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CerefolinNAC® Caplets


CerefolinNAC® is an orally administered medical food for use only under medical supervision for the dietary management
of certain metabolic processes identified with early memory loss.
Each oval coated blue colored caplet contains:
Dietary Ingredients:
L-methylfolate Calcium (as Metafolin®)*
N-acetylcysteine, Microcrystalline Cellulose, Opadry II Blue 07F90856 (Hypromellose, Talc, Titanium Dioxide, Polyethylene
Glycol, FD&C Blue #2-Aluminum Lake, Saccharin Sodium), and Magnesium Stearate (Vegetable Source), L-methylfolate
Calcium, Methylcobalamin.
CerefolinNAC® caplets do not contain sugar, lactose, yeast or gluten.

L-methylfolate or 6(S)-5-Methyltetrahydrofolate, [6(S)-5-MTHF], is the primary biologically active isomer of folate1 and the
form of folate in circulation2. It is also the form which is transported across membranes into peripheral tissues3, particularly
across the blood brain barrier4. In the cell, 6(S)-5-MTHF is used in the methylation of homocysteine to form methionine and
tetrahydrofolate (THF)1. THF is the immediate acceptor of one carbon units for the synthesis of thymidine-DNA, purines
(RNA and DNA) and methionine5. Folic acid, the synthetic form of folate, must undergo enzymatic reduction by
methylenetetrahydrofolate reductase (MTHFR) to become biologically active6. Certain genetic mutations of MTHFR result
in a cel ’s inability to convert folic acid to 6(S)-5-MTHF7.
Metafolin® (L-methylfolate calcium) is a substantially diastereoisomerically pure source of L-methylfolate containing not more
than 1% D-methylfolate which results in
not more than 0.06 milligrams of D-methylfolate in CerefolinNAC®.
D-methylfolate or 6(R)-5-methyltetrahydrofolate [6(R)-5-MTHF] is the other diastereoisomer of folate. Studies administering doses of 2.5
mg per day or higher resulted in plasma protein binding of D-methylfolate higher than L-methylfolate causing a significantly higher renal
clearance of L-methylfolate when compared to D-methylfolate.8 Further, D-methylfolate is found to be stored in tissues in the body, mainly
in the liver. D-methylfolate is not metabolized by the body and has been hypothesized to inhibit regulatory enzymes related to folate and
homocysteine metabolism and reduces the bioavailability of L-methylfolate.9

Methylcobalamin (Methyl-B12) is one of two forms of biologically active vitamin B12. Methyl-B12 is the principal form of
circulating vitamin B12, hence the form which is transported into peripheral tissue. Methyl-B12 is absorbed by a specific
intestinal mechanism which uses intrinsic factor and by a diffusion process in which approximately 1% of the ingested dose
is absorbed. Cyanocobalamin and hydroxycobalamin are forms of the vitamin that require conversion to Methyl-B12 via the
intermediate glutathionyl- B12.
N-acetylcysteine (NAC) is a precursor to glutathione (GSH) one of the body’s most potent natural antioxidants. NAC is
converted to GSH intracellularly. The presence of appropriate amounts of intracellular GSH helps to maintain the ability of
the neurovascular tissue to metabolize vitamin B12 and to reduce or eliminate oxidative stress in these tissues. NAC
significantly lowers plasma homocysteine concentrations10,11, and increases total antioxidant capacity (TAC)12, thus
correcting the characteristic pattern of changes in cognitively impaired patients with hyperhomocysteinemia 13,14,15.

Absorption and Elimination: L-methylfolate is a water soluble molecule which is primarily excreted via the kidneys16. In a study of subjects with coronary artery disease (n=21), peak plasma levels were reached in 1-3 hours following ORAL/PARENTERAL administration9. Peak concentrations of were found to be more than seven times higher than folic acid (129 ng ml-1 vs. 14.1 ng ml-1) following ORAL/PARENTERAL administration. The mean elimination half-life is approximately 3 hours after 5mg of oral L-methylfolate, administered daily for 7 days. The mean values for Cmax, Tmax, and AUC0-12 were 129 ng ml-1, 1.3 hr., and 383 respectively. Distribution: Red blood cells (RBCs) appear to be the storage depot for folate, as RBC levels remain elevated for periods in excess of 40 days following discontinuation of supplementation16. Plasma protein binding studies showed that L-methylfolate is 56% bound to plasma proteins9.

CerefolinNAC® is indicated for the distinct nutritional requirements of individuals under treatment for early memory loss26
with particular emphasis for those individuals diagnosed with or at risk for neurovascular oxidative stress15,17,18 and/or
hyperhomocysteinemia19; mild to moderate cognitive impairment with or without vitamin B12 deficiency10,14,20, vascular
dementia13,14,21 or Alzheimer’s disease13,14,17,22.
CerefolinNAC® should always be used under medical supervision.

There have been rare reports of hypersensitivity (allergic-like reactions) to CerefolinNAC®. Therefore, a known
hypersensitivity to any components in the product is a contraindication to its use for any indication.

Folic acid when administered as a single agent in doses above 0.1mg daily, may obscure the detection of B12 deficiency
(specifically, the administration of folic acid may reverse the hematological manifestations of B12 deficiency, including
pernicious anemia, while not addressing the neurological manifestations). L-methylfolate may be less likely than folic acid to
mask vitamin B12 deficiency23,24. Folate therapy alone is inadequate for the treatment of a B12 deficiency. The 2 mg of
methylcobalamin contained in CerefolinNAC® has been shown to provide an adequate amount of cobalamin to address
this precaution25. NAC should be avoided by nursing mothers. NAC clearance is reduced in those with chronic liver
disease as well as in pre-term newborns. Headaches may be intensified in those taking NAC and nitrates for the treatment
of angina. While the incidence of renal stones is low, those that do form renal stones, particularly cysteine stones should
avoid CerefolinNAC®. Do not administer CerefolinNAC® to critically ill patients. NAC and its sulfhydryl metabolites could
produce a false-positive result in the nitroprusside test for ketone bodies used in diabetes. CerefolinNAC® should be used
with caution in those with a history of peptic ulcer disease since NAC may disrupt the gastric mucosal barrier.
Patient Information:

CerefolinNAC® is a medical food 27 for use only under medical supervision and direction.
Drug Interactions;

CerefolinNAC®added to other Drugs: High dose folic acid may result in decreased serum levels for pyrimethamine and
first-generation anticonvulsants (carbamazepine, fosphenytoin, phenytoin, phenobarbital, primidone, valproic acid,
valproate).28,29 This may possibly reduce first generation anticonvulsants effectiveness and/or increase the frequency of
seizures in susceptible patients.28,29 While the concurrent use of folic acid and first generation anticonvulsants or
pyrimethamine may result in decreased efficacy of anticonvulsants, no such decreased effectiveness has been reported
with the use of 6(S)-5-Methyltetrahydrofolic acid (as L-methylfolate; Metafolin®). Nevertheless, caution should be used
when prescribing CerefolinNAC® among patients who are receiving treatment with first generation anticonvulsants or
pyrimethamine. Pyridoxal 5’-phosphate should not be given to patients receiving the drug levodopa, because the action of
levodopa is antagonized by pyridoxal 5’-phosphate. However, pyridoxal 5’-phosphate may be used concurrently in patients
receiving a preparation containing both carbidopa and levodopa. Capecitabine (Xeloda®) toxicity may increase with the
addition of leucovorin (5-formyltetrahydrofolate) (folate).

Drugs added to CerefolinNAC®: Antibiotics may alter the intestinal microflora and may decrease the absorption of
methylcobalamin. Cholestyramine, colchicines or colestipol may decrease the enterohepatic re-absorption of
methylcobalamin. Metformin, para-aminosalicylic acid and potassium chloride may decrease the absorption of
methylcobalamin. Nitrous oxide can produce a functional methylcobalamin deficiency. Several drugs are associated with
lowering serum folate levels or reducing the amount of active folate available. First generation anticonvulsants
(carbamazepine, fosphenytoin, phenytoin, phenobarbital, primidone, valproic acid, valproate)28,29 and lamotrigine30 (a
second-generation anticonvulsant) may decrease folate plasma levels. Information on other second-generation
anticonvulsants impact on folate levels is limited and cannot be ruled out. Diavalproex sodium,31 topiramate,32 gabapentin,33
pregabalin,34 levetiracetam,35 tiagabine,36 zonisamide,37 have not reported the potential to lower folate in their respective
prescribing information. Methotrexate, alcohol (in excess), sulfasalazine, cholestyramine, colchicine, colestipol, L-dopa,
methylprednisone, NSAIDs (high dose), pancreatic enzymes (pancrelipase, pancratin), pentamidine, pyrimethamine,
smoking, triamterene, and trimethoprim may decrease folate plasma levels. Warfarin can produce significant impairment in folate status after a 6-month therapy.

While allergic sensitization has been reported following both oral and parenteral administration of folic acid, allergic
sensitization has not been reported with the use of oral L-methylfolate. Mild transient diarrhea, polycythemia vera, itching,
transitory exanthema and the feeling of swelling of the entire body have been associated with methylcobalamin. Nausea,
vomiting, headache, other gastrointestinal symptoms, and rash (with or without mild fever) have been associated with NAC.
There are rare reports of renal stone formation with NAC.
Usual adult dose is one caplet daily under medical supervision. CerefolinNAC® is not recommended for use with children
under the age of twelve.
CerefolinNAC® must be administered under medical supervision.

Available as an oval coated blue colored caplet. Debossed with “PAL” on one side and “600” on the other. Commercial
product is supplied in bottles of 90 caplets. Sample product is supplied in a bottle containing three caplets.
Commercial Product (90 caplets)
Use under medical/physician supervision. *Pamlab LLC does not represent these product codes to actual National Drug Codes (NDCs). NDC format codes are product codes adjusted according to standard industry practice to meet the formatting requirements of pharmacy and health insurance computer systems. Storage;

Store at controlled room temperature 15oC to 30oC (59oF to 86oF) (See USP). Protect from heat, light and moisture.
Some or all of the following patents may apply:
U.S. Patent No. 5,563,126

1 Donaldson, K. and K. JC., Naturally occurring forms of folic acid. II. Enzymatic conversion of methylenetetrahydrofolic
acid to prefolic A-methyl-tetrahydrofolate. J Biol Chem, 1962. 237: p. 1298-304.
2 Sweeney, M.R., J. McPartlin, and J. Scott, Folic acid fortification and public health: report on threshold doses above which
unmetabolised folic acid appear in serum. BMC Public Health, 2007. 7: p. 41
3 Wagner, C., Cellular folate binding proteins; function and significance. Annu Rev Nutr, 1982. 2: p. 229-48. 4 Spector, R. and A.V. Lorenzo, Folate transport in the central nervous system. Am J Physiol, 1975. 229(3): p. 777-82. 5 Selhub, J., Folate, vitamin B12 and vitamin B6 and one carbon metabolism. J Nutr Health Aging, 2002. 6(1): p. 39-42.
6 Wright, A.J., J.R. Dainty, and P.M. Finglas, Folic acid metabolism in human subjects revisited: potential implications
for proposed mandatory folic acid fortification in the UK. Br J Nutr, 2007: p. 1-9.
7 Chen, Z., A.C. Karaplis, S.L. Ackerman, I.P. Pogribny, S. Melnyk, S. Lussier-Cacan, M.F. Chen, A. Pai, S.W. John, R.S
.Smith, T. Bottiglieri, P. Bagley, J. Selhub, M.A. Rudnicki, S.J. James, and R. Rozen, Mice deficient in
methylenetetrahydrofolate reductase exhibit hyperhomocysteinemia and decreased methylation capacity, with
neuropathology and aortic lipid deposition. Hum Mol Genet, 2001. 10(5): p. 433-43.
8 Stroes E, van Faasen E, et al. Folic acid reverts dysfunction of endothelial nitric oxide synthase. Circ Res 2000; 86:1129-
9Willems FF, Boers GH, Blom HJ, et al. Pharmacokinetic Study on the Utilization of 5-methyltetrahydrofolate and Folic Acid
in Patients with Coronary Artery Disease. Br J Pharmacol 2004;141:825-830.

10 Lehmann M, Regland B, Blennow K, and Gottfries CG: Vitamin B12-B6-Folate Treatment Improves Blood-Brain Barrier
Function in Patients with Hyperhomocysteinaemia and Mild Cognitive Impairment. Dementia and Geriatric Cognitive
Disorders 2003;16:145-150.
11 Hultberg, B., Andersson, A., Masson, P., Larson, M., and Tunek, A. Plasma Homocysteine and Thiol Compound
Fractions After Oral Administration of N-Acetylcysteine. Scand.J.Clin.Lab Invest 1994;54(6):417-22.
12 Ventura, P., Panini, R., Abbati, G., Marchetti, G., and Salvioli, G. Urinary and Plasma Homocysteine and Cysteine Levels
During Prolonged Oral N-Acetylcysteine Therapy. Pharmacology 2003;68(2):105-14.
13 McCaddon A and Davies G: Co-administration of N-acetylcysteine, vitamin B12 and folate in cognitively impaired
hyperhomocysteinaemic patients. International Journal of Geriatric Psychiatry 2005;20(10):998-1000.
14 McCaddon A and Davies G: Clinical effects of co-administering N-acetylcysteine, vitamin B12 and folate in cognitively
impaired hyperhomocysteinaemic patients. Haematologica Reports 2005:1(3):49-50. Poster presentation at the 5th
Homocysteine Conference in Milan, Italy June 26th – June 30th 2005.
15 Guidi I, Galimberti D, Lonati S, Novembrino C, Bamonti F, Tiriticco M, Fenoglio C, Venturelli E, Baron P, Bresolin N and
Scarpini E: Oxidative imbalance in patients with mild cognitive impairment and Alzheimer’s disease. Neurobiology of Aging
16 5-Methyltetrahydrofolate.(Monograph), Alternative Medicine Review, 2006. 11(4):330-337
17 Adair JC, Knoefel JE and Morgan N: Controlled trial of N-acetylcysteine for patients with probable Alzheimer’s disease.
Neurology 2001;57:1515-1517.
18 Boyd-Kimball D, Sultana R, Abdul HM and Butterfield DA: ∂-Glutamylcysteine Ethyl Ester-Induced Up-Regulation of
Glutathione Protects Neurons Against Aβ (1-42)-Mediated Oxidative Stress and Neurotoxicity: Implications for Alzheimer’s
Disease. Journal of Neuroscience Research 2005;79:700-706.
19 Wiklund O, Fager G, Andersson A, Lundstam U, Masson P and Hultberg B: N-acetylcysteine treatment lowers plasma
homocysteine but not serum lipoprotein(a) levels. Atherosclerosis 119 (1996) 99-106.
20 PDR® For Nutritional Supplements, 2001;ISBN: 1-56363-364-7: 477-86.
21 Nilsson K, Gustafson L, and Hultberg B: Improvement of cognitive functions after cobalamin/folate supplementation in
elderly patients with dementia and elevated plasma homocysteine. International Journal of Geriatric Psychiatry
22 Seshadri S, Beiser A, Selhub J, Jacques PF, Rosenberg IH, D’Agostino RB, Wilson PWF, and Wolf PA: Plasma
Homocysteine As A Risk Factor For Dementia And Alzheimer’s Disease. New England Journal of Medicine 2002:Vol346,
No. 7:476-483.
23 B Akoglu, M Schrott, H Bolouri, A Jaffari, E Kutschera, WF Caspary and D Faust: The Folic Acid Metabolite L-5-
Methyltetrahydrofolate Effectively Reduces Total Serum Homocysteine Level in Orthotopic Liver Transplant Recipients: A
Double-Blind Placebo-Controlled Study. European Journal of Clinical Nutrition (2007), 1–6

24 Scott JM, Weir DG: The Methylfolate Trap. A Physiological Response in Man to Prevent Methyl Group Deficiency in
Kwashiokor and an Explanation for Folic-Acid-Induced Exacerbation of Subacute Combined Degeneration in Pernicious
Anemia; Lancet. 1981 2:337-340
25 Kuzminski AM, Del Giacco EJ, Allen RH, et al.: Effective Treatment Of Cobalamin Deficiency With Oral Cobalamin. Blood
1998; 92:1191-1198.
26 Durga J et al. Effect of a 3 year folic acid supplementation on cognitive function in older adults in the FACIT trial; a randomized,
double blind, controlled trial. The Lancet 2007;369:208-216.
27 United States Food and Drug Administration Title 21 Code of federal Regulations 101.9(j)(8).
28 PDR for Nutritional Supplements, (n.19) pp. 157-67.
29 Leucovorin Calcium (folinic acid) For Injection Prescribing Information:December 2003; Mayne Pharma (USA) Inc.
30 Lamictal® (lamotrigine) Prescribing Information:August 2005; GlaxoSmithKline.
31 Depakote® (divalproex sodium) Prescribing Information:January 2006; Abbott Laboratories.
32 Topamax® (topiramate) Prescribing Information:June 2005; ORTHO-McNEIL NEUROLOGICS, INC.
33 Neurontin® (gabapentin) Prescribing Information:December 2005; Parke-Davis.
34 Lyrica® (pregabalin) Prescribing Information:March 2006; Parke-Davis.
35 Keppra® (levetiracetam) Prescribing Information: March 2007; UCB, Inc.
36 Gabitril (tiagabine) Prescribing Information: March 2005: Cephalon, Inc.
37 Zonegran® (zonisamide) Prescribing Information: December 2004: Elan Pharma International Ltd.; licensed to Eisai Inc
Metafolin® is a registered trademark of Merck KGaA, Darmstadt, Germany. Certain rights to CEREFOLIN®NAC were
granted under a license from COBALZ Limited, Chester, United Kingdom, CH1 1NZ.
Distributed by:
PAMLAB, L.L.C. Covington, LA 70433


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