What Is NIM811? Definition and What Research Reports

NIM811 in one paragraph

NIM811 — written in the chemical literature as N-methyl-4-isoleucine-cyclosporin (N-MeIle₄-cyclosporin) — is a semi-synthetic analogue of cyclosporin A, the cyclic eleven-amino-acid peptide originally isolated from a soil fungus. A single amino-acid position in the cyclosporin ring is altered, and the resulting molecule is classified in published pharmacology as a non-immunosuppressive cyclophilin inhibitor: it retains binding to the cyclophilin family of proteins while being described as separated from the immunosuppressive activity that defines cyclosporine as a transplant drug. In practice the term "NIM811" is used in papers as the name of a research compound used to probe what happens when cyclophilins — including mitochondrial cyclophilin D — are blocked in a given disease model. It is not a growth-hormone-type peptide, not a receptor agonist, and not an approved medicine; it belongs to the cyclic peptide / macrocycle category alongside cyclosporine itself.

What kind of molecule it is

• Class: cyclic undecapeptide (macrocyclic peptide), structurally a cyclosporin analogue rather than a linear synthetic peptide.
• Origin of the scaffold: cyclosporin A, a fungal natural product; NIM811 is produced by chemical modification of that scaffold.
• Molecular target described in the literature: cyclophilins, a family of peptidyl-prolyl isomerases; the 2017 paper that reported NIM811 ameliorated experimental allergic encephalomyelitis describes the compound in its title simply as a "cyclophilin inhibitor" (PMID 28789840).
• Typical framing: a pharmacological tool compound in preclinical mitochondrial and neurotrauma research.
• Naming: "NIM811" is a development code, not a trade name; no consumer product name is attached to it in the peer-reviewed record.

Where the term comes from and how it is used

Because cyclosporine's immunosuppressive action and its cyclophilin binding can be separated chemically, analogues such as NIM811 became useful to researchers who wanted to test the consequences of cyclophilin inhibition without the confound of broad immune suppression. That is why the compound turns up across quite different literatures — liver surgery, spinal cord injury, neuroinflammation and fibrosis signalling — rather than in a single therapeutic area. When a paper says it "treated animals with NIM811," the usual intent is to ask whether cyclophilin-dependent processes, particularly the mitochondrial permeability transition, contribute to the injury being modelled.

In peptide-education contexts the term is most often encountered as a glossary item: readers meet it next to cyclosporin A and cyclophilin D and want to know which category it belongs to. The short answer is that it is a modified natural-product peptide studied in animals and cells, not a compound with an established clinical role described in the verified literature summarised here.

What the published literature reports

The studies below are the papers cited on this page. Each is preclinical — laboratory animals or cultured cells — and each answers a narrow question inside its own model.

Liver injury and regeneration after massive hepatectomy

A 2011 report in Transplantation stated that NIM811 prevented mitochondrial dysfunction, attenuated liver injury and stimulated liver regeneration after massive hepatectomy in the model studied (PMID 21131897). This is the work most often referenced when NIM811 is discussed as a mitochondrial permeability transition inhibitor, because the study linked the compound's effect to preserved mitochondrial function rather than to immune modulation (PMID 21131897).

Spinal cord contusion

A 2018 paper in the Journal of Neurotrauma was designed as a dose-response study and reported that post-injury treatment with NIM811 promoted recovery of function in adult female rats after spinal cord contusion (PMID 28967329). The dose-response framing means researchers compared more than one dose level within the same rodent model; the numerical dose values are left to the source paper and are not reproduced here (PMID 28967329).

Experimental allergic encephalomyelitis

A 2017 study in the Journal of Neuroimmunology reported that the cyclophilin inhibitor NIM811 ameliorated experimental allergic encephalomyelitis, a laboratory model used to study inflammatory demyelination (PMID 28789840). Results in that model describe the model itself and do not establish an outcome in any human condition (PMID 28789840).

TGF-β signal transduction

A 2016 report in Molecular Medicine Reports found that NIM811 downregulated transforming growth factor-β signal transduction, with the authors describing both in vivo and in vitro experiments (PMID 26573209). TGF-β signalling is a pathway frequently studied in fibrosis, and the study is generally cited for that mechanistic observation rather than for a clinical endpoint (PMID 26573209).

Summary table

Tolerability and adverse events: What Studies Report

The four papers summarised here are animal and cell studies whose stated endpoints were efficacy-type measures — mitochondrial function and liver regeneration after hepatectomy (PMID 21131897), functional recovery after spinal cord contusion across dose levels (PMID 28967329), disease severity in experimental allergic encephalomyelitis (PMID 28789840) and TGF-β pathway activity (PMID 26573209). None of them is a human safety trial, and this entry therefore does not present a human adverse-event profile for NIM811. Statements about tolerability in people cannot be drawn from rodent and cell-culture endpoints. This page is for educational purposes only and is not medical advice; consult a licensed physician about any medical question or any compound discussed in the research literature.

Related terms readers often confuse

• Cyclosporin A: the parent natural-product peptide and an approved immunosuppressant; NIM811 is a modified version described as non-immunosuppressive.
• Cyclophilin D: a mitochondrial protein in the cyclophilin family, commonly discussed alongside the mitochondrial permeability transition in papers such as the 2011 hepatectomy study (PMID 21131897).
• Cyclophilin inhibitor: a drug class label, not a single molecule; NIM811 is one member of it (PMID 28789840).

Limits of what this entry can say

Three limits are worth stating plainly. First, every finding summarised above is model-specific: an effect in a rat contusion model or in a hepatectomy model describes that model (PMID 28967329). Second, dose figures, routes and treatment windows vary between models and are not transferable, so they are left in the source papers. Third, a glossary entry is a definition, not an evidence review; anyone tracking this compound would read the primary articles and any newer literature published since them. NIM811 does not appear in the cited record as an approved therapy, and nothing on this page describes its use.

References

• NIM811 prevents mitochondrial dysfunction, attenuates liver injury, and stimulates liver regeneration after massive hepatectomy (Transplantation, 2011)
• NIM811 downregulates transforming growth factor-β signal transduction in vivo and in vitro (Molecular Medicine Reports, 2016)
• Cyclophilin inhibitor NIM811 ameliorates experimental allergic encephalomyelitis (Journal of Neuroimmunology, 2017)
• Post-Injury Treatment with NIM811 Promotes Recovery of Function in Adult Female Rats after Spinal Cord Contusion: A Dose-Response Study (Journal of Neurotrauma, 2018)