Therapeutic carbon monoxide (CO) is being investigated as a way to limit injury to transplanted organs, especially damage that can occur when blood flow returns after a period without oxygen. Researchers are testing inhaled CO, CO-releasing compounds, and treatments applied to organs during preservation. Most supporting evidence is preclinical, and the available trial records do not establish that CO improves transplant outcomes in people. CO is also toxic when it disrupts oxygen delivery, so this research depends on tightly controlled exposure—not ordinary CO exposure or self-treatment.
Why researchers are studying CO in transplantation
Transplanted organs can experience ischemia-reperfusion injury: stress and damage associated with reduced blood flow during procurement or preservation, followed by the return of blood flow. That injury can contribute to inflammation and cellular damage in a graft. Researchers are investigating whether carefully controlled CO exposure could reduce some of that harm.
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CO is produced naturally in the body when heme is broken down by heme oxygenases. Experimental literature describes effects on several heme and non-heme signaling targets, with reported anti-inflammatory, anti-apoptotic, antioxidant, and vascular effects. These effects depend on the tissue, dose, route, and timing; they do not amount to one settled mechanism or show that giving CO will protect a transplanted organ in clinical practice.
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Studies explore different ways to deliver CO. The key distinction is whether exposure is systemic—reaching the recipient’s body—or localized to the graft before implantation.
#1 Best Overall
| Approach | What it involves | What the evidence does and does not show |
|---|---|---|
| Inhaled CO | The recipient inhales a controlled amount, producing systemic exposure that requires clinical and COHb monitoring. COHb means carboxyhemoglobin, CO bound to hemoglobin. | Kidney-transplant protocols and experimental work have examined this route. Registry records do not provide efficacy results establishing a transplant benefit. |
| CO-releasing molecules or prodrugs | A compound releases CO under particular conditions. Different compounds have different chemistry and release behavior. | Kidney and other organ models have been studied, but findings from one compound or animal model cannot be assumed to apply to another or to people. |
| Ex vivo organ delivery | CO is introduced into preservation solution or another delivery material while the organ is outside the recipient, aiming to treat the graft before implantation. | This is a research direction intended to localize exposure. The available evidence does not establish routine clinical use or human benefit. |
Comparing these approaches requires more than asking whether CO was used. Relevant distinctions include the organ and model, route and timing, dose and exposure control, how localized delivery is, which graft outcomes were measured, and whether the evidence is from cells, animals, or people. The reviewed evidence does not establish a clinically superior route.
What the evidence says so far
Preclinical findings
A 2025 transplantation-focused review summarizes rodent and large-animal work, delivery strategies, and early clinical research. It describes translational promise while noting unresolved questions, including how a brief CO exposure might produce durable protection of a graft.
Rank #2
In a porcine kidney ischemia-reperfusion study, lower tested concentrations of the CO-releasing molecule CORM-3 were associated with improved renal-function measures. At higher tested concentrations, renal hemodynamics and function were poor. These model-specific findings illustrate why dose control matters; they are not dosing guidance for people.
A 2025 study reported CORM-A1 delivery and outcomes in rat and swine renal ischemia models. Its translational relevance is a research possibility, not evidence of established benefit for human transplant recipients.
Rank #3
Human trial records
ClinicalTrials.gov record NCT00531856 concerns a Phase 2 study of inhaled CO safety and tolerability in kidney-transplant recipients. The record lists the study as withdrawn, actual enrollment as zero, no results posted, actual completion in August 2011, and its last update on October 19, 2016. Because no participants were enrolled, this record supplies no evidence of safety or efficacy in participants.
A separate 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 has no results posted; recruitment status may have changed since that record. The protocol planned to examine safety and preliminary kidney-function and delayed-graft-function outcomes. In that protocol, delayed graft function means at least one dialysis treatment within seven days after transplant; this is a trial definition, not an estimate of how often delayed graft function occurs.
Why therapeutic CO is not ordinary CO exposure
CO binds hemoglobin and interferes with oxygen delivery. Toxicity varies with concentration and exposure duration, which makes route, dose, timing, and monitoring central to any therapeutic investigation. A controlled research protocol with clinical monitoring is not comparable to household exposure, and experimental findings do not make uncontrolled exposure safe. No one should try to use CO or CO-releasing compounds to treat an organ outside a regulated medical or research setting.
What would be needed to establish a transplant benefit
Promising animal results can justify further study, but they cannot show that a treatment improves outcomes in people. Human evidence would need to establish safety and assess relevant transplant outcomes under controlled conditions. Until such results are available, therapeutic CO remains an experimental strategy for limiting graft injury—not a proven way to prevent rejection, improve graft survival, or protect a transplant recipient.
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