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Tacrolimus Basic information
Overview Indication and administrations Pharmacodynamics Mode of action Side effects References
Product Name:Tacrolimus
Synonyms:(2-propenyl)-,(3s-(3r*(e(1s*,3s*,4s*)),4s*,5r*,8s*,9e,12r*,14r*,15s*,16r*,18s*;,19s*,26ar*))-;16-dimethoxy-4,10,12,18-tetramethyl-8-3-(2-(4-hydroxy-3-methoxycyclohexyl)-1;15,19-Epoxy-3H-pyrido[2,1-c][1,4]oxaazacyclotricosine-1,7,20,21(4H,23H)-tetrone, 5,6,8,11,12,13,14,15,16,17,18,19,24,25,26,26a-hexadecahydro-5,19-dihydroxy-3-[2-(4-hydroxy-3-methoxycyclohexyl)-1-methylethenyl]-14,16-dimethoxy-4,10,12,18-tetramethyl-8-(2-propenyl)-, [3S-[3R*[E(1S*,3S*,4S*)],4S*,5R*,8S*,9E,12R*,14R*,15S*,16R*,18S*,19S*,26aR*]]-;L 679934;Protopic;FK-506:FR-900506;Fujimycin Prozraf
MF:C44 H69 N O12
Product Categories:Inhibitors;API;Active Pharmaceutical Ingredients;Immunosuppressant.;Chiral Reagents;Fujimycin, Prograf;Intermediates & Fine Chemicals;Pharmaceuticals;antibiotic;APIs
Mol File:104987-11-3.mol
Tacrolimus Structure
Tacrolimus Chemical Properties
Melting point 113-115°C
Boiling point 871.7±75.0 °C(Predicted)
density 1.19±0.1 g/cm3(Predicted)
Fp 2℃
storage temp. Sealed in dry,Store in freezer, under -20°C
solubility DMSO: >3 mg/mL
form solid
color white
Water Solubility Freely soluble in DMSO or ethanol. Poorly soluble in water.Soluble in dimethyl sulfoxide, ethanol, water, acetone, chloroform, ethyl acetate, ether, methanol and dimethyl formamide.
CAS DataBase Reference104987-11-3(CAS DataBase Reference)
Safety Information
Hazard Codes T,Xi,Xn,F
Risk Statements 25-36/37/38-36-20/21/22-11
Safety Statements 45-36-26-36/37-16-60-20
RIDADR UN 2811 6.1/PG 3
WGK Germany 3
RTECS KD4201200
HazardClass 6.1
HS Code 29349990
Hazardous Substances Data104987-11-3(Hazardous Substances Data)
MSDS Information
Tacrolimus Usage And Synthesis
OverviewTacrolimus (also FK-506 or Fujimycin) is an immunosuppressive drug whose main use is after organ transplant to reduce the activity of the patient's immune system and so the risk of organ rejection. It is also used in a topical preparation in the treatment of severe atopic dermatitis, severe refractory uveitis after bone marrow transplants, and the skin condition vitiligo. Tacrolimus was first extracted from the fermentation broth of Streptomyces tsukuba, a soil microbe found in Tsukuba, Japan.1 The name tacrolimus is derived by taking the ‘t’ for Tsukuba, the name of the mountain where the soil sample was extracted, ‘acrol’ for macrolide and ‘imus’ for immunosuppressant.[2] Although structurally unrelated to cyclosporin, tacrolimus shows a similar spectrum of immunosuppressive effects to this agent at the cellular and molecular level. Initial studies indicated that tacrolimus was a powerful immunosuppressant, displaying approximately 100-fold greater in vitro potency than cyclosporin in inhibiting T cell activation. Subsequent in vivo studies have shown tacrolimus to be effective both in suppressing spontaneous and experimental autoimmune disease, and in preventing allograft and xenograft rejection in animal models of organ transplantation.
Initially, tacrolimus was used for systemic immunosuppression of patients who had undergone allograft transplants to stop them from rejecting their new grafts. Soon, however, through the benefit of the serendipity of science, it was noticed that tacrolimus could produce favorable results in skin disorders in some of the patients who had undergone transplantation. The discovery of tacrolimus has thus lead to greater understanding of skin pathology, for example of atopic dermatitis.[3] Subsequently, other topical applications of tacrolimus were reported and the use of this agent in dermatology is gradually expanding.

Figure 1 The chemical structure of Tacrolimus
Indication and administrationsIt is used after allogenic organ transplant to reduce the activity of the patient's immune system and so the risk of organ rejection. It was first approved by the FDA in 1994 for use in liver transplantation, this has been extended to include kidney, heart, small bowel, pancreas, lung, trachea, skin, cornea, and limb transplants. It has also been used in a topical preparation in the treatment of severe atopic dermatitis.
PharmacodynamicsTacrolimus was absorbed topically by intact skin at rates of 3.1, 4.9 and 6.8 ng/cm2 per hour, for the 0.03%, 0.1% and 0.3% ointment concentrations, respectively.[1,2] Interestingly, tacrolimus was absorbed regardless of occlusion at significantly higher rates in damaged skin, with percutaneous penetration of 40 ng/cm2 per hour. Thus, while on topical therapy, the patient’s skin will absorb progressively lower quantities of the agent as the lesions heal. This self-regulatory property of tacrolimus is a major advantage, as it should result in fewer adverse effects over the course of treatment.[4] In one randomized, double-blind study, a 3-week course of twice daily, topically applied tacrolimus ointment 0.03%, 0.1% and 0.3% resulted in blood concentrations below 0.25 ng/mL in most patients.[5] This low systemic absorption rate is typical of the majority of clinical cases. The mean time taken to attain the highest blood concentration of tacrolimus is between 5 and 6 h after application in adults and 2.5 h in children.[6] In another study, the bioavailability of topical tacrolimus was found to be lower than 0.5%. 6 Furthermore, tacrolimus does not seem to
accumulate, either in the skin or blood, following repeated applications.[7] When taken orally, the absorption of tacrolimus is erratic and poor. The bioavailability of the drug ranges from 5% to 67%. 8 Intravenous administration of tacrolimus has resulted in the highest relative tissue concentrations in the spleen, lung and kidneys, followed by heart, skin and muscle, then fat and bone marrow and finally by liver, bone and blood.[9]
During topical administration, there is no evidence of cutaneous metabolism. Systemically, tacrolimus metabolism is mediated by the cytochrome P450 3A4 isoenzyme. It is metabolized in the liver, by CYPIA and CYPIIIA.[8] In vitro studies have identified eight different metabolites. When SMS 201-995 is administered via the intraperitoneal route, the effects of tacrolimus are enhanced and thus may enable lower doses of the latter to be used.[10]
When administered systemically, tacrolimus is eliminated in bile. It is cleared at 2.25 L/h, with a half-life of 40 h. 1 It has been found that paediatric transplant patients under 6 years old have higher weight-normalized clearance of tacrolimus, as compared with older children and adults.
Mode of actionTacrolimus is a prodrug that enters the T cells and binds to immunophilins, forming a complex that binds competitively and blocks calmodulin.[2] This has the spin-off effect of not activating phosphatase calcineurin, which disables the dephosphorylation of NF-AT and subsequently inhibits entry of NF-AT into the nucleus, suppressing gene transcription. The final result is a decreased responsiveness of T cells to antigens.
Tacrolimus can also exert a broad range of immunomodulatory effects on various skin disorders by binding to cell surface steroid receptors and inhibiting mast cell adhesion, inhibiting the release of mediators from mast cells and basophils, decreasing intercellular adhesion molecule-1 and E-selectin lesional blood vessel expression, and downregulating the expression of IL-8 receptor and Fcε RI on Langerhans cells.[11-13] Langerhans cells are considered to be important in the pathophysiology of many inflammatory diseases.[14] There is speculation that the features involved in the activation of Langerhans cells are common with T-cell activation; in other words, there is a dependence on calcineurin in the activation of Fcε RI-specific transcription factor.[15] Tacrolimus may downregulate the expression of FcεRI. Langerhans cells and other CD1a+ skin dendritic cells are important targets of tacrolimus.[14]
It has also been suggested that tacrolimus is able to increase levels of p53.2 Topical tacrolimus has been shown to decrease cytokine mRNA levels of IL-1α, IL-1β and macrophage inflammatory protein (MIP)-2, which results in lymph node cell proliferation.16,17 Tacrolimus inhibits the transcription and release of cytokines, for example, IL-2, Il-3, IL-4, IL-5, interferon-γ, tumor necrosis factor-α, and granulocyte-monocyte colony stimulating factor.[18] Additionally, the production of T-helper 1 (Th1) and Th2 cytokines is inhibited by tacrolimus.[18]
Side effects Owing to its potent activity as an immunosuppressant, tacrolimus has a number of adverse effects when administered orally or intravenously following transplant operations. Nephrotoxicity, represented by elevated creatinine, blood urea nitrogen, hyperkalaemia and reduction of the glomerular filtration rate, as well as vasoconstrictive effects, such as hypertension are among the most serious adverse effects.[19-22] There are also various neurotoxic adverse effects that can occur with systemic therapy. The major ones include mutism, aphasia, encephalopathy, seizures, psychosis, coma and focal disturbances. These reactions have an incidence of 5–10%. [23,24] Minor adverse effects such as headaches, transient, tremors, paraesthesias, photophobias, somnolence and insomnia occur in approximately 20% of individuals.[25,26] Systemic tacrolimus can also cause adverse reactions in the gastrointestinal system, causing diarrhoea, nausea, constipation, anorexia and vomiting. Respiratory disorders such as dyspnoea, pleural effusion and atelectasis, and cutaneous disorders, such as pruritus or a rash may develop. Other adverse effects include fever, pain, peripheral oedema, arthralgia and asthenia. Hypersensitivity reactions may also occur and may be due castor oil derivatives in the parenteral formulation.[24]
  1. 1 Ruzicka T, Assmann T, Homey B. Tacrolimus: The drug for the turn of the millennium? Arch Dermatol 1999; 135: 574–580.
  2. Lawrence ID. Tacrolimus (FK506): experience in dermatology. Dermatol Ther 1998; 5: 74–84.
  3. Michel G, Kemeny L, Homey B, Ruzicka T. FK506 in the treatment of inflammatory skin disease: promises and perspectives. Immunol Today 1996; 17: 106–108.
  4. Bieber T. Topical tacrolimus (FK506): a new milestone in the management of atopic dermatitis. J Allergy Clin Immunol 1998; 102: 555–557.
  5. Ruzicka T, Bieber T, Schopf E et al. A short-term trial of tacrolimus ointment for atopic dermatitis. N Engl J Med 1997; 337: 816–821.
  6. Alaiti S, Kang S, Fiedler VC et al. Tacrolimus (FK506) ointment for atopic dermatitis: a phase I study in adults and children. J Am Acad Dermatol 1998; 38: 69–76.
  7. Hanifin JM, Chan S. Biochemical and immunologic mechanisms in atopic dermatitis: New targets for emerging therapies. J Am Acad Dermatol 1999; 41: 72–77.
  8. Laurema AI, Granlund H, Reitamo S. Use of the newer immunosuppressive agents in dermatology. Bio Drugs 1997; 8: 96–106.
  9. Shirbacheh MV, Jones JW, Harralson TA et al. Pharmacokinetics of intra-arterial delivery of tacrolimus to vascularly isolated rabbit forelimb. J Pharmacol Exp Ther 1999; 289: 1196–1201.
  10. Perego C, Lattuada D, Casnici C et al. Evidence that SMS 201–995 enhances the immunosuppressive effect of FK506. Int J Immunopharmacol 1998; 20: 479–490.
  11. Fleischer AB. Treatment of atopic dermatitis: Role of tacrolimus ointment as a topical noncorticosteroid therapy. J Allergy Clin Immunol 2000; 104: S126–S130.
  12. Wollenberg A, Bieber T. FK-506/Tacrolimus. In: Burg G, Dummer RG, editors. Strategies for Immunointerventions in Dermatology. Springer-Verlag, Heidelberg, 1997: 53–57.
  13. Columbo M, Bochner BS, Marone G. Human skin mast cells express functional beta1 integrins that mediate adhesion to extracellular martix proteins. J Immunol 1995; 154: 6058–6064.
  14. Panhans-Groß A, Novak N, Kraft S et al. Human epidermal Langerhans’ cells are targets for the immnosuppressive macrolide tacrolimus (FK506). J Allergy Clin Immunol 2001; 107: 345–352.
  15. Reitamo S. Tacrolimus: a new topical immunomodulatory therapy for atopic dermatitis. J Allergy Clin Immunol 2001; 107: 445–448.
  16. Nagai H, Hiyama H, Matsuo A et al. FK-506 and cyclosporin A potentiate the IgE antibody production by contact sensitization with hapten in mice. J Pharmacol Exp Ther 1997; 283: 321–327.
  17. Homey B, Assmann T, Vohr H-W et al. Topical FK506 suppresses cytokine and costimulatory molecule expression in epidermal and local draining lymph node cells during primary skin immune responses. J Immunol 1998; 160: 5331–5340.
  18. Leung DYM, Soter NA. Cellular and immunologic mechanisms in atopic dermatitis. J Am Acad Dermatol 2001; 44: S1–S12.
  19. Nash RA, Etzioni R, Storb R et al. Tacrolimus (FK506) alone or in combination with methotrexate or methylprednisolone for the prevention of acute graft-versus-host disease after marrow transplantation from HLA-matched siblings: a single-center study. Blood 1995; 85: 3746–3753.
  20. Nielsen FT, Leyssac PP, Kemp E et al. Nephrotoxicity of FK-506 in the rat. Studies on glomerular and tubular function, and on the relationship between efficacy and toxicity. Nephrol Dial Transplant 1995; 10: 334–340.
  21. Nasr IS. Topical tacrolimus in dermatology. Clin Exp Dermatol 2000; 25: 250–254.
  22. Compendium of Pharmaceuticals Specialties, 35th edn. Webcom Limited, Toronto, 2000: 1287–1292.
  23. Manez R, Jain A, Marino IR, Thomson AW. Comparative evaluation of tacrolimus (FK506) and cyclosporin A as immunosuppressive agents. Transplant Rev 1995; 9: 63–76.
  24. Nousari Hossein C, Sragovich A, Kimyai-Asadi A et al. Mycophenolate mofetil in autoimmune and inflammatory skin disorders. J Am Acad Dermatol 1999; 40: 265–268.
  25. Ohashi Y, Minegishi M, Fujie H et al. Successful treatment of steroid-resistant severe acute GVHD with 24-h continuous infusion of FK506. Bone Marrow Transplant 1997; 19: 625–627.
  26. Jegasothy BV, Ackerman CD, Todo S et al. Tacrolimus (FK506) – A new therapeutic agent for severe recalcitrant psoriasis. Arch Dermatol 1992; 128: 781–785.
DescriptionTacrolimus, isolated from the microorganism Streptomyces tsukubaensis, is a macrolide immunosuppressant developed by Fujisawa for organ transplantation. It displays similar but more potent immunosuppressive activity than cyclosporin. It inhibits both cell mediated and humoral immune responses. In animal models of organ transplantation, tacrolimus has been shown to prolong survival of hepatic, renal, cardiac, small intestine, pancreatic and skin allografts and to reverse cardiac and renal allograft rejection. It has been used effectively in humans as rescue or primary immunosuppressant therapy in liver or kidney transplantation. Compared to cyclosporin, tacrolimus causes reduced incidence of infectious complications and of hypertension and hypercholesterolemia for the allograft recipients. In common with cyclosporin, tacrolimus binds with high affinity to a family of cytoplasmic immunosuppressant binding proteins, the immunophilins. This tight complex is proposed as the biologically active moiety that interacts with intracellular molecules involved in signal transduction.It inhibits phosphatase activity of calcineurin, an action that may impair the generation and/or activation of nuclear transcription factors required for lymphokine (particularly interleukin-2) gene expression. Tacrolimus has also been reported to have potential in multiple sclerosis, psoriasis, rheumatoid arthritis and uveitis associated with Behcet‘s disease.
Chemical PropertiesWhite Crystalline Solid
OriginatorFujisawa (Japan)
UsesAn immunosuppressant that blocks T cell proliferation in vitro by inhibiting the generation of several lymphokines, especially IL-2. Shown to inhibit the activity of FK-506 binding protein, thereby reversing its effects on sarcoplasmic reticulum Ca+2 release.
UsesFK-506 (Tacrolimus) is a macrolide immunosuppressive drug that is mainly used after allogeneic organ transplant to reduce the activity of the patient's immune system
UsesTacrolimus (fujimycin) was discovered as a potent inhibitor of IL2 production in a targeted search for novel immunosuppressants. Tacrolimus acts by blocking T cell proliferation in vitro by inhibiting the generation of several lymphokines, notably the original target IL-2. Tacrolimus inhibits the activity of FK-506 binding protein, Ca2+-dependent phosphatase and calcineurin, and activates NF-κB through phosphorylation and degradation of IκBα.
Usestreatment of Cushing's syndrome
UsesFor use after allogenic organ transplant to reduce the activity of the patient's immune system and so the risk of organ rejection. It was first approved by the FDA in 1994 for use in liver transplantation, this has been extended to include kidney, heart,
DefinitionChEBI: Tacrolimus is a macrolide containing a 23-membered lactone ring, originally isolated from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis.
IndicationsTacrolimus is a macrolide lactone originally derived from Streptomyces tsukubaensis. Although structurally unrelated to cyclosporine, tacrolimus has a very similar mechanism of action; that is, it blocks the production of proinflammatory cytokines by T lymphocytes by inhibiting calcineurin.Tacrolimus, however, appears to be 10 to 100 times as potent as an immunosuppressive. Oral tacrolimus (FK506) is used for prevention of organ rejection in recipients of renal and hepatic transplants.
IndicationsTacrolimus (Prograf) is a second-generation immunosuppressive agent that has been approved for use in liver transplantation. Its efficacy for other transplantations is being evaluated. It has properties similar to those of cyclosporine except that weight for weight it is 10 to 100 times more potent. It is a macrolide antibiotic that selectively inhibits transcription of a specific set of lymphokine genes in T lymphocytes (e.g., IL-2, IL-4, and interferon-) and binds to cytoplasmic proteins in lymphocytes. Although the binding proteins (cytophilins) for cyclosporine and tacrolimus are different, they share similar functions in that the cytophilins are important for the intracellular folding of proteins. It is speculated that these proteins are important in regulating gene expression in T lymphocytes and that both drugs somehow interfere in this process.
Absorption of tacrolimus from the gastrointestinal (GI) tract is variable. It is extensively metabolized in the liver and excreted in the urine.As with cyclosporine, nephrotoxicity is its principal side effect.
Manufacturing ProcessThe novel 17-allyl-1,14-dihydroxy-12-[2-(4-hydroxy-3-methoxycyclohexyl)-1- methylvinyl]-23,25-dimethoxy-13,19,21,27-tetramethyl-11,28-dioxa-4- azatrcyclo[,9]octacos-18-ene-2,3,10,16-tetraone (FR-900506), substance can be produced by culturing a FR-900506 substance(s)-producing strain belonging to the genus Streptomyces (e.g. Streptomyces tsukubaensis No. 9993, FERM BP-927) in a nutrient medium.
A culture medium (160 ml) containing glycerin (1%), corn starch (1%), glucose (0.5%), cottonseed meal (1%), dried yeast (0.5%), corn steep liquor (0.5%) and calcium carbonate (0.2%) (adjusted to pH 6.5) was poured into each of ten 500 ml-Erlenmeyer flasks and sterilized at 120°C for 30 min. A loopful of slant culture of Streptomyces tsukubaensis No. 9993 was inoculated to each of the medium and cultured at 30°C for 4 days on a rotary shaker. The resultant culture was inoculated to a medium containing soluble starch (5%), peanut powder (0.5%), dried yeast (0.5%), gluten meal (0.5%), calcium carbonate (0.1%) and Adekanol (deforming agent, Trade Mark, maker Asasi Denka Co.) (0.1%) (150 liters) in a 200-liter jar-fermentor, which had been sterilized at 120°C for 20 min in advance, and cultured at 30C for 4 days under aeration of 150 liters/minutes and agitation of 250 rpm.
Isolation and Purification
The cultured broth thus obtained was filtered with an aid of diatomaseous earth (5 kg). The mycelial cake was extracted with acetone (50 liters), yielding 50 liters of the extract. The acetone extract from mycelium and the filtrate (135 L) were combined and passed through a column of a non-ionic adsorption resin "Diaion HP-20" (Trade Mark, maker Mitsubishi Chemical Industries Ltd.) (10 L). After washing with water (30 L) and 50 % aqueous acetone (30 L), elution was carried out with 75 aqueous acetone. The eluate (30 liters) was evaporated under reduced pressure to give residual water (2 L). This residue was extracted with ethyl acetate (2 L) three times. The ethyl acetate extract was concentrated under reduced pressure to give an oily residue. The oily residue was mixed with twice weight of acidic silica gel (special silica gel grade 12, maker Fuji Devison Co.), and this mixture was slurried in ethyl acetate. After evaporating the solvent, the resultant dry powder was subjected to column chromatography of the same acidic silica gel (800 ml) which was packed with n-hexane. The column was developed with nhexane (3 L), a mixture of n-hexane and ethyl acetate (4:1 v/v, 3 L) and ethyl acetate (3 L). The fractions containing the object compound were collected and concentrated under reduced pressure to give an oily residue. The oily residue was dissolved in a mixture of n-hexane and ethyl acetate (1:1 v/v, 30 ml) and subjected to column chromatography of silica gel (maker Merck Co., Ltd. 230-400 mesh) (500 ml) packed with the same solvents system. Elution was carried out with a mixture of n-hexane and ethyl acetate (1:1 v/v, 2 liters and 1:2 v/v, 1.5 L) and ethyl acetate (1.5 L). Fractions containing the first object compound were collected and concentrated under reduced pressure to give crude FR-900506 substance (3 g) in the form of yellowish powder.
This powder of the FR-900506 substance could be transformed into a form of white crystals by recrystallization thereof from acetonitrile. Melting point: 127°-129°C.
Brand namePrograf (Astellas); Protopic (Astellas).
Therapeutic FunctionImmunosuppressive
Clinical UseA topical formulation (Protopic) has recently been approved for treatment of moderate to severe atopic dermatitis in children and adults who have not responded to other therapies. Levels of systemic absorption are low even when applied to a relatively large body surface area.
Side effectsLocal irritant reactions (burning, stinging, erythema) are a common side effect, but these usually resolve within the first few days of treatment. The major benefit of topical tacrolimus over topical corticosteroids is that tacrolimus does not cause atrophy, striae, or telangiectasia, even with chronic use.
Veterinary Drugs and TreatmentsTacrolimus has recently been studied at the University of Tennessee College of Veterinary Medicine where investigators found it equally effective as cyclosporine and effective for cyclosporine-resistant cases of KCS. It exerts its effects through a mechanism similar to that of cyclosporine, however exact mechanisms of action in causing tear production are still being determined.
Veterinary Drugs and TreatmentsTacrolimus ointment may be of benefit in veterinary patients in the adjunctive treatment of atopic dermatitis, discoid lupus erythematosus, pemphigus erythematosus or foliaceous, pinnal vascular disease, alopecia areata, vitiligo and for perianal fistulas (terminal phase or maintenance treatment after cyclosporine therapy). Unlike topical corticosteroids, tacrolimus or pimecrolimus do not have atrophogenic or metabolic effects associated with long-term or large area treatment.
Tacrolimus acts similarly as cyclosporine, namely inhibiting T-lymphocyte activation primarily by inhibiting the phosphatase activity of calcineurin. It also inhibits the release of inflammatory cytokines and mediators from mast cells and basophils.
Tacrolimus Preparation Products And Raw materials
Raw materialsEthyl acetate-->Celite-->Starch-->Yeast extract-->Active Calcium
Preparation ProductsTacroliMus Methyl Acryl Aldehyde
Tag:Tacrolimus(104987-11-3) Related Product Information
TACROLIMUS HYDRATE/TSUKUBAENOLIDE HYDRATE 1-OCTEN-3-YL BUTYRATE 1-(2-methylpiperidin-1-yl)acetone H-HOMOPRO-OME HCL 1-piperidinoacetone D(+)-Pipecolinic acid 1-ETHYL-PIPERIDINE-2-CARBOXYLIC ACID HYDROCHLORIDE N-Dodecanoyl-L-alanine Tacrolimus N-LAUROYLSARCOSINE 2-(dibutylamino)acetic acid 1-methyl-piperidine-2-carboxylicacidmethylester 1-ACETYL-2-PIPERIDINECARBOXYLIC ACID N,N-DI-N-PROPYL-L-ALANINE 2-(TETRAHYDRO-PYRAN-2-YL)-ETHYLAMINE N-LAUROYL-L-ALANINE Ethyl pipecolinate N,N-Diethyldodecanamide