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Therapeutic carbon monoxide (CO) is being investigated as a way to limit ischemia-reperfusion injury in transplanted organs. Researchers have studied inhaled CO, CO-releasing compounds, and delivery to organs during preservation. Most supporting evidence is preclinical, and available transplant trial records do not establish that CO improves outcomes in people. CO is also toxic when it interferes with oxygen delivery, so controlled exposure and careful monitoring are essential.
Why study carbon monoxide in transplantation?
CO is best known as a toxic gas, but the body also produces it in small amounts when heme is broken down by heme oxygenases. Research into therapeutic CO asks whether carefully controlled exposure can influence biological processes involved in tissue injury; it does not make accidental exposure or self-administration safe.
One proposed target is ischemia-reperfusion injury. A donor organ can experience reduced blood flow during procurement and preservation, followed by renewed blood flow after transplantation. That transition can contribute to inflammation and cellular damage. Researchers have therefore tested whether CO given to a donor or recipient, or delivered to the organ before implantation, might reduce some of that injury.
Experimental studies and reviews describe possible anti-inflammatory, anti-apoptotic, antioxidant, and vascular effects. CO can act on heme and non-heme signaling targets, but the pathways and outcomes vary with tissue, route, timing, and dose. There is no single established mechanism that explains every reported effect.
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How can researchers target CO to an organ?
The main approaches differ in where CO is delivered and how much of the recipient’s body is exposed. No approach has been shown to be clinically superior.
| Approach | How delivery is intended to work | Evidence and limitation |
|---|---|---|
| Inhaled CO | The recipient inhales CO, creating systemic exposure. Research protocols require control of exposure and monitoring, including carboxyhemoglobin (COHb) and clinical measures. | Human kidney-transplant protocols appear in trial registries, but the records described below provide no efficacy results. |
| CO-releasing molecules or prodrugs | A compound releases CO under particular conditions. The compounds differ in chemistry and release behavior, and studies have tested them in kidney and other organ models. | Evidence includes animal models. Findings from one compound or model cannot be assumed to apply to another or to human transplantation. |
| Ex vivo organ delivery | CO is dissolved or introduced into preservation solution or another delivery material so the graft can be treated before implantation, with the aim of limiting systemic exposure. | This is a research direction, not evidence of routine clinical benefit or established practice. |
Comparisons between these approaches need to account for the organ and model studied, route, timing, dose, exposure control, degree of localization, measured graft outcomes, and evidence tier. A result in cells or animals cannot by itself show that a treatment will help transplant recipients.
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What does the evidence show so far?
Reviews and preclinical studies
A 2025 transplantation-focused review describes findings from rodent and large-animal models, different CO delivery strategies, and early clinical work. It presents the approach as promising but notes an unresolved translational question: how a brief CO exposure could produce durable protection of a graft.
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In a porcine kidney ischemia-reperfusion study, lower tested concentrations of the CO-releasing molecule CORM-3 were associated with improved renal-function measures, while higher tested concentrations were associated with poor renal hemodynamics and function. A 2025 study of CORM-A1 reports delivery and outcomes in rat and swine renal ischemia models. These are model-specific findings; neither establishes a dose or benefit for people.
Rank #3
Human transplant trial records
ClinicalTrials.gov record NCT00531856 describes a Phase 2 study of inhaled CO safety and tolerability in kidney-transplant recipients. The registry lists it as withdrawn, with actual enrollment of zero, no results posted, actual completion in August 2011, and a last update dated October 19, 2016. Because no participants were enrolled, this record is not evidence of safety or efficacy in recipients.
The ISRCTN record for PRO-K-001, ISRCTN42763074, describes a Phase 2 randomized, placebo-controlled study of inhaled CO after deceased-donor kidney transplantation. Its 2024 record lists the study as ongoing/recruiting and reports no results. The protocol is intended to examine safety and preliminary kidney-function and delayed-graft-function outcomes. For that protocol, delayed graft function is defined as at least one dialysis treatment within seven days after transplant; this is a study definition, not an estimate of how often the outcome occurs. Registry status can change, so the dated record should not be treated as confirmation of current recruitment.
These records do not demonstrate that inhaled CO prevents rejection, improves graft survival, or benefits transplant recipients. Animal results and trial plans are reasons for further investigation, not proof of clinical effectiveness.
Why dose and safety control matter
CO binds to hemoglobin and reduces the blood’s ability to deliver oxygen. The risk depends on factors including exposure concentration and duration. The therapeutic hypothesis therefore depends on precise control of dose, timing, route, and monitoring—not simply on CO being present in the body naturally.
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The CORM-3 kidney findings illustrate why dose cannot be generalized: lower tested concentrations and higher tested concentrations were associated with different renal outcomes in that animal model. Those concentrations are not human dosing advice. A controlled research protocol is fundamentally different from household CO exposure or self-treatment.
What would establish whether this can help patients?
The key next step is reliable human evidence showing that a defined delivery approach is acceptably safe and improves clinically meaningful transplant outcomes. Results need to be interpreted for the specific organ, route, timing, dose, and patient population studied. Until such evidence is available, therapeutic CO remains an experimental strategy rather than an established way to protect a transplanted organ.
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