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A brief background on activities reported for curcumin and turmeric essential oil is provided as an introduction for pharmacological studies conducted on BCM-95. The pharmacological properties reported for standard curcumin, which include antioxidant, anti-inflammatory, antibacterial, and anticancer activities, have been recently reviewed.1,3 In vitro reports of enhanced peroxisome proliferator-activated receptor gamma (PPAR-g) expression along with modulation of nitric oxide synthase (NOS) and glutathione are indicative of antioxidant activity. The anti-inflammatory mechanisms identified for curcumin include reduction of nuclear factor-kappa B (NF-kB) activation, cyclooxygenase-2 (COX-2) expression, as well as pro-inflammatory cytokines interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNF-a) production. Interactions (inhibition, inhibition of protein expression, or other types of activities) with the above targets have shown to provide clinically measurable benefits. These targets translate into clinical improvements in RA, psoriasis, and other inflammatory states.4 There is strong evidence from preclinical studies that curcumin has antitumor actions, including pro-apoptotic and anti-angiogenic effects, as well as modulation of the cell cycle, growth factor expression, and signal transduction pathways.4,23 Another area of promising preliminary research is the use of curcumin to treat age-related cognitive impairment and Alzheimer’s disease.21,52,53

Activity-guided fractionation of a turmeric extract revealed anti-inflammatory activity due to the essential oil of turmeric as well as the curcuminoids. Both components of turmeric inhibited production of the inflammatory mediator prostaglandin E2 in cultured cells exposed to lipopolysaccharide, but only the curcuminoids inhibited expression of the COX-2 enzyme.54 Further studies on the essential oil found that it had antioxidant and anti-inflammatory activities when administered orally to mice at a dose of 100 mg/kg body weight.41 Calculations based upon body surface area suggest that a similar amount of oil might be administered following consumption of about 8 g of turmeric by a 60-kg human.55 This is a relatively large dose. However, the data suggest that turmeric essential oil might contribute to the pharmacological effects of turmeric, in addition to enhancing the bioavailability of the curcuminoids.

BCM-95 (Curcugreen)

Antioxidant/Anti-inflammatory Activities

ORAC assay

The ORAC (oxygen radical absorbance capacity) assay provides a measure of the scavenging capacity of antioxidants against the peroxyl radical, one of the most common reactive oxygen species in the human body. The activity is measured against Trolox, a water-soluble vitamin E analog, which serves as a calibration standard. Results of the ORAC assay are reported as micromole (µmol) Trolox equivalent (TE) per gram. Two lots of BCM-95 were tested in the ORAC assays and reported to have a total of 13,11556 and 15,50457 µmol TE/g. The water-soluble fraction of the two lots displayed antioxidant capacities of 7,61356 and 12,61757 µmol TE/g, which was calculated to be 58% and 81% of the total activity. The remainder of the activity was due to lipid-soluble components. In essence, BCM-95 exhibited significant antioxidant activity in this in vitro assay.

Turmeric Curcuma longa
Photo ©2019 Steven Foster



BCM-95 has demonstrated anti-inflammatory activity in animal models using the carrageenan rat paw assay and obesity-associated low-grade inflammation in a study of obese cats.58,59 BCM-95, as part of a multi-ingredient supplement, reduced exercise-induced increases in inflammatory markers in racehorses.60


The anti-inflammatory effects of BCM-95, compared to a “regular turmeric extract” (an ethyl acetate extract containing 95% curcuminoids as determined using spectrophotometry) and diclofenac sodium (an NSAID), were assessed using the carrageenan rat paw model.58 Wistar albino rats (sex not given) were divided into 17 groups of six animals each. Vehicle control, BCM-95, turmeric extract (each individually at 10, 20, 40, 60, 80, 150, and 200 mg/kg), or diclofenac sodium (5 and 10 mg/kg) were orally administered to the animals. Thirty minutes after administration of the test agents, carrageenan (0.1 mL of 1% suspension) was injected into the animals’ hind paw. The paw volumes were measured before dosing, three hours, and six hours after administration of the carrageenan using a digital plethysmometer. The percent inhibition of paw volume compared to control was calculated for each test agent. As expected, the diclofenac control significantly inhibited the swelling of the rat paws at both doses. The regular turmeric extract did not significantly inhibit swelling at any of the doses tested. BCM-95 appeared to have a bell-shaped response curve, with significant effects with doses of 20, 40, and 60 mg/kg. There was no significant effect with the lower dose of 10 mg/kg or the higher doses of 80, 150, and 200 mg/kg. The authors of the study concluded that the addition of the essential oil to the curcumin extract, as formulated in BCM-95, substantially increased the anti-inflammatory effect in this model. The effective doses of BCM-95 were as effective as diclofenac sodium in reducing the swelling of the rat paws.


The effect of BCM-95 on obesity-associated low-grade inflammation was examined in obese cats using an eight-week crossover study design with a four-week washout period between treatments.59 European domestic shorthair neutered cats (N = 8; 3 males, 5 females) classified as obese were divided into two groups. Their diets were supplemented with BCM-95 or citrus polyphenols. BCM-95 was given as 0.09% of the diet. The citrus polyphenols, hesperidin (Natural Orange Extract; Exquim SA; Barcelona, Spain) and naringin (Citroflavonoids Soluble; Exquim SA), were given together at a concentration of 0.05% and 0.1% of the diet, respectively. The levels of the polyphenols in the cats’ diet were intended to reflect levels of polyphenols recommended for human consumption. At baseline and at the end of the treatment period, blood was collected from the animals. The concentrations of plasma acute-phase proteins amyloid A, haptoglobin, and alpha-1-acid glycoprotein were determined. In addition, peripheral blood mononuclear cells (PBMCs) were isolated from the blood samples and the levels of cytokine messenger RNA (mRNA) expression were determined. The addition of BCM-95 to the diet caused a significant decrease in the level of haptoglobin in blood compared to baseline (P < 0.02), but had no significant effect on the other acute-phase proteins. The citrus polyphenols caused significant decreases in both haptoglobin and alpha-1-acid glycoprotein, but had no effect on amyloid A. Of the panel of 10 cytokine mRNA levels analyzed, only IL-2 mRNA levels were decreased by BCM-95, and interferon-gamma (IFN-g) mRNA levels were reduced by the citrus flavonoids, both in comparison to baseline levels. The authors suggested that a greater effect on PBMC cytokine levels might be observed with a higher dose of BCM-95. This study indicated that BCM-95, at low levels in the diet, might reduce levels of acute-phase plasma proteins, which are associated with chronic inflammation sometimes related to obesity.


A controlled, parallel-group, randomized study with thoroughbred racehorses measured the effect of training with and without a multi-ingredient supplement on inflammatory markers in the blood.60 The study included 25 thoroughbred racehorses (18-21 months old) monitored over an eight-week training period on a grass track. Half of the animals received a supplement twice daily with meals. The supplement (Double Diamond®; Equine Nutriceuticals, LLC; Franklin Lakes, New Jersey) contained 1.6 g curcumin (BCM-95), 1.6 g boswellia (Boswellia serrata, Burseraceae) extract (BosPure®; 75% boswellic acids and 10% 3-O-acetyl-11-keto-b-boswellic acid; DolCas Biotech, LLC; Landing, New Jersey), 400 mg coenzyme Q10 (Hydro Q Sorb®; Tishcon Corp.; Westbury, New York), 4 g GlycoCarn® glycine propionyl-l-carnitine HCl (Sigma-Tau HealthScience USA, Inc.; Gaithersburg, Maryland), and 10 g d-ribose. The study included four tests of increasing exercise intensity (from 8.0 to 14 m/second) over the 10-week testing period. Peripheral blood samples were collected before each exercise test, as well as immediately afterwards and two hours afterwards. The samples were analyzed for the presence of lactic acid, oxidative stress (lipid peroxidation measured via malondialdehyde), and inflammatory cytokine gene expression (IL-1, IL-6, TNF-a, IFN-g, and granzyme B). There was a positive correlation between the intensity of the exercise and the levels of lactate, malondialdehyde, and pro-inflammatory cytokine gene expression. The supplement group showed a decrease in PBMC gene expression for cytokine IL-1b levels over time, reaching significance in the fourth test. This effect was observed in blood samples taken before, immediately after, and two hours after the exercise. No change was observed in the control group. There were no significant differences in the other variables measured. The authors concluded that the supplement enhanced adaptation to exercise by reducing the expression of the gene for the pro-inflammatory cytokine IL-1b.

Cytotoxicity and Antitumor Effects

A series of in vitro and in vivo studies by one research group documents the potential use of BCM-95 in the prevention and treatment of colon cancer.61-65 Another group of researchers used a mouse model to evaluate the effectiveness of curcumin (BCM-95) to prevent the progression of cancer caused by a chemical agent.66

A series of in vitro 2D and 3D models were used to examine the effects of BCM-95 and/or 5-fluorouracil (5-FU) on the malignancy of colorectal cancer cells. 5-FU is widely used as a chemotherapeutic agent for the treatment of many types of cancers. It has a chemical structure similar to the nucleotides uracil and thymine, and acts by inhibiting cellular proliferation and inducing apoptosis. However, high rates of metastasis and recurrence of colorectal cancer is common, primarily thought to be the result of a progressive resistance to the drug. Boosting the effectiveness of 5-FU is important as it has been estimated that more than 15% of patients with colorectal cancer are resistant to the drug.61

One paper examined the ability of curcumin to enhance the effectiveness of 5-FU in an in vitro model of colorectal cancer.61 In vitro experiments were conducted with cancerous colorectal cell lines with and without resistance to 5-FU. The studies reported that pretreatment of cancer cells with BCM-95 curcumin (0-20 µM) significantly (P < 0.05) enhanced the effectiveness of 5-FU (0-20 µM). The combination of curcumin plus 5-FU increased disintegration of cancerous colonies, enhanced cell death (apoptosis), and inhibited cell growth. The effects of curcumin in enhancing chemosensitivity to 5-FU were further supported by its ability to effectively suppress development of cancer stem cells. Cancer stem cells are a subset of cells that exhibit the stem cell characteristics of self-renewal and pluripotency (capable of differentiating into one of many cell types). Cancer stem cells are thought to be involved in the spread of cancer by forming distant metastasis.

Another paper explored the effects of BCM-95 and 5-FU on the interactions between tumor cells and stromal fibroblasts in an in vitro co-culture model.62 Stromal fibroblasts play a dynamic role in initiating and enhancing carcinogenesis through upregulation of several chemical mediators. The studies showed that mediator “crosstalk” was increased in the presence of 5-FU (0-10 µM), but dramatically decreased in the presence of curcumin (0-10 µM), inducing biochemical changes that sensitized cancer stem cells to 5-FU treatment. The authors suggested that modulation of this synergistic crosstalk by curcumin might suppress metastasis.

Another experiment used a sophisticated 3D in vitro culture model (an alginate-based 3D scaffold) that mimicked the tumor microenvironment in vivo.63 In this model, the colon cancer cells encapsulated in alginate proliferated in 3D-colonospheres. During cultivation of cells in alginate, 3 stages of cells were observed: proliferating, invasive, and adherent cells. Tumor-promoting factors were significantly increased in the proliferating and invasive cells compared to the adherent cells.

Studies conducted with this model revealed that the addition of BCM-95 (dose given as 5 µM curcumin) enhanced the ability of 5-FU to decrease proliferation and invasion. The studies indicated that these actions occurred through the transcription factor, NF-kB. NF-kB plays an important role in cell survival, proliferation, invasion, angiogenesis, metastasis, and chemoresistance. NF-kB is constituently activated in human colorectal cancer cells and is associated with disease progression. It is theorized that agents that suppress NF-kB activation might reduce chemoresistance and thus improve clinical outcomes for colorectal cancer. In these experiments, curcumin caused a downregulation of NF-kB activation and NF-kB-regulated gene products.

Chemosensitizing effects of BCM-95 were validated in a xenograft mouse model.64 Tumors resistant to 5-FU were established by subcutaneous injection of resistant cancer cells into athymic nude mice. Once the average tumor reached 50 mm2, the animals were divided into four groups of 10 animals each. Treatments were administered via intraperitoneal (IP) injection for 40 days. Treatment with 5-FU (20 mg/kg, IP, every two days) did not significantly reduce tumor growth (measured as tumor volume), demonstrating the resistant nature of the cells. In contrast, treatment with BCM-95 (dose given as curcumin 50 mg/kg, IP, daily) significantly reduced tumor volume compared to controls. The combination of BCM-95 plus 5-FU had an additive effect in reducing tumor volume. Mathematical models indicated that the fraction of the tumor cells resistant to 5-FU was 67%. The addition of BCM-95 reduced the degree of resistance by 30%.

Further experiments using the xenograft mouse model explored the combination of BCM-95 with BosPure, a preparation made from B. serrata gum resin containing three boswellic acids (acetyl-a-boswellic acid, acetyl-b-boswellic acid, and acetyl-11-keto-b-boswellic acid [AKBA]; provided by DolCas Biotech, LLC).65 Boswellia serrata gum resin is a traditional remedy for inflammatory conditions. As in the previous study, xenograft tumors were established in mice by subcutaneous injection of colorectal cancer cells. The animals were divided into four groups with 10 animals in each group. Treatments or vehicle controls were injected intraperitoneally daily for three weeks, starting seven days after the injection of cancer cells. BCM-95 was administered in a dose of 25 mg/kg, with and without AKBA in a dose of 75 mg/kg. Administration of either BCM-95 or the boswellic acid suppressed tumor growth at a similar rate and the combination of the two had a synergistic effect (ratio of expected:observed tumor volume > 1). On day 20, the size of tumor in the curcumin group was 58% compared to controls; in the AKBA group, the tumor was 63% compared to controls; and both agents together resulted in a tumor size of 33% of the controls. Gene-expression arrays revealed that curcumin and AKBA regulated distinct cancer-signaling pathways including key cell-cycle regulatory genes. Combined bioinformatics and in silico analysis identified apoptosis, proliferation, and cell-cycle regulatory signaling pathways as key modulators of curcumin and AKBA-induced anticancer effects. Micro RNAs (miRNAs) are a class of small non-coding RNA molecules that play critical roles in the regulation of gene expression. Curcumin and AKBA induced upregulation of tumor-suppressive miR-34a and down-regulation of oncogenic‡‡ miR-27a in colorectal cancer cells.

Other researchers used a mouse model to evaluate the effectiveness of BCM-95 and metformin (a medication for type 2 diabetes) either alone or in combination to prevent the progression of tumors caused by 4-nitroquinoline-oxide (4NQO).66 The study used C57BL/6 mice (N = 60; four to six weeks old), which were initially divided into two groups — a control arm (n = 10) administered with plain drinking water and a treatment arm (n = 50) administered with 4NQO in drinking water (50 ppm) for a period of 17 weeks. Administration of the carcinogen was then stopped and the “treatment” mice (n = 45) were divided into four arms, with treatments administered in their drinking water as follows: arm 1 (n = 15) with plain water, arm 2 (n = 15) with BCM-95 (64 µg/mL), arm 3 (n = 15) with metformin (5 mg/mL), and arm 4 (n = 15) given both BCM-95 and metformin. The average tumor volume in the 4NQO control was 6.65 ± 2.37 mm3. Tumor volume was reduced by BCM-95 (to 2.54 mm3) and metformin (to 1.45 mm3) individually and even more so when the agents were administered together (0.693 ± 0.034 mm3) (no statistics given). The average number of lesions in the 4NQO control (0.6 ± 0.22) was reduced by BCM-95 and metformin individually and even more so when the agents were administered in combination (0.375 ± 0.17) (again, no statistics given). The overall probability of survival for the combination arm was calculated as improved compared to the individual treatments (P = 0.0006). Further details were not available.§§

Antidepressant Activities

Rodent models were used to assess the potential antidepressant activity of BCM-95 when given acutely (in the last 24 hours before evaluation) and when administered for two weeks (“chronic studies”).67 In the acute studies, BCM-95 and the standard antidepressant drugs fluoxetine and imipramine were given to Swiss albino mice in three oral doses 24 hours, five hours, and one hour before evaluating the animals in a forced swimming test, tail suspension test, and measurement of locomotor activity. The chronic study evaluated the mice after 14 days of administration of test agents in a forced swimming test that included an activity wheel. The chronic administration study was repeated using Wistar albino rats. Each experiment was conducted with seven groups of animals with at least six animals in each group. The groups for the studies conducted with mice were the following: group 1, vehicle control (5% gum acacia); group 2, BCM-95 low dose (50 mg/kg); group 3, BCM-95 higher dose (100 mg/kg); group 4, fluoxetine (20 mg/kg); group 5, imipramine (15 mg/kg); group 6, BCM-95 (100 mg/kg) plus fluoxetine; and group 7, BCM-95 (100 mg/kg) plus imipramine. The doses of BCM-95 used in rats were 35 and 70 mg/kg. In the acute forced swimming test with mice, all test groups with the exception of BCM-95 at 50 mg/kg showed a significant decrease in time spent immobile compared to the vehicle control (P < 0.05). The effect of 100 mg/kg BCM-95 was similar to that of fluoxetine and imipramine. The addition of BCM-95 to the antidepressants did not lead to a greater effect. In this assay, swimming time, in comparison to control, was significantly increased by fluoxetine and imipramine but not by either dose of BCM-95. Conversely, climbing time increased significantly, but only for the higher-dose BCM-95 group and not for the groups on standard antidepressants. Immobility time in the tail suspension assay was decreased by all test agents. The chronic study conducted with rats showed an increase in the number of rotations of the activity wheel with all test agents compared to the control group. In summary, BCM-95 demonstrated antidepressant activity similar to that of fluoxetine and imipramine in rodent models. When BCM-95 was added to fluoxetine or imipramine, there were no additive effects.

Antiepileptic Effects

Studies with Swiss albino mice assessed the antiepileptic and memory retention activity of BCM-95, alone and in combination with the two most commonly prescribed antiepileptic drugs, phenytoin and sodium valproate.68 Antiepileptic activity was evaluated using models of maximal electroshock (MES)- or pentylenetetrazole (PTZ)-induced seizures after oral dosing of the mice for 14 days with the test agents.

For the MES test, animals were divided into six groups, each group having six animals. Group 1 received 5% gum acacia and served as vehicle control. Groups 2 and 3 received BCM-95 in doses of 50 mg/kg and 100 mg/kg, respectively. Group 4 received 50 mg/kg phenytoin. Groups 5 and 6 received phenytoin in therapeutic (50 mg/kg) and sub-therapeutic (25 mg/kg) doses, respectively, in combination with BCM-95 (100 mg/kg). An electroconvulsiometer was used with ear electrodes to deliver the shock at an intensity of 36 mA for 0.2 s. BCM-95 in doses of 50 mg/kg and 100 mg/kg did not produce any significant effects (P = 0.33) on tonic flexion or hind limb extension as compared to the vehicle control group. Phenytoin in a dose of 50 mg/kg abolished the tonic extension phase completely, but did not show any significant difference (P > 0.05) on clonic convulsion as compared to vehicle control. BCM-95, at a dose of 100 mg/kg (but not at 50 mg/kg), produced significant (P < 0.01) reduction in duration of the clonic phase as compared to vehicle control and the phenytoin group. There were no additive effects due to combining curcumin (BCM-95) and phenytoin.

PTZ-induced seizures were caused by intraperitoneal injection in a dose of 95 mg/kg. Animals were divided into six groups each having six animals. Group 1 received 5% gum acacia and served as vehicle control. Groups 2 and 3 received BCM-95 in doses of 50 mg/kg and 100 mg/kg, respectively. Group 4 received 800 mg/kg of sodium valproate. Groups 5 and 6 received sodium valproate in therapeutic (800 mg/kg) and sub-therapeutic (400 mg/kg) doses, respectively, in combination with BCM-95 (100 mg/kg). In the vehicle-treated group, myoclonic jerks followed by tonic-clonic seizure and death were observed. BCM-95 in a dose of 100 mg/kg increased latency for onset of myoclonic jerks and seizures as well as decreased incidence, total duration of seizure, and mortality compared to the vehicle control group (P < 0.001). Sodium valproate completely prevented incidence of tonic-clonic convulsions and mortality as compared to vehicle control. BCM-95 showed no significant additive effect when combined with sodium valproate.

An elevated plus-maze test was used to study the effect of drugs and/or seizures on memory retention in the MES and PTZ groups. The maze test was performed on days 13 and 14, after recovery from seizure. Neither BCM-95 nor the antiepileptic drugs had any significant effect on memory retention compared to vehicle control.

Hepatoprotective Effects

The ability of BCM-95 to prevent liver injury caused by carbon tetrachloride (CCl4) was tested in male albino Sprague Dawley rats.69 In rats administered a low dose of CCl4 (5 mL/kg body weight via gavage) for three months, liver injury was observed, determined by effects on serum and liver biochemistry. BCM-95 was administered at a daily dose of 300 mg/kg body weight orally via gavage for the same period of time. The experiment included a control group, for a total of three groups, and all groups contained six animals. By week 12, the animals given CCl4 weighed less than the control group, but those given CCl4 plus BCM-95 had a body weight comparable to the controls. Liver injury in the CCl4 group was observed as an increase in clotting time (the liver is responsible for the production of coagulation factors), increases in liver transaminases (alanine aminotransferase/ glutamic-pyruvic transaminase [ALT/GPT] and aspartate aminotransferase/glutamic-oxaloacetic transaminase [AST/GOT]), and an increase in lactate dehydrogenase (LDH) in both the serum and the liver. BCM-95 was able to ameliorate the increases in clotting time, liver transaminases, and LDH, but not restore them to the levels in the control animals. CCl4 reduced the ratio of albumin to globulin in the blood serum (A/G ratio) and this was also partially ameliorated by BCM-95. Cholesterol levels were increased in both the serum and the liver following treatment with CCl4. This change was also partially reversed by BCM-95. In addition, BCM-95 partly reduced the increase in serum bilirubin and collagen in the liver. In summary, BCM-95 at a dose of 300 mg/kg body weight partially prevented liver injury in rats to which a low dose of CCl4 was administered.

The same protocol was used to examine the effect of BCM-95 on alcoholic hepatitis induced in rats administered alcohol diluted to 10% in water and fed via intragastric tube daily for three months.70 In this study, alcoholic hepatitis was observed by altered liver function tests and increased accumulation of lipids (cholesterol and triglycerides) as well as collagen in the liver. As in the CCl4 model, alcohol caused increases in clotting time, liver transaminases (ALT/GPT and AST/GOT), and LDH levels, in both the serum and the liver. BCM-95 was again able to reduce clotting time, liver transaminases, and LDH concentrations, but not restore them to the levels observed in the control animals. BCM-95 partly normalized the reduced A/G ratio, as well as the increases in serum cholesterol and bilirubin. BCM-95 also reduced elevated cholesterol or triglyceride levels, and decreased amounts of soluble protein and collagen in the liver caused by the administration of alcohol. In summary, BCM-95 at a dose of 300 mg/kg body weight partially prevented liver injury induced by alcohol in rats.