Teduglutide targets the glucagon-like peptide-2 receptor (GLP-2R), which is a G protein-coupled receptor 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-1 (IGF-1), nitric oxide, and keratinocyte growth factor (KGF). Teduglutide also activates the expression of nuclear receptor subfamily 4 group A member 1 (NR4a1/nur77) and intestinal farnesoid X receptor (FXR) signaling in human hepatic stellate cells. Through GLP-2R binding, teduglutide stimulates cellular proliferation and inhibits apoptosis in intestinal epithelial cells, leading to increased mucosal surface area.

In vitro, teduglutide (2.5 μM, 36 hours) activates the expression of NR4a1/nur77 in human hepatic stellate cells. It increases the proliferation and decreases apoptosis of all intestinal epithelial cells in the short intestinal neonatal piglet model. Teduglutide promotes the proliferation of intestinal epithelial cells through activation of the GLP-2 receptor signaling pathway, which stimulates cellular proliferation and inhibits apoptosis. These in vitro activities demonstrate the compound's direct effects on intestinal cell survival and growth, which underlie its therapeutic efficacy in short bowel syndrome.

In vivo, teduglutide has demonstrated significant efficacy in multiple animal models. In Mdr2⁻/⁻ mice, treatment with teduglutide via intraperitoneal injection improved liver inflammation, fibrosis, and reactive bile duct cell phenotypes. It promotes Fxr-Fgf15/19 signaling in the gut, resulting in decreased Cyp7a1 and increased Cyp2c70 expression in the liver, contributing to hepatoprotective and antifibrotic effects. In a neonatal piglet model of short bowel syndrome, teduglutide (0.1 mg/kg/day) improved mucosal surface area and acute nutrient handling capacity. In clinical studies, teduglutide decreased stomal output or fecal fluid and macronutrient excretion, resulted in enhanced gastrointestinal fluid absorption of approximately 750-1000 mL/day, and increased villus height and crypt depth of the intestinal mucosa.

Non-cellular enzyme/receptor binding assays for teduglutide typically involve measuring its binding affinity to the GLP-2 receptor using surface plasmon resonance (SPR) or radioligand binding assays. In a typical SPR assay, recombinant GLP-2 receptor protein is immobilized on a sensor chip, and varying concentrations of teduglutide are flowed over the chip. The association and dissociation rates are measured, and the equilibrium dissociation constant (KD) is calculated. Alternatively, competitive binding assays using radiolabeled GLP-2 and membrane preparations from cells overexpressing the GLP-2 receptor can be employed to determine the IC50 for displacement of the labeled ligand.

In vitro cellular assays for teduglutide typically employ intestinal epithelial cell lines or primary intestinal epithelial cells to assess proliferation and anti-apoptotic effects. Cells are seeded in multi-well plates and treated with various concentrations of teduglutide for 24-72 hours. Cell proliferation is assessed using BrdU incorporation assays, MTT assays, or cell counting. Apoptosis is evaluated by flow cytometry using Annexin V/PI staining or by measuring caspase-3/7 activity. The expression of proliferation markers (e.g., Ki-67) and anti-apoptotic proteins (e.g., Bcl-2) can be analyzed by Western blotting or immunofluorescence.

In vivo animal studies for teduglutide typically utilize rodent models of intestinal resection or short bowel syndrome. In the neonatal piglet model, ileojejunal resection is performed, and teduglutide is administered subcutaneously at doses of 0.1 mg/kg/day. In Mdr2⁻/⁻ mouse models of sclerosing cholangitis, teduglutide is administered via intraperitoneal injection. Efficacy endpoints include measurement of intestinal mucosal surface area, villus height, crypt depth, and nutrient absorption capacity. Liver inflammation and fibrosis are assessed by histological analysis and measurement of serum biomarkers. Body weight, stool output, and fluid balance are also monitored as functional outcomes.

Absorption, Distribution and Excretion
The pharmacokinetic characteristics of terduglutide administered subcutaneously conform to a one-compartment model, with first-order kinetics in the abdomen, arm, and thigh. The pharmacokinetics of terduglutide exhibit a linear relationship with increasing dose. The absolute bioavailability after subcutaneous injection is 88%; the time to peak concentration (Tmax) after subcutaneous injection is 3–5 hours; the peak plasma concentration (Cmax) in patients with short bowel syndrome (SBS) after subcutaneous injection of 0.05 mg/kg is 36 ng/mL; the area under the curve (AUC) in patients with short bowel syndrome (SBS) after subcutaneous injection of 0.05 mg/kg is 0.15 µg•hr/mL; terduglutide does not accumulate after multiple subcutaneous injections.
Urine
Volume of distribution (Vd), healthy subjects = 103 mL/kg
Plasma clearance, healthy subjects = 123 mL/hr/kg; this value indicates that terdugraftide is primarily cleared by the kidneys.
In healthy subjects, the volume of distribution of terdugraftide (103 mL/kg) is similar to that of blood volume.
In healthy subjects, the absolute bioavailability of subcutaneously administered Gattex is 88%, with peak plasma terdugraftide concentrations reached 3–5 hours after administration. In patients with short bowel syndrome (SBS), after subcutaneous administration of a dose of 0.05 mg/kg, the median peak concentration (Cmax) of terdugraftide was 36 ng/mL, and the median area under the curve (AUC0-inf) was 0.15 μghr/mL. No accumulation of terdugraftide was observed after repeated subcutaneous administration.
/Breast milk/ It is unclear whether Gattex is present in human breast milk. Terdugratide is secreted into the milk of lactating rats, with the highest concentration detected in milk after a single subcutaneous injection of 25 mg/kg being 2.9% of the plasma concentration. Terdugratide is a recombinant analog of human glucagon-like peptide-2 and has recently been approved for the treatment of short bowel syndrome in adults. This study aimed to investigate the effects of renal function and age on the pharmacokinetics of terdugratide. This was an open-label study with six parallel groups (6 subjects per group). Three renal impairment groups (moderate, severe, and end-stage renal disease) were compared with healthy subjects with normal renal function, and the baseline characteristics of the healthy subjects were matched to those of the renal impairment groups. At least two elderly subjects (≥65 years) were included in each group. Each subject received a single subcutaneous injection of 10 mg terdugratide. Plasma concentrations of terdugratide were determined using validated liquid chromatography-tandem mass spectrometry, and the main pharmacokinetic parameters (AUCinf and Cmax) were calculated. Patients with end-stage renal disease had approximately 2.59-fold and 2.08-fold higher area under the concentration-time curve (AUCinf) and maximum plasma concentration (Cmax) of terdugraft, respectively, compared to healthy subjects. Patients with moderate to severe renal impairment also showed slightly higher AUCinf and Cmax. Comparison of healthy subjects <65 years of age and older healthy subjects revealed very similar pharmacokinetic characteristics between the two groups. In this study population, the major pharmacokinetic parameters of terdugraft increased with increasing renal impairment. These results suggest that the daily dose of terdugraft should be reduced by 50% for patients with moderate to severe renal impairment and end-stage renal disease. We found that age had no effect on the pharmacokinetics of terdugraft in healthy subjects. Treatment was well tolerated, and no safety issues were observed.

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Metabolism/Metabolites
Although formal studies have not been conducted, as terdugraft is a peptide drug, it is expected to degrade 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 terduglutide has not been studied in humans. However, it is expected that terduglutide will be degraded into small peptides and amino acids via a catabolic pathway, similar to the catabolic metabolism of endogenous GLP-2.

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Biological Half-Life
The terminal half-life in healthy subjects is 2 hours; terminal half-life in SBS patients = 1.3 hours. The mean terminal half-life of terduglutide in healthy subjects is approximately 2 hours, and the mean terminal half-life in patients with short bowel syndrome (SBS) is 1.3 hours.
Pharmacokinetic properties of teduglutide are well-characterized from clinical studies. Due to the single amino acid substitution at the N-terminus, teduglutide is resistant to DPP-IV-mediated degradation, resulting in an extended half-life compared to native GLP-2. Following subcutaneous administration, teduglutide is absorbed and reaches peak plasma concentrations within 3-5 hours. The terminal half-life is approximately 1.3 hours in humans. Teduglutide is metabolized via proteolytic degradation into smaller peptides and amino acids, similar to endogenous GLP-2. Renal clearance is the primary route of elimination for the peptide fragments. The compound is administered as a once-daily subcutaneous injection at a dose of 0.05 mg/kg.

Toxicity Summary
Identification and Use: Terdugranitide is a biosynthetic (recombinant DNA-derived) analog of human glucagon-like peptide-2 (GLP-2), a pleiotropic hormone that promotes intestinal mucosal growth and affects intestinal function. This product is indicated for the treatment of adult patients with short bowel syndrome (SBS) who require parenteral nutrition support. Human Exposure and Toxicity: Based on pharmacological activity and studies in animals, this drug may cause proliferative changes, including tumors. In clinical studies, gastrointestinal polyps (e.g., colorectal polyps, duodenal polyps, and peristomal polyps, including hyperplastic polyps and villous adenomas) have been detected in patients treated with this drug. Several patients treated with terdugranitide have reported malignant tumors, including one patient who had previously received abdominal radiotherapy for Hodgkin's lymphoma and developed metastatic adenocarcinoma of unknown origin, and two patients with a history of smoking and developed lung cancer (squamous cell carcinoma and non-small cell carcinoma). Animal studies: In a two-year carcinogenicity study, subcutaneous injections of terduglutide in rats at doses of 3, 10, and 35 mg/kg/day (approximately 60, 200, and 700 times the recommended human daily dose of 0.05 mg/kg, respectively) significantly increased the incidence of bile duct and jejunal adenomas in male rats. In a two-year carcinogenicity study in mice, subcutaneous injections of terduglutide at doses of 1, 3.5, and 12.5 mg/kg/day (approximately 20, 70, and 250 times the recommended human daily dose of 0.05 mg/kg, respectively) significantly increased the incidence of papillary adenomas of the gallbladder; at a high dose of 12.5 mg/kg/day (approximately 250 times the recommended human dose), it also induced jejunal adenocarcinoma in male mice. Animal studies have shown that subcutaneous injection of terduglutide at doses up to 50 mg/kg/day (approximately 1000 times the recommended human daily dose of 0.05 mg/kg) has no effect on embryo-fetal development in pregnant rats and rabbits. A rat prenatal and postnatal development study showed that subcutaneous injection of terduglutide at doses up to 50 mg/kg/day (approximately 1000 times the recommended human daily dose of 0.05 mg/kg) had no adverse effects on prenatal and postnatal development. Furthermore, subcutaneous injection of terduglutide at doses up to 50 mg/kg/day (approximately 1000 times the recommended human daily dose of 0.05 mg/kg) also had no adverse effects on fertility and reproductive function in male and female rats. Terduglutide was negative in the Ames test, the Chinese hamster ovary cell chromosomal aberration test, and the in vivo mouse micronucleus test.

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Effects during pregnancy and lactation
◉ Overview of use during lactation
Because Teduglutide is a large protein molecule with a molecular weight of 3752 Da, its concentration in breast milk is likely to be very low. Furthermore, Teduglutide has a low oral absorption rate, so it is unlikely to be absorbed by breastfed infants. Two breastfed infants appeared to have no adverse effects while their mothers were using Teduglutide, but long-term data are currently unavailable. Infants should be closely monitored during breastfeeding when using Teduglutide until more data are available.
◉ Effects on breastfed infants
One mother used Teduglutide during pregnancy and postpartum lactation. She breastfed her infant for 6 months (breastfeeding duration not specified). No adverse effects on the infant were reported.
A woman who took Teduglutide due to partial gastrointestinal resection became pregnant and delivered a healthy infant. She breastfed her infant and restarted the medication 1 month postpartum. During treatment, she breastfed her infant for 4 months (feeding extent not specified). The infant experienced no side effects during breastfeeding.
◉ Effects on breastfeeding and breast milk
As of the revision date, no relevant published information was found.

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Drug Interactions
Tetugglutide may increase intestinal absorption of the drug and should therefore be used with caution in patients receiving oral treatment with central nervous system medications (e.g., benzodiazepines, antipsychotics), medications requiring dose adjustment, or medications with a narrow therapeutic index.
Toxicological data for teduglutide are well-established from clinical trials and post-marketing surveillance. Teduglutide is generally well-tolerated. Common adverse effects include gastrointestinal symptoms such as abdominal pain, nausea, and diarrhea, as well as injection site reactions, headache, and upper respiratory tract infections. Serious adverse effects are rare but may include intestinal obstruction, gallbladder disease, and pancreatitis. Long-term studies have not demonstrated significant carcinogenic risk, but monitoring for colorectal polyps is recommended. Teduglutide is contraindicated in patients with a history of malignancy of the gastrointestinal tract and in patients with known hypersensitivity to the drug or its components.

[1].Teduglutide (ALX-0600), a dipeptidyl peptidase IV resistant glucagon-like peptide 2 analogue, improves intestinal function in short bowel syndrome patients. Gut. 2005 Sep;54(9):1224-31.

[2].Teduglutide Study Group. Teduglutide, a novel mucosally active analog of glucagon-like peptide-2 (GLP-2) for the treatment of moderate to severe Crohn's disease. Inflamm Bowel Dis. 2010 Jun;16(6):962-73.

Teduglutide is a polypeptide composed of 33 amino acid residues with the following sequence: 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. It is a glucagon-like peptide-2 receptor agonist used to treat short bowel syndrome. Teduglutide has multiple functions, including acting as a glucagon-like peptide-2 receptor agonist, a metabolite, an antioxidant, and a protectant. Teduglutide is a glucagon-like peptide-2 (GLP-2) analog. It consists of 33 amino acids and is produced using recombinant DNA technology-modified E. coli strains. Teduglutide differs from GLP-2 only in one amino acid (alanine is replaced by glycine). The significance of this amino acid substitution is that terdulglutide has a longer duration of action than endogenous GLP-2 because it is more resistant to the proteolytic activity of dipeptidyl peptidase-4. The FDA approved it on December 21, 2012.

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Drug Indications
Terdulglutide is indicated for the treatment of adult and pediatric patients aged 1 year and older who require parenteral nutrition support for short bowel syndrome (SBS).
FDA Label
Revestive is indicated for the treatment of patients aged 1 year and older with short bowel syndrome (SBS). Patients should be stable after a period of bowel adaptation post-surgery. Revestive is indicated for the treatment of patients aged 1 year and older with short bowel syndrome. Patients should be stable after a period of bowel adaptation post-surgery.
Treatment of Short Bowel Syndrome

Mechanism of Action

Tedugglutide is an analogue of natural human glucagon-like peptide-2 (GLP-2), a peptide secreted by L cells in the distal intestine after eating. GLP-2 increases intestinal and portal venous blood flow and inhibits gastric acid secretion. Tedugglutide binds to glucagon-like peptide-2 receptors located in enteroendocrine cells, submucosal myofibroblasts, and enteric neurons in the submucosal and myenteric plexuses. This leads to the release of insulin-like growth factor (IGF)-1, nitric oxide, and keratinocyte growth factor (KGF). These growth factors may contribute to increasing the growth and surface area of gastric mucosal crypt cells. Ultimately, intestinal absorption is enhanced.
Compared to natural GLP-2, tedugglutide has a similar affinity for the human and rat GLP-2 receptor (GLP-2R). Receptor binding leads to increased intracellular cyclic adenosine monophosphate (cAMP) levels and activates multiple downstream signaling pathways, such as protein kinase A (PKA), cAMP response element-binding protein (CREB), and activator protein-1 (AP-1). Terdugratin's potency against GLP-2R is comparable to that of natural GLP-2, but its enhanced biological activity, resulting in a prolonged circulating half-life, is due to its resistance to DPP-IV cleavage. Terdugratin is an analog of natural human glucagon-like peptide-2 (GLP-2), a peptide secreted by L cells in the distal intestine. GLP-2 is known to increase intestinal and portal venous blood flow and inhibit gastric acid secretion. Terdugratin binds to glucagon-like peptide-2 receptors located in intestinal endocrine cell subsets, submucosal myofibroblasts, and enteric neurons in the submucosal and myenteric plexus. Activation of these receptors leads to the local release of various mediators, including insulin-like growth factor (IGF)-1, nitric oxide, and keratinocyte growth factor (KGF).

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Therapeutic Use
/Clinical Trials/ ClinicalTrials.gov is a registry and results database that lists publicly and privately funded human clinical studies conducted worldwide. The website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov provides summary information on the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure under investigation); the title, description, and design of the study; participation requirements (eligibility criteria); the location of the study; contact information for the study location; and links to relevant information from other health websites, such as the NLM's MedlinePlus (for patient health information) and PubMed (for citations and abstracts of academic articles in the medical field). The database contains terdugraftide.
Tettex for injection (recombinant DNA source) is indicated for the treatment of adult patients with short bowel syndrome (SBS) who require parenteral nutrition support. /Included on US product labels/
/Therapeutic Use/ Currently available medications for treating Crohn's disease (CD) include aminosalicylates, corticosteroids, antibiotics, immunomodulators, and biologics (infliximab, cetrus, adalimumab, and natezumab). These drugs primarily target the immune and inflammatory pathways of Crohn's disease (CD), while drugs targeting the impaired intestinal barrier function in CD patients are scarce. Glucagon-like peptide-2 (GLP-2) is an incretin with significant nutritional effects on the intestinal mucosa. Teduglutide, an analogue of GLP-2, has been approved by the US Food and Drug Administration (FDA) for the treatment of short bowel syndrome. This article explores the potential use of teduglutide in CD patients. Due to the limited number of randomized, placebo-controlled trials currently available on teduglutide for CD, data on its efficacy in treating CD are lacking. This article uses the Medline database, searching for keywords including: teduglutide, GLP-2, CD, and inflammatory bowel disease. Based on the available data, it can be concluded that this drug appears to be a promising treatment for CD, but further trials are needed to determine the role of terduglutide in CD treatment.

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Drug Warnings
Based on animal pharmacological activity and study results, Gattex may cause proliferative changes, including tumorigenesis. For patients at high risk of malignancy, Gattex should only be considered when the benefits outweigh the risks. For patients with active gastrointestinal malignancies (gastrointestinal tract, hepatobiliary, pancreas), Gattex treatment should be discontinued.
For patients with active non-gastrointestinal malignancies, the clinical decision on whether to continue using Gattex should be based on a risk-benefit ratio consideration. In controlled clinical trials of terdugraftide at the recommended dose for short bowel syndrome, adverse reactions were reported in 5% or more of patients, with a higher incidence in the treatment group than in the placebo group. These adverse reactions included gastrostomy complications (in patients with an ostomy), abdominal pain, upper respiratory tract infection, nausea, abdominal distension, vomiting, fluid retention, flatulence, allergic reactions, appetite disturbances, sleep disturbances, cough, and skin bleeding. Reports of injection site reactions and headache were also common in all clinical studies. Terdugraftide may increase intestinal absorption and should therefore be used with caution in patients concurrently receiving oral central nervous system medications (e.g., benzodiazepines, antipsychotics), medications requiring dose adjustment, or medications with a narrow therapeutic index. Terdugraftide increases fluid absorption, which may induce or exacerbate congestive heart failure. Fluid overload and congestive heart failure have been reported in patients receiving terdugraftide in clinical trials. In controlled clinical trials, 9 out of 77 patients (11.7%) receiving 0.05 mg/kg terdugraft daily reported fluid overload, compared to 4 out of 59 patients (6.8%) receiving placebo. Fluid status should be routinely monitored, and parenteral nutrition support adjusted accordingly. Patients with cardiovascular disease (e.g., heart failure, hypertension) should be monitored for fluid overload, especially during the initiation of terdugraft treatment. If fluid overload occurs, parenteral nutrition support should be reduced, and terdugraft treatment should be reassessed, especially in patients with cardiovascular disease. If clinically significant deterioration of cardiac function occurs, the need for continued terdugraft treatment should be reassessed. For more complete (14) drug warnings regarding terdugraft, please visit the HSDB record page.

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Pharmacodynamics
After daily administration of terdugraftide, increased gastrointestinal fluid absorption (750-1000 mL/day) was observed. Increased intestinal villus height and crypt depth were also observed. Furthermore, decreased stool weight was observed. Terdugraftide does not prolong the QTc interval.

Teduglutide is an FDA-approved therapeutic agent (marketed as REVESTIVE®) for the treatment of short bowel syndrome in adult patients who are dependent on parenteral nutrition. It was first approved by the FDA in 2012. The compound is also being investigated in clinical trials for other indications including intestinal failure, Crohn's disease, and sclerosing cholangitis. Teduglutide represents a significant advance in the management of short bowel syndrome, offering patients the potential to reduce or eliminate parenteral nutrition dependence. The mechanism of action involves GLP-2 receptor-mediated promotion of intestinal adaptation, including increased villus height and crypt depth, enhanced nutrient absorption, and reduced intestinal motility and gastric acid secretion. The compound is supplied as a lyophilized powder for reconstitution and is administered via subcutaneous injection.

C164H252N44O55S

3752.08247999998

3749.8

197922-42-2

Teduglutide TFA

16139605

H-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-Asp-OH
L-histidyl-glycyl-L-alpha-aspartyl-glycyl-L-seryl-L-phenylalanyl-L-seryl-L-alpha-aspartyl-L-alpha-glutamyl-L-methionyl-L-asparagyl-L-threonyl-L-isoleucyl-L-leucyl-L-alpha-aspartyl-L-asparagyl-L-leucyl-L-alanyl-L-alanyl-L-arginyl-L-alpha-aspartyl-L-phenylalanyl-L-isoleucyl-L-asparagyl-L-tryptophyl-L-leucyl-L-isoleucyl-L-glutaminyl-L-threonyl-L-lysyl-L-isoleucyl-L-threonyl-L-aspartic acid

HGDGSFSDEMNTILDNLAARDFINWLIQTKITD

White to off-white solid powder

1.016

55

60

126

264

9030

38

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

CILIXQOJUNDIDU-ASQIGDHWSA-N

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

(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

Teduglutide; ALX-0600; ALX0600; Gattex; 197922-42-2; revestive;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~13.33 mM)
H2O : ~22.22 mg/mL (~5.92 mM)

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.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*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).

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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)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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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).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)