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Benfotiamine powder (99.7% pure)
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SYNONYMS: Benfotiamine = Benfotiamin = Benfothiamine = S-benzoylthiamine-O-monophosphate
CAS# = 22457-89-2
A small measuring spoon is provided that measures a dose of 90 mg of pure benfotiamine powder. There are 333 doses per 30 grams of powder. Total daily dosage = 90 - 270 mg/day.
Benfotiamine is an inhibitor of Advanced Glycation Endproduct (AGE) formation.
Pharmacokinetics of thiamine derivatives especially of benfotiamine.
Int J Clin Pharmacol Ther 1996 Feb; 34(2): 47-50.
Pharmacokinetic data of orally administered lipid-soluble thiamine analogues like benfotiamine are reviewed and assessed. It is quite clear that benfotiamine is absorbed much more better than water-soluble thiamine salts: maximum plasma levels of thiamine are about 5 times higher after benfotiamine, the bioavailability is at maximum about 3.6 times as high as that of thiamine hydrochloride and better than other lipophilic thiamine derivates. The physiological activity (alphaETK) increased only after benfotiamine was given. Due to its excellent pharmacokinetic profile benfotiamine should be preferred in treatment of relevant indications.
A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy.
Exp Clin Endocrinol Diabetes 1996; 104(4): 311-6.
Stracke H, Lindemann A, Federlin K.
In a double-blind, randomized, controlled study, the effectiveness of treatment with a combination of Benfotiamine (an Allithiamine, a lipid-soluble derivative of vitamin B1 with high bioavailability) plus vitamin B6/B12 on objective parameters of neuropathy was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement (p = 0.006) of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold. Long-term observation of 9 patients with verum over a period of 9 months support the results. Therapy-specific adverse effects were not seen. The results of this double-blind investigation, of the long-term observation and of the reports in the literature support the contention that the neurotropic benfotiamine-vitamin B combination represents a starting point in the treatment of diabetic polyneuropathy.
Benfotiamin inhibits intracellular formation of advanced Glycation endproducts in vivo.
Diabetes. 2000 May; 49(Suppl1): A143(P583).
Lin J, Alt A, Liersch J, Bretzel RG, Brownlee MA, Hammes HP.
We have demonstrated previously that intracellular formation of the advanced glycation end product (AGE) N-[Epsilon]-(carboxymethyl)lysine (CML) inversely correlates with diabetic vascular complications independently from glycemia (Diabetologia 42, 603, 1999). Here, we studied the effect of benfotiamine, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in-vitro on the intracellular formation of (CML) and methylglyoxal-derived AGE in red blood cells. Blood was collected from 6 Type 1 diabetic patients (2m, 4f, age 31.8 ± 5.5 years; diabetes duration 15.3 ± 7.0 years) before and after treatment with 600 mg/day benfotiamine for 28 days. In addition to HbA1c (HPLC), CML and methylglyoxal were measured using specific antibodies and a quantitative blot technique. While treatment with benfotiamine did not affect HbA1c levels (at entry: 7.18 ± 0.86%; at conclusion 6.88 ± 0.88%; p not significant), levels of CML decreased by 40% (737 ± 51 arbitrary units/mg protein (AU) vs 470 ± 86 AU; p<0.01). The levels of intracellular methylglyoxal were reduced by almost 70% (1628 ± AU vs 500 ± 343 AU; p<0.01). The data indicate that thiamine derivatives are effective inhibitors of both intracellular glycoxidation and AGE formation.
Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy.
Nat Med 2003 Mar; 9(3): 294-9.
Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M.
Three of the major biochemical pathways implicated in the pathogenesis of hyperglycemia induced vascular damage (the hexosamine pathway, the advanced glycation end product (AGE) formation pathway and the diacylglycerol (DAG)-protein kinase C (PKC) pathway) are activated by increased availability of the glycolytic metabolites glyceraldehyde-3-phosphate and fructose-6-phosphate. We have discovered that the lipid-soluble thiamine derivative benfotiamine can inhibit these three pathways, as well as hyperglycemia-associated NF-kappaB activation, by activating the pentose phosphate pathway enzyme transketolase, which converts glyceraldehyde-3-phosphate and fructose-6-phosphate into pentose-5-phosphates and other sugars. In retinas of diabetic animals, benfotiamine treatment inhibited these three pathways and NF-kappaB activation by activating transketolase, and also prevented experimental diabetic retinopathy. The ability of benfotiamine to inhibit three major pathways simultaneously might be clinically useful in preventing the development and progression of diabetic complications.
Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy.
Arzneimittelforschung 1999 Mar; 49(3): 220-4.
Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P.
The therapeutic effectiveness of a benfotiamine (CAS 22457-89-2)-vitamin B combination (Milgamma-N), administered in high (4 x 2 capsules/day, = 320 mg benfotiamine/day) and medium doses (3 x 1 capsules/day), was compared to a monotherapy with benfotiamine (Benfogamma) (3 x 1 tablets/day, = 150 mg benfotiamine/day) in diabetic patients suffering from painful peripheral diabetic neuropathy (DNP). In a 6-week open clinical trial, 36 patients (aged 40 to 70 yrs) having acceptable metabolic control (HbA1c < 8.0%) were randomly assigned to three groups, each of them comprising 12 participants. Neuropathy was assessed by five parameters: the pain sensation (evaluated by a modified analogue visual scale), the vibration sensation (measured with a tuning fork using the Riedel-Seyfert method) and the current perception threshold (CPT) onthe peroneal nerve at 3 frequencies: 5, 250 and 2000 Hz). Parameters were registered at the beginning of the study and at the end of the 3rd and 6th week of therapy. An overall bneneficial therapeutic effect on the neuropathy status was observed in all three groups during the study, and a significant improvement in most of the parameters studied appeared already at the 3rd week of therapy (p < 0.01). The greatest change occurred in the group of patients receiving the high dose of benfotiamine (p < 0.01 and 0.05, resp., compared to the othr groups). Metabolic control did not change over the study. It is concluded that benfotiamine is most effective in large doses, although even in smaller daily dosages, either in combination or in monotherapy, it is effective.
Prevention of cardiac autonomic neuropathy in dogs with Benfotiamin.
In Gries FA, Federlin K. Benfotiamin in the Therapy of Polyneuropathy.
New York: Georg Thieme Verlag, 1998; 45-9.
Experimentally-induced diabetes of the dog leads to disturbances in the autonomous neurological function of the heart after approximately 3 months of continuously- observed diabetes. As signs of autonomic cardiac neuropathy, the heart rate variability and Valsalva ratio clearly fell in the untreated diabetic animals. Oral benfotiamin, administered from the sixth day after diabetes-induction, prevented or at least delayed these changes. According to the results, treatment with fat-soluble benfotiamin can play an important role in the therapy and prevention of cardiac autonomic neuropathy, apart from any effect on diabetic metabolic disturbances.
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