IngredientesMyristoleic acid, chemically known as (9Z)-tetradec-9-enoic acid, is a monounsaturated omega-5 fatty acid with the molecular formula C₁₄H₂₆O₂ and a molecular weight of 226.35 g/mol. It features a 14-carbon chain with a cis double bond between the ninth and tenth carbons, classifying it as a long-chain fatty acid biosynthesized from myristic acid via the enzyme stearoyl-CoA desaturase-1. Naturally occurring myristoleic acid predominantly exists in the cis (Z)-configuration at the 9-position double bond, while the trans isomer is rare and not commonly found in biological systems. Its CAS number is 544-64-9, and it is also known by the synonyms cis-9-tetradecenoate, FA 14:1, and oleomyristic acid.
As a monounsaturated fatty acid, myristoleic acid exhibits weak UV absorption around 200 nm attributable to the carbon-carbon double bond. It is chemically stable under normal conditions but susceptible to oxidation at the unsaturated site, leading to rancidity in lipid mixtures. It has a role as an apoptosis inducer, a plant metabolite, and an EC 3.1.1.1 (carboxylesterase) inhibitor.
Cetyl myristoleate is a fatty acid ester or, more specifically, a cetylated fatty acid (CFA). It is the cetyl ester of myristoleic acid. Chemically designated as hexadecyl (Z)-tetradec-9-enoate, with the molecular formula C₃₀H₅₈O₂, it consists of myristoleic acid esterified with cetyl alcohol and is classified as a cetylated fatty acid (CFA), a group of compounds where fatty acids are combined with cetyl alcohol. The compound is identified by CAS number 64660-84-0, ChemSpider ID 4947787, PubChem CID 6443825, and UNII 87P8K33Q5X.
Cetyl myristoleate has been prepared synthetically by an esterification reaction between myristoleic acid and cetyl alcohol, catalyzed by p-toluenesulfonic acid monohydrate. In the dietary supplement trade it is commonly abbreviated as CMO or CM and is frequently marketed under brand names such as Celadrin and Cetyl-M, often as part of a broader cetylated fatty acid complex (CFA or CMC) that may include cetyl oleate, cetyl palmitoleate, cetyl laurate, and cetyl myristate alongside cetyl myristoleate as the principal active component.
Myristoleic acid is an omega-5 fatty acid biosynthesized from myristic acid by the enzyme stearoyl-CoA desaturase-1, but it is uncommon in nature. One of the major sources of this fatty acid is the seed oil from plants of the family Myristicaceae, comprising up to 30 per cent of the oil in some species. Concentrations reach 19.4–26.3% of total fatty acids in Pycnanthus angolensis (African nutmeg) seeds and 20.37% in Horsfieldia pandurifolia seeds, highlighting these as primary botanical sources.
The fat known as kombo butter comes from the seeds of Pycnanthus kombo (Myristicaceae family) found in West Central Africa and represents a rich commercial source. Preferred natural sources of myristoleic acid also include beef tallow and seeds of Pycnanthus kombo. Myristoleic acid is a constituent of Serenoa repens (saw palmetto), and appears to have activity against LNCaP prostate-cancer cells. It is also found in natural compounds such as nutmeg, butter, and milk.
Myristoleic acid can be synthesized from myristic acid — found in palm seed oil, coconut oil, and butter — by the enzyme stearoyl-CoA desaturase (SCD)-1 in various organisms, including humans. Myristoleic acid levels in humans can also be modulated by the gut microbiome, and several studies have shown that microbes can produce or consume myristoleic acid.
Whereas myristoleic acid is commonly found in fish oils, whale oils, and dairy butter, CMO is known to exist only naturally in sperm whale oil and in a small gland in the male beaver. It is also present naturally in Swiss albino mice, which was the original observation that launched scientific study of the compound. Because natural animal sources are limited or protected (sperm whales are endangered), all commercially available CMO for dietary supplement use is produced synthetically from myristoleic acid and cetyl alcohol. Cetyl myristoleate has been available over-the-counter in the United States as a dietary supplement since the 1990s, following its initial discovery and patenting in the 1970s.
Cetyl myristoleate was isolated for the first time by Dr. Harry Diehl at the Laboratory of Chemistry of the National Institute of Arthritis, Metabolic, and Digestive Diseases in Bethesda, Maryland. Dr. Diehl had tried to unsuccessfully induce polyarthritis in Swiss albino mice using Freund's adjuvant (heat-killed desiccated Mycobacterium butyricum) but realized that they were immune. Further investigation revealed that cetyl myristoleate was what was causing the mice to be immune to becoming arthritic.
To isolate the protective factor, Diehl and collaborator Everette L. May extracted tissues from 80 male Swiss albino mice (totaling 2,300 g) using chloroform and methylene chloride, followed by concentration and purification steps involving acetone precipitation, silica gel chromatography with pentane:diethyl ether (20:1), and further rechromatography with carbon tetrachloride:ether mixtures. The active nonpolar component, yielding 0.15 g of oil, was identified as cetyl myristoleate (cis-9-cetyl myristoleate) through alkaline hydrolysis, which separated it into cetyl alcohol and myristoleic acid, confirmed by melting points, elemental analysis, infrared spectroscopy, gas chromatography–mass spectrometry, and nuclear magnetic resonance.
The findings were first published in 1994 in the peer-reviewed American Journal of Pharmaceutical Sciences. The paper (Diehl HW, May EL, J Pharm Sci 1994;83:296–9, PMID 8207671) remains the foundational reference for all subsequent research. Diehl subsequently obtained a US patent on the compound. Since early 1991, desiccated oral cetyl myristoleate has been available to the public and has been used extensively to treat inflammatory disease states such as arthritis.
There is no documented pre-modern or traditional ethnomedical history of cetyl myristoleate as a discrete supplement, as it was unknown to earlier cultures as an isolated compound. Its parent fatty acid, myristoleic acid, occurs in foods long used across many cultures (dairy products, nutmeg), but no specific traditional preparation or therapeutic application of myristoleate as a named ingredient has been recorded in the peer-reviewed ethnobotanical or pharmacopeial literature. The compound's history is therefore entirely a product of modern biochemical research beginning in the latter twentieth century.
Myristoleic acid is the bioactive parent fatty acid within the CMO ester. Myristoleic acid is a substrate for the cytochrome P450 enzyme CYP102D1, which mediates cell metabolism. Because it is an amphipathic acid, it may be able to integrate into cell membranes, creating structural defects and causing cell death at high concentrations.
Cetylated fatty acids are a group of naturally occurring fats of plant and/or animal origin. In commercial preparations, cetyl myristoleate is typically the dominant component but is usually accompanied by other cetylated fatty acid esters. In limited comparisons, cetyl oleate, also found in Swiss albino mice, gave lesser protection, whereas cetyl myristate and cetyl elaidate (the trans-isomer of cetyl oleate) appeared to be virtually ineffective. This suggests the cis-9 double bond geometry of myristoleic acid is critical for activity.
The precise mechanism of action of cetyl myristoleate and its parent myristoleic acid has not been fully established in the peer-reviewed literature. Several mechanistic hypotheses have been advanced, ranging from eicosanoid modulation to N-myristoylation interference.
Although not fully established, the most likely mechanism of action of cetyl myristoleate is the decrease of production of prostaglandins and leukotrienes through the inhibition of the lipoxygenase and cyclooxygenase pathways of arachidonic acid metabolism. More specifically, CM may act by inhibition of the 5-lipoxygenase pathway, which is responsible for the metabolism of leukotrienes, potent inflammatory mediators, from the arachidonic acid cascade. Cetyl myristoleate is thought to inhibit cyclooxygenase and lipoxygenase pathways in arachidonic acid metabolism, thereby reducing the production of pro-inflammatory prostaglandins and leukotrienes.
In order for the tyrosine kinase Src to be activated, trafficking to the inner plasma membrane via myristoylation is of importance. A previous study reported that myristoleic acid derived from myristic acid inhibited N-myristoyltransferase, an essential enzyme for the myristoylation process. This pathway has implications for osteoclast function, as described further under bone biology below.
It is thought that CM may work through a mechanism similar to — but distinct from — polyunsaturated fatty acids. There is some evidence that n-5 and n-9 fatty acids form oxygenated metabolites through transcellular processing and that these exert anti-inflammatory effects. A striking difference between the effect of CMO and PUFAs is the longer-lasting effects CMO appears to have, which may be due to some type of "reprogramming" of T cells.
A secondary, non-immunological mechanism proposed in the literature is that, as a long-chain fatty acid ester with surfactant properties, cetyl myristoleate may improve the lubricating quality of synovial fluid, reducing mechanical friction in affected joints. This is a widely cited hypothesis in clinical commentary but has not been formally demonstrated in controlled human synovial fluid studies.
In animal studies, cetyl myristoleate was first reported to block inflammation and prevent adjuvant-induced arthritis at very high doses in rats. Cetyl myristoleate (CM) was reported by Diehl and May to block inflammation and prevent adjuvant-induced arthritis in rats. CM is the ester of cis-9-tetradecenoic acid (myristoleic acid) and 1-hexadecanol (cetyl alcohol), and was originally isolated as a natural product from a NIH Swiss albino mouse strain that was resistant to adjuvant-induced arthritis. When tested in a rat adjuvant arthritis model, this compound was shown to have striking anti-arthritic properties, albeit when used in very high doses.
To replicate these findings, Hunter et al. (2003, Pharmacol Res 47:43–47) synthesized pure CM and tested it in a collagen-induced arthritis model. They tested CM's anti-arthritic properties in a collagen-induced arthritis model in DBA/1LacJ mice. Multiple intraperitoneal injections of CM in 450 and 900 mg/kg doses resulted in a significantly lower incidence of disease and caused a modest but significant diminution in clinical signs in those mice that developed arthritis. CM administered in daily oral doses of 20 mg/kg also reduced the incidence of arthritis and caused a small reduction in the clinical signs in mice that developed arthritis. The authors noted the protective effect was less dramatic than originally reported.
A separate rat study using near-identical methodology to the original Diehl/May protocol arrived at a different conclusion: the proposed arthro-preventive action of cetyl myristoleate, an OTC product sold as a nutritional supplement, could not be confirmed, using an almost identical bioassay (adjuvant-induced polyarthritis in rats) as that described in the original report. This failure to replicate introduces significant uncertainty into the animal evidence base.
A 32-week (8-week cycle, 4 in-hospital and 4 in follow-up), multicentric, double-blind, randomized, placebo-controlled parallel trial (Siemandi, 1997) compared the efficacy of cis-9-cetyl myristoleate alone, and cis-9-cetyl myristoleate plus glucosamine hydrochloride, sea cucumber, and hydrolyzed cartilage, administered over a period of 30 days, with placebo, for the treatment of various forms of autoimmune diseases commonly characterized as arthritis and psoriasis. Out of a dose of 90 grams of total fatty acid esters, 18 grams constituted cis-9-cetyl myristoleate. After 32 weeks of observation, cetyl myristoleate had clearly superior efficacy in terms of reducing the frequency of arthritic episodes when compared to control groups of patients who received a mixture of natural compounds or a placebo. This study has been cited widely but the full dataset has not been published in an indexed peer-reviewed journal, limiting its independent verification.
In the Hesslink et al. (2002) study evaluating a formulation with a CFA mixture, 64 patients with knee osteoarthritis received either a combination of CFAs (six capsules or 2.1 g per day) or a placebo for 68 days. The CFA group showed a statistically significant improvement in knee flexion, whereas knee extension remained unchanged in both groups.
A 2025 double-blind, placebo-controlled, randomized trial published in the European Journal of Clinical Nutrition enrolled 60 patients (mean age: 66.0 ± 7.7 years, 85% female) with grade 3–4 knee osteoarthritis and a pain intensity of >4 cm on the visual analog scale (VAS), randomized 1:1 to receive either 1.5 g of oral CFA or a placebo for 60 days. The primary outcome was the change in pain intensity (VAS); secondary outcomes included changes in range of motion (ROM), WOMAC, and the safety profile. After 60 days of CFA assumption, the mean reduction in pain intensity (VAS) was −1.7 cm (95% CI [−2.0, −1.4]), showing a statistically significant difference compared to placebo.
Kraemer et al. (2004, J Rheumatol 31:767–74, PMID 15088305) conducted a randomized controlled trial examining a topical CFA cream. The objective was to examine the effect of a topical cream consisting of cetylated fatty acids on functional performance in patients diagnosed with osteoarthritis (OA) of one or both knees. Forty patients diagnosed with knee OA were randomly assigned to one of two topical treatment groups: cetylated fatty acid (CFA) (n=20; age 62.7 ± 11.7 yrs) or placebo (n=20; age 64.6 ± 10.5 yrs). Patients were tested at baseline, 30 minutes after initial treatment, and after 30 days of cream application twice per day. The conclusion was that use of a CFA topical cream is an effective treatment for improving knee range of motion, ability to ascend/descend stairs, ability to rise from sitting, walk and sit down, and unilateral balance.
A 2025 randomized, double-blind, placebo-controlled trial in Scientific Reports specifically investigated topical CFA cream in hand osteoarthritis. Patients fulfilling the American College of Rheumatology criteria for hand OA participated; eligible patients were over 40 years of age, had at least one tender joint, and had a joint pain visual analog score of 30–60 mm. Patients received topical CFA (n=36) or placebo (n=36) twice daily for six weeks. The primary outcome was the Functional Index for Hand Osteoarthritis (FIHOA) at 2, 4, and 6 weeks. Previous studies have reported that topical CFAs are effective in all knee OA patients, with slightly higher evidence for those with advanced disease.
The aim of one study was to investigate the possible mechanisms of Celadrin cetylated fatty acids action at the cellular level in inflammation-related pain relief and chondrogenesis. For this, the effects of the cetylated fatty acids mixture from Celadrin were tested on an in vitro scaffold-free three-dimensional mesenchymal stem cells culture model of chondrogenesis. This work was preclinical in nature and does not directly demonstrate clinical efficacy.
There is some clinical evidence for the benefits of CFAs, which may contain cetyl myristoleate, in arthritic patients. One pilot study found that cetyl myristoleate may be beneficial against fibromyalgia, and there have been other studies. However, these low-quality clinical trials provide only limited scientific evidence of efficacy. The evidence base consists of a modest number of small, short-duration trials that predominantly test CFA mixtures rather than isolated cetyl myristoleate. Independent replication by research groups unaffiliated with the supplement industry is limited, and no Cochrane-level systematic review of CMO specifically has been published.
While preclinical studies in animal models demonstrated promising anti-arthritic effects, human clinical data have not fully replicated these results, indicating modest benefits primarily for osteoarthritis symptom management rather than disease modification. The Siemandi trial included patients with autoimmune forms of arthritis, but the full publication data are limited. Nutraceuticals containing CM are widely used for indications of pain and inflammation relief, and with the exception of a short report suggesting a positive clinical effect of cerasomol-CM in patients with fibromyalgia, no follow-on studies have been published to confirm any biological properties of this fatty acid ester. Evidence for rheumatoid arthritis specifically is considered preliminary and insufficient to draw firm conclusions.
The primary evidence for CMO in fibromyalgia is an open (uncontrolled) pilot study. The purpose was to investigate the efficacy and tolerability of CMO (cerasomol-cis-9-cetyl myristoleate) in the treatment of fibromyalgia. The design was an open study: 21 days' treatment following a 7-day baseline without treatment. Thirteen adult patients with fibromyalgia were enrolled. Following a 7-day pre-treatment baseline, patients were treated with a mixture of CMO plus sea cucumber and shark cartilage extracts. All treatments were administered orally.
Ten fibromyalgia patients completed the study. One subject did not record baseline symptoms. Two patients had to discontinue treatment because of adverse effects. One patient had severe indigestion and the other developed muscle spasms and a skin rash. The mean scores for the severity of pain, fatigue, and sleep disturbance during the baseline were 2.63, 2.50, and 2.33 respectively. These improved to 1.70, 1.83, and 1.73 during the last 7 days of CMO treatment. There were individual differences in CMO treatment response with five patients showing good response and five showing little or no response.
There are few studies that examine the effectiveness of cetylated fatty acid preparations in diseases other than osteoarthritis. Those that exist are either pilot or low-quality trials with no follow-up and have a small number of subjects. The fibromyalgia evidence base is therefore considered preliminary, based on an uncontrolled pilot study only.
Preclinical research has identified myristoleic acid as a modulator of bone remodeling. Myristoleic acid inhibited RANKL-induced osteoclast formation in vitro, especially at later stages of differentiation. Myristoleic acid attenuated the tyrosine phosphorylation of c-Src and Pyk2, which associates with Src, by RANKL. When myristoleic acid was co-administered with soluble RANKL into mice, RANKL-induced bone loss was substantially prevented. These data suggest that myristoleic acid is capable of blocking the formation of large multinucleated osteoclasts and bone resorption likely through suppressing activation of Src and Pyk2. The dosage used in the mouse model was myristoleic acid at 2 mg/kg, intraperitoneally every 24 hours for 4 days. This evidence is entirely preclinical (in vitro and murine). No human clinical trials examining myristoleic acid's effects on bone density or fracture risk have been identified in the indexed literature.
Prostatic tumors are well known to progress to hormonal therapy-resistant terminal states, and at this stage there are no chemotherapeutic agents to affect clinical outcome. In a 2001 study by Iguchi et al. (Prostate 47:59–65), it was demonstrated that the extract from S. repens and myristoleic acid induces mixed cell death of apoptosis and necrosis in LNCaP cells. Quantitatively, myristoleic acid induces apoptosis and necrosis in human prostate cancer LNCaP cells at a rate of 8.8% and 8.1%, respectively. These data suggest that myristoleic acid may be an attractive antitumor agent for prostate cancer; however, further studies are needed to examine the effects of myristoleic acid on primary tumors. This evidence is limited to in vitro cell-line work and cannot be extrapolated to a clinical anticancer effect in humans.
Myristoleic acid inhibits Candida albicans germination in vitro with a minimal inhibitory concentration (MIC) of 9 µM. Myristoleic acid found in the by-products of making cheese is one of three fatty acids that are most active at inhibiting Candida albicans germination. This is in vitro evidence only; no human clinical data examining myristoleic acid as an antifungal agent have been identified.
Myristoleic acid has been shown to inhibit the growth of Selenomonas artemidis, a bacterium found in high amounts in patients with periodontal disease. Again, this represents in vitro data only.
Myristoleic acid may also play an important protective role against nonalcoholic fatty liver disease (NAFLD). High-fat/high-sucrose diet-fed mice supplemented with nobiletin had reduced signs of NAFLD along with increased systemic levels of myristoleic acid. When fed myristoleic acid, these mice displayed reduced body weight, total triglycerides, total cholesterol, and free cholesterol, and reversed hepatocyte ballooning or degeneration. These results suggest that myristoleic acid oral supplementation may be a viable treatment for NAFLD and other chronic liver diseases. This evidence is preclinical (murine) only.
Cetyl myristoleate is available in capsule (oral) or cream (topical) dosage forms. Oral administration is recommended with meals to avoid abdominal discomfort.
Dosages vary across the published clinical studies:
In the Kraemer et al. (2004) topical study, 40 patients with knee OA were assigned to a cetylated fatty acid cream or placebo, applied twice per day for 30 days. In the 2025 hand OA trial, patients received topical CFA (n=36) or placebo (n=36) twice daily for six weeks.
In a study with rats with arthritis, cetyl myristoleate administered at a dose of approximately 350–375 mg/kg was shown to have an anti-arthritic effect. In the Hunter et al. (2003) mouse collagen-induced arthritis model, multiple intraperitoneal injections of CM in 450 and 900 mg/kg doses were used; CM administered in daily oral doses of 20 mg/kg also showed effects. These animal doses are pharmacologically very high and are not directly translatable to human supplemental doses.
No major side effects were reported in clinical trials for both topical and oral cetylated fatty acid preparations. However, specific adverse events were documented in the fibromyalgia open pilot study: two patients had to discontinue treatment because of adverse effects — one patient had severe indigestion and the other developed muscle spasms and a skin rash. In addition to the two withdrawals, one further fibromyalgia patient reported gastrointestinal symptoms.
Early animal research and subsequent use in humans demonstrated few adverse reactions to cetyl myristoleate, including gastrointestinal upset, with increased gas or belching. After starting liquid cetyl myristoleate, all patients in one fibromyalgia report initially reported poorer overall health (lasting 2–5 days), followed by rapid improvement and an overall sense of enhanced well-being.
The interactions of cetylated fatty acid preparations with other drugs and the long-term safety profile are largely unknown. The safety profile is relatively unknown, given the lack of well-designed long-term clinical studies.
Although cetyl myristoleate is sold as a dietary supplement, its possible benefits in the treatment of any medical condition are not completely established and the Federal Trade Commission has taken legal action against supplement manufacturers for inaccurate claims.
As a monounsaturated fatty acid, myristoleic acid is chemically stable under normal conditions but susceptible to oxidation at the unsaturated site, leading to rancidity in lipid mixtures. This has practical implications for storage and shelf-life of oral formulations.
Intake of alcohol, excess sugars, nicotine, or acidic foods may alter local pH levels, potentially influencing the three-dimensional structure and chemical properties of liquid cetyl myristoleate. The efficacy of liquid cetyl myristoleate may have been less in patients who consumed these substances. Such alteration in structure and function may have reduced the absorption and assimilation of liquid cetyl myristoleate into the gastrointestinal tract. These observations are from an open clinical report and should be regarded as hypothesis-generating rather than established interactions.
Some people may be allergic to cetylated fatty acid preparations; two fibromyalgia patients withdrew from one study. Skin rash was documented as an adverse event in one of those withdrawals.
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Cetyl myristoleate (CMO) has been evaluated in multiple human trials for various forms of arthritis, including osteoarthritis and psoriatic arthritis. A 1997 multicenter, double-blind, placebo-controlled RCT (Siemandi, n=382) found 63% of CMO-treated patients showed improvement versus 15% on placebo. A 2002 RCT of 64 patients with knee OA published in the Journal of Rheumatology found significant improvement in range of motion versus placebo. Evidence quality is limited by small sample sizes and methodological gaps, but preclinical and clinical data consistently support an anti-arthritic effect.
The Siemandi 1997 RCT explicitly included autoimmune arthritis patients and concluded CMO appeared to provide relief to autoimmune inflammatory diseases, potentially long-term. CMO's proposed immune-modulating mechanism — involving modulation of cytokine signaling via N-myristoylation pathways — provides a plausible mechanistic basis for benefit in autoimmune conditions. Evidence is limited to arthritis-spectrum autoimmune disease.
Myristoleic acid has been identified in vitro as one of three fatty acids most active at inhibiting Candida albicans germination, based on research on cheese by-product fatty acids. This is in vitro evidence only, derived from the free acid form of the myristoleate moiety.
Research into CMO suggests it may protect joint cartilage through anti-inflammatory mechanisms and joint lubrication, reducing mechanical and inflammatory damage to cartilage. In animal models of collagen-induced arthritis — which involves synovitis and cartilage/bone erosions — CMO treatment reduced both incidence and severity of disease. In vitro studies also indicate potential tissue-protective effects at specific concentrations.
CMO's primary documented mechanism is inhibition of the lipoxygenase and cyclooxygenase pathways of arachidonic acid metabolism, reducing prostaglandin and leukotriene production. Multiple clinical trials showing reductions in joint pain, swelling, and inflammatory scores provide indirect human evidence of anti-inflammatory activity. The mechanism parallels that of NSAID drugs, though evidence is limited to musculoskeletal contexts.
Multiple small clinical trials support CMO's analgesic effects in chronic musculoskeletal pain conditions including knee osteoarthritis and low back pain. A study on axial discogenic low back pain (n=27) found significant reductions in ODI and numeric pain scores after four weeks. A 2002 double-blind RCT of 64 patients with chronic knee pain found significant functional improvement in range of motion. Evidence quality is moderate with small sample sizes.
An open pilot study (Edwards et al., J Nutr Environ Med, 2001) investigated CMO in 13 fibromyalgia patients over 21 days. Ten patients completed the study; mean pain, fatigue, and sleep disturbance scores improved meaningfully, with five showing good response. Wikipedia confirms this pilot study as evidence of potential benefit, though notes low evidence quality and the absence of a follow-up placebo-controlled trial.
Several clinical trials have used range of motion as a primary or secondary outcome for CMO. The 1997 Siemandi RCT measured range of motion across arthritis populations; the 2002 knee OA RCT found statistically significant improvement in knee flexion (10.1 degrees vs. 1.1 degrees on placebo). A knee OA trial using a plant-derived CFA extract reported CMO effective at alleviating knee pain and improving function.
Myristoleic acid has been shown in vitro to be the only one of 45 fatty acids surveyed capable of inhibiting Selenomonas artemidis — a bacterium found in high amounts in patients with periodontal disease — at concentrations below 100 µg/mL. This is in vitro evidence only, from the free acid form of the ingredient.
Myristoleic acid — the free acid form of the myristoleate moiety in CMO — has been identified as the cytotoxic component in saw palmetto (Serenoa repens) that induces apoptosis and necrosis in human prostate cancer LNCaP cells (Iguchi et al., Prostate, 2001). This is in vitro evidence only; no clinical trials of CMO for prostate conditions have been published.
Rheumatoid arthritis (RA) was one of the specific indications studied in the Siemandi 1997 multicenter RCT, which enrolled patients with RA alongside osteoarthritis and psoriatic arthritis. Animal work by Diehl and May (1994) also specifically demonstrated protective effects against adjuvant-induced polyarthritis. CMO's proposed immune-modulating mechanism is particularly relevant to RA's autoimmune pathology. Evidence remains preliminary and trial quality limited.
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