay a flat 2 percent fee, and coverage runs across all indications and modalities, so the same account carries from preclinical DMPK into IND-enabling tox without re-papering a new master agreement.

Source DMPK / ADME with one contract

Compare transparent quotes from qualified DMPK / ADME CROs, then contract once. Free for buyers.

Compare quotes