| Size | Price | |
|---|---|---|
| 500mg | ||
| 1g | ||
| Other Sizes |
Teduglutide Acetate (Gattex; Revestive) is a polypeptide composed of 33-amino acids. It is a glucagon-like peptide-2 (GLP-2) analog that has been approved as an orphan drug for use in the treatment of SBS-short bowel syndrome. Teduglutide works by promoting mucosal growth and possibly restoring gastric emptying and secretion. Teduglutide differs from naturally occurring GLP-2 by a single amino acid: an alanine replaced by a glycine, which blocks breaking down of the molecule by dipeptidyl peptidase and increases the half-life from 7 minutes (GLP-2) to about 2 hours, while retaining its biological activity.
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
The pharmacokinetic profile of teduglutide (when administered subcutaneously) is described by a one-compartment model with first order absorption in the abdomen, arm, and thigh. With escalating doses, teduglutide demonstrates linear pharmacokinetics. Absolute bioavailability, SubQ = 88%; Tmax, SubQ = 3-5 hours; Cmax, 0.05 mg/kg SubQ, SBS patients = 36 ng/mL; AUC, 0.05 mg/kg SubQ, SBS patients = 0.15 µg•hr/mL; Teduglutide does not accumulate following multiple subcutaneous administrations. Urine Vd, healthy subjects = 103 mL/kg Plasma clearance, healthy subjects = 123 mL/hr/kg; This value indicates that teduglutide is primarily cleared by the kidney. In healthy subjects, teduglutide has a volume of distribution (103 mL/kg) similar to blood volume. In healthy subjects, Gattex administered subcutaneously had an absolute bioavailability of 88% and reached maximum plasma teduglutide concentrations at 3-5 hours after administration. Following a 0.05 mg/kg subcutaneous dose in SBS subjects, the median peak teduglutide concentration (Cmax) was 36 ng/mL and the median area under the curve (AUC0-inf) was 0.15 ug*hr/mL. No accumulation of teduglutide was observed following repeated subcutaneous administrations. /MILK/ It is not known whether Gattex is present in human milk. Teduglutide is excreted in the milk of lactating rats, and the highest concentration measured in milk was 2.9% of the plasma concentration following a single subcutaneous injection of 25 mg/kg. Teduglutide is a recombinant analog of human glucagon-like peptide-2 that has recently been approved for the treatment of short bowel syndrome in adults. This study was designed to study the influence of renal function and age on teduglutide pharmacokinetics. This was an open-label study with six parallel groups (6 subjects each). Three groups with renal impairment (moderate, severe and end-stage renal disease) were compared to healthy subjects with normal renal function, which were matched to the renal-impaired subjects with respect to demographics. At least two elderly subjects (=65 years) were enrolled per group. A single dose of 10 mg teduglutide was subcutaneously administered to each subject. Teduglutide plasma concentrations were measured using a validated liquid chromatography method with tandem mass spectrometric detection, and the primary pharmacokinetic variables (AUCinf and Cmax) were calculated. Area under the concentration versus time curve extrapolated to infinity (AUCinf) and maximum plasma concentration (Cmax) of teduglutide in subjects with end-stage renal disease were approximately 2.59- and 2.08-fold higher, respectively, than those of healthy subjects. The AUCinf and Cmax were also slightly higher in subjects with moderate and severe renal impairment. Comparison of healthy subjects aged <65 years with healthy elderly subjects revealed very similar pharmacokinetics in both subgroups. In our study population, the primary pharmacokinetic parameters of teduglutide increased with increased severity of renal impairment. These results suggest that the daily dose of teduglutide should be reduced by 50 % in patients with moderate and severe renal impairment and end-stage disease. We found no effect of age on the pharmacokinetics of teduglutide in healthy subjects. The treatment was well tolerated, and there were no safety concerns. Metabolism / Metabolites Although a formal investigation has not been conducted, it is expected because teduglutide is a peptide-based drug, it will be degraded into smaller peptides and amino acids via catabolic pathways. The cytochrome P450 enzyme system is not involved in the metabolism of this drug. The metabolic pathway of teduglutide was not investigated in humans. However, teduglutide is expected to be degraded into small peptides and amino acids via catabolic pathways, similar to the catabolism of endogenous GLP-2. Biological Half-Life Terminal half-life, healthy subjects = 2 hours; Terminal half-life, SBS patients = 1.3 hours Teduglutide has a mean terminal half-life of approximately 2 hours in healthy subjects and 1.3 hours in short bowel syndrome (SBS) subjects. |
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| Toxicity/Toxicokinetics |
Toxicity Summary
IDENTIFICATION AND USE: Teduglutide is a biosynthetic (recombinant DNA origin) analog of human glucagon-like peptide-2 (GLP-2), a pleiotropic hormone that enhances intestinal mucosal growth and affects intestinal function. It is indicated for the treatment of adult patients with short bowel syndrome (SBS) who are dependent on parenteral support. HUMAN EXPOSURE AND TOXICITY: Based on the pharmacologic activity and findings in animals, the drug has the potential to cause hyperplastic changes including neoplasia. In clinical studies, GI tract polyps (e.g., colorectal, duodenal, and peristomal polyps, including hyperplastic polyps and villous adenomas) have been detected in patients receiving the drug. Malignancies have been reported in several patients receiving teduglutide, including metastatic adenocarcinoma of unconfirmed origin in a patient who had received prior abdominal irradiation for Hodgkin lymphoma and lung cancer (squamous and non-small cell carcinoma) in 2 patients with a history of smoking. ANIMAL STUDIES: In a 2-year carcinogenicity study in rats at subcutaneous doses of 3, 10 and 35 mg/kg/day (about 60, 200 and 700 times the recommended daily human dose of 0.05 mg/kg, respectively), teduglutide caused statistically significant increases in the incidences of adenomas in the bile duct and jejunum of male rats. In a 2-year carcinogenicity study in mice at subcutaneous doses of 1, 3.5 and 12.5 mg/kg/day (about 20, 70 and 250 times the recommended daily human dose of 0.05 mg/kg, respectively), teduglutide caused a significant increase in papillary adenomas in the gall bladder; it also caused adenocarcinomas in the jejunum in male mice at the high dose of 12.5 mg/kg/day (about 250 times the recommended human dose). In animal studies, no effects on embryo-fetal development were observed in pregnant rats given subcutaneous teduglutide at doses up to 50 mg/kg/day (about 1000 times the recommended daily human dose of 0.05 mg/kg) or pregnant rabbits given subcutaneous doses up to 50 mg/kg/day (about 1000 times the recommended daily human dose of 0.05 mg/kg). A pre- and postnatal development study in rats showed no evidence of any adverse effect on pre- and postnatal development at subcutaneous doses up to 50 mg/kg/day (about 1000 times the recommended daily human dose of 0.05 mg/kg). Teduglutide at subcutaneous doses up to 50 mg/kg/day (about 1000 times the recommended daily human dose of 0.05 mg/kg) was found to have no adverse effect on fertility and reproductive performance of male and female rats. Teduglutide was negative in the Ames test, chromosomal aberration test in Chinese hamster ovary cells, and in vivo mouse micronucleus assay. Effects During Pregnancy and Lactation ◉ Summary of Use during Lactation Because it is a large protein molecule with a molecular weight of 3752 Da, the amount in milk is likely to be very low. Teduglutide is also poorly absorbed orally so absorption by a breastfed infant is unlikely. Two breastfed infants apparently experienced no adverse effects during maternal use of teduglutide, but no long-term data are available. Until more data are available, teduglutide should be used with careful infant monitoring during breastfeeding. ◉ Effects in Breastfed Infants One mother used teduglutide during pregnancy and postpartum while breastfeeding. She breastfed her infant (extent not stated) for 6 months. No mention was made of any adverse effects in the infant. A woman taking teduglutide because of removal of a portion of her gastrointestinal tract became pregnant and delivered a healthy infant. She breastfed her infant and the drug was restarted 1 month after delivery. She breastfed (extent not stated) her infant for another 4 months during treatment. The infant experienced no side effects during breastfeeding. ◉ Effects on Lactation and Breastmilk Relevant published information was not found as of the revision date. Interactions Teduglutide may increase intestinal absorption of drugs and should be used with caution in patients receiving concomitant oral therapy with CNS agents (e.g., benzodiazepines, antipsychotic agents), drugs that require dosage titration, or drugs that have a narrow therapeutic index. |
| References | |
| Additional Infomation |
Teduglutide is a 33-membered polypeptide consisting of His, Gly, Asp, Gly, Ser, Phe, Ser, Asp, Glu, Met, Asn, Thr, Ile, Leu, Asp, Asn, Leu, Ala, Ala, Arg, Asp, Phe, Ile, Asn, Trp, Leu, Ile, Gln, Thr, Lys, Ile, Thr and Asp residues joined in sequence. A glucagon-like peptide-2 receptor agonist used for the treatment of short-bowel syndrome. It has a role as a glucagon-like peptide-2 receptor agonist, a metabolite, an antioxidant and a protective agent.
Teduglutide is a glucagon-like peptide-2 (GLP-2) analogue. It is made up of 33 amino acids and is manufactured using a strain of Escherichia coli modified by recombinant DNA technology. Teduglutide differs from GLP-2 by one amino acid (alanine is substituted by glycine). The significance of this substitution is that teduglutide is longer acting than endogenous GLP-2 as it is more resistant to proteolysis from dipeptidyl peptidase-4. FDA approved on December 21, 2012. Drug Indication Teduglutide is indicated for the treatment of adults and pediatric patients 1 year of age and older with Short Bowel Syndrome (SBS) who are dependent on parenteral support. FDA Label Revestive is indicated for the treatment of patients aged 1 year and above with Short Bowel Syndrome (SBS). Patients should be stable following a period of intestinal adaptation after surgery. Revestive is indicated for the treatment of patients aged 1 year and above with Short Bowel Syndrome. Patients should be stable following a period of intestinal adaptation after surgery. Treatment of short bowel syndrome Mechanism of Action Teduglutide is an analog of naturally occurring human glucagon-like peptide-2 (GLP-2), a peptide secreted by L-cells of the distal intestine in response to meals. GLP-2 increases intestinal and portal blood flow and inhibit gastric acid secretion. Teduglutide binds to the glucagon-like peptide-2 receptors located in enteroendocrine cells, subepithelial myofibroblasts and enteric neurons of the submucosal and myenteric plexus. This causes the release of insulin-like growth factor (IGF)-1, nitric oxide and keratinocyte growth factor (KGF). These growth factors may contribute to the increase in crypt cell growth and surface area of the gastric mucosa. Ultimately, absorption through the intestine is enhanced. Teduglutide binds to the human and rat GLP-2 receptor (GLP-2R) with similar affinity compared to native GLP-2. Receptor binding results in intracellular cyclic adenosine 3'-5'- monophosphate (cAMP) levels and activation of several downstream signaling pathways such as protein kinase A (PKA), cAMP response element-binding protein (CREB), and activator protein-1(AP-1). The potency of teduglutide is equivalent to native GLP-2 for the GLP-2R with enhanced biological activity due to resistance to DPP-IV cleavage, resulting in a longer half-life in the circulation. Teduglutide is an analog of naturally occurring human glucagon-like peptide-2 (GLP-2), a peptide secreted by L-cells of the distal intestine. GLP-2 is known to increase intestinal and portal blood flow, and inhibit gastric acid secretion. Teduglutide binds to the glucagon-like peptide-2 receptors located in intestinal subpopulations of enteroendocrine cells, subepithelial myofibroblasts and enteric neurons of the submucosal and myenteric plexus. Activation of these receptors results in the local release of multiple mediators including insulin-like growth factor (IGF)-1, nitric oxide and keratinocyte growth factor (KGF). Therapeutic Uses /CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Teduglutide is included in the database. Gattex (teduglutide [rDNA origin]) for injection is indicated for the treatment of adult patients with short bowel syndrome (SBS) who are dependent on parenteral support. /Included in US product label/ /EXPL THER/ The currently available medications for treatment of Crohn's disease (CD) include aminosalicylates, corticosteroids, antibiotics, immunomodulators and biologic agents (infliximab, certolizumab pegol, adalimumab and natalizumab). These agents target the immune and inflammatory pathways of CD, while there is a shortage of agents that target the barrier functions of the gut that are impaired in CD. Glucagon-like peptide 2 is an enterogastrone with strong trophic effects on the intestinal mucosa. Teduglutide, the analog of glucagon-like peptide has been already approved by the US Food and Drug Administration as a treatment of short bowel syndrome. This review discusses the potential use of teduglutide in patients with CD. As there has been only one randomized placebo controlled trial of teduglutide in CD, there is a shortage of data regarding the efficacy of this agent in CD. The literature search was performed using Medline database with the use of the following key words: teduglutide, glucagon-like peptide-2, CD and inflammatory bowel disease. Based on available data, it can be concluded that this agent seems to be a promising medication in CD and further trials are required to define the place of teduglutide in treatment of CD. Drug Warnings Based on the pharmacologic activity and findings in animals, Gattex has the potential to cause hyperplastic changes including neoplasia. In patients at increased risk for malignancy, the clinical decision to use Gattex should be considered only if the benefits outweigh the risks. In patients with active gastrointestinal malignancy (GI tract, hepatobiliary, pancreatic), Gattex therapy should be discontinued. In patients with active non-gastrointestinal malignancy, the clinical decision to continue Gattex should be made based on risk-benefit considerations. Adverse effects reported in controlled clinical trials in 5% or more of patients receiving teduglutide at the recommended dosage for the management of short bowel syndrome, and occurring more frequently with the drug than with placebo, include GI stomal complication (in patients with a stoma), abdominal pain, upper respiratory tract infection, nausea, abdominal distention, vomiting, fluid overload, flatulence, hypersensitivity, appetite disorder, sleep disturbance, cough, and skin hemorrhage. Across all clinical studies of the drug, injection site reactions and headache also were reported frequently. Teduglutide may increase intestinal absorption of drugs and should be used with caution in patients receiving concomitant oral therapy with CNS agents (e.g., benzodiazepines, antipsychotic agents), drugs that require dosage titration, or drugs that have a narrow therapeutic index. Teduglutide increases fluid absorption, which can precipitate or exacerbate congestive heart failure. Both fluid overload and congestive heart failure have been reported in clinical trials in patients receiving teduglutide. In controlled clinical trials, fluid overload was reported in 9 of 77 patients (11.7%) receiving teduglutide 0.05 mg/kg daily and 4 of 59 patients (6.8%) receiving placebo. Fluid status should be monitored routinely and parenteral support volume adjusted accordingly. Patients with cardiovascular disease (e.g., cardiac insufficiency, hypertension) should be monitored for fluid overload, especially during initiation of teduglutide therapy. If fluid overload occurs, parenteral support volume should be reduced and teduglutide therapy should be reassessed, especially in patients with cardiovascular disease. If clinically important cardiac deterioration occurs, the need for continued therapy with teduglutide should be reassessed. For more Drug Warnings (Complete) data for Teduglutide (14 total), please visit the HSDB record page. Pharmacodynamics An enhancement of gastrointestinal fluid absorption (750-1000 mL/day) was observed following daily administrations of teduglutide. An increase in villus height and crypt depth of the intestinal mucosa was also noted. A decrease in fecal weight has also been observed. Teduglutide does not prolong the QTc interval. |
| Exact Mass |
3750.802
|
|---|---|
| CAS # |
287714-30-1
|
| PubChem CID |
16139605
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| Appearance |
Typically exists as solid at room temperature
|
| LogP |
-15.2
|
| Hydrogen Bond Donor Count |
55
|
| Hydrogen Bond Acceptor Count |
60
|
| Rotatable Bond Count |
126
|
| Heavy Atom Count |
264
|
| Complexity |
9030
|
| Defined Atom Stereocenter Count |
38
|
| SMILES |
CC[C@H](C)[C@@H](C(=O)N[C@@H]([C@@H](C)O)C(=O)N[C@@H](CC(=O)O)C(=O)O)NC(=O)[C@H](CCCCN)NC(=O)[C@H]([C@@H](C)O)NC(=O)[C@H](CCC(=O)N)NC(=O)[C@H]([C@@H](C)CC)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC1=CNC2=CC=CC=C21)NC(=O)[C@H](CC(=O)N)NC(=O)[C@H]([C@@H](C)CC)NC(=O)[C@H](CC3=CC=CC=C3)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](C)NC(=O)[C@H](C)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC(=O)N)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H](CC(C)C)NC(=O)[C@H]([C@@H](C)CC)NC(=O)[C@H]([C@@H](C)O)NC(=O)[C@H](CC(=O)N)NC(=O)[C@H](CCSC)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H](CO)NC(=O)[C@H](CC4=CC=CC=C4)NC(=O)[C@H](CO)NC(=O)CNC(=O)[C@H](CC(=O)O)NC(=O)CNC(=O)[C@H](CC5=CN=CN5)N
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| InChi Key |
CILIXQOJUNDIDU-ASQIGDHWSA-N
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| InChi Code |
InChI=1S/C164H252N44O55S/c1-21-77(11)126(156(255)187-95(44-46-114(167)214)141(240)206-130(83(17)211)160(259)186-93(42-33-34-49-165)140(239)202-129(80(14)24-4)159(258)208-131(84(18)212)161(260)200-111(163(262)263)66-125(230)231)203-151(250)100(54-76(9)10)189-145(244)103(57-88-67-175-92-41-32-31-40-90(88)92)192-147(246)105(60-116(169)216)199-157(256)127(78(12)22-2)204-152(251)102(56-87-38-29-26-30-39-87)190-149(248)109(64-123(226)227)195-137(236)94(43-35-50-174-164(171)172)183-134(233)82(16)179-133(232)81(15)180-142(241)98(52-74(5)6)188-146(245)104(59-115(168)215)194-150(249)110(65-124(228)229)196-143(242)99(53-75(7)8)198-158(257)128(79(13)23-3)205-162(261)132(85(19)213)207-153(252)106(61-117(170)217)193-139(238)97(48-51-264-20)185-138(237)96(45-47-120(220)221)184-148(247)108(63-122(224)225)197-155(254)113(72-210)201-144(243)101(55-86-36-27-25-28-37-86)191-154(253)112(71-209)182-119(219)70-177-136(235)107(62-121(222)223)181-118(218)69-176-135(234)91(166)58-89-68-173-73-178-89/h25-32,36-41,67-68,73-85,91,93-113,126-132,175,209-213H,21-24,33-35,42-66,69-72,165-166H2,1-20H3,(H2,167,214)(H2,168,215)(H2,169,216)(H2,170,217)(H,173,178)(H,176,234)(H,177,235)(H,179,232)(H,180,241)(H,181,218)(H,182,219)(H,183,233)(H,184,247)(H,185,237)(H,186,259)(H,187,255)(H,188,245)(H,189,244)(H,190,248)(H,191,253)(H,192,246)(H,193,238)(H,194,249)(H,195,236)(H,196,242)(H,197,254)(H,198,257)(H,199,256)(H,200,260)(H,201,243)(H,202,239)(H,203,250)(H,204,251)(H,205,261)(H,206,240)(H,207,252)(H,208,258)(H,220,221)(H,222,223)(H,224,225)(H,226,227)(H,228,229)(H,230,231)(H,262,263)(H4,171,172,174)/t77-,78-,79-,80-,81-,82-,83+,84+,85+,91-,93-,94-,95-,96-,97-,98-,99-,100-,101-,102-,103-,104-,105-,106-,107-,108-,109-,110-,111-,112-,113-,126-,127-,128-,129-,130-,131-,132-/m0/s1
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| Chemical Name |
(2S)-2-[[(2S,3R)-2-[[(2S,3S)-2-[[(2S)-6-amino-2-[[(2S,3R)-2-[[(2S)-5-amino-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[(2S,3R)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]acetyl]amino]-3-carboxypropanoyl]amino]acetyl]amino]-3-hydroxypropanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-4-carboxybutanoyl]amino]-4-methylsulfanylbutanoyl]amino]-4-oxobutanoyl]amino]-3-hydroxybutanoyl]amino]-3-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-4-oxobutanoyl]amino]-4-methylpentanoyl]amino]propanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-carboxypropanoyl]amino]-3-phenylpropanoyl]amino]-3-methylpentanoyl]amino]-4-oxobutanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-4-methylpentanoyl]amino]-3-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-hydroxybutanoyl]amino]hexanoyl]amino]-3-methylpentanoyl]amino]-3-hydroxybutanoyl]amino]butanedioic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
An Extension Study of Teduglutide in Japanese Participants With Short Bowel Syndrome Who Completed 24 Weeks of Treatment in SHP633-306 or TED-C14-004
CTID: NCT03596164
Phase: Phase 3 Status: Completed
Date: 2023-03-15
Products are for research use only; We do not sell to patients
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