PTH (IC50 = 2 nM)[1]; Teriparatide targets and binds to the parathyroid hormone 1 receptor (PTH1R, Gene ID:5745). PTH1R is a G protein-coupled receptor (GPCR) expressed on osteoblasts and bone stromal cells. As a PTH1R agonist, teriparatide exerts its effects by activating the cyclic AMP (cAMP) signaling pathway and the bone anabolic signaling pathway.
Teriparatide targets and activates the parathyroid hormone type 1 receptor (PTH1R), a G protein-coupled receptor (GPCR) expressed on osteoblasts and bone stromal cells. Activation of PTH1R stimulates the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway, which promotes bone formation. When administered intermittently, this results in net bone anabolism, increased bone mineral density (BMD), and reduced fracture risk.

Teriparatide is a polypeptide that acts as a PTH1 receptor agonist. It can also cause cancer according to state or federal government labeling requirements. It is a polypeptide that consists of the 1-34 amino-acid fragment of human PARATHYROID HORMONE, the biologically active N-terminal region. The acetate form is given by intravenous infusion in the differential diagnosis of HYPOPARATHYROIDISM and PSEUDOHYPOPARATHYROIDISM.

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In HEK293 cells, teriparatide acetate acts as a PTH1R agonist with an IC₅₀ value of 2 nM. In vitro studies demonstrate that teriparatide does not directly act on regulatory T cells (Tregs) but may regulate their number and function through indirect mechanisms. In cultured human peripheral blood CD4⁺CD25⁺ T cells, teriparatide treatment failed to increase the relative number of Tregs or induce TGFβ mRNA expression, suggesting an indirect mechanism of action mediated by the in vivo microenvironment.

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In cell-based assays, teriparatide activates PTH1R with high potency, stimulating intracellular cAMP production. It enhances the expression of osteogenic markers, including alkaline phosphatase (ALP), osteocalcin (OCN), collagen type I alpha 2 (COL1A2), bone sialoprotein, and Runx2, promoting osteoblast differentiation and bone matrix mineralization.

Teriparatide acetate hydrate, also known as human parathyroid hormone-(1-34) acetate hydrate, enhances cortical thickness and porosity in female New Zealand white rabbits (20 μg/kg IV; once daily for 4 weeks)[1].

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In an orchiectomized (testicular excision) rat model, intermittent administration of teriparatide (PTH 1-34, 0.5 μg/kg/day for 60 days) significantly promoted peri-implant bone repair. Treated animals exhibited bone volume fraction (BV/TV), trabecular thickness (Tb.Th), and bone-implant contact (BIC) parameters restored to healthy control levels, with bone turnover markers (mineral apposition rate, neoformed bone area) significantly higher than untreated osteoporotic animals. In mouse models, intermittent PTH treatment increased regulatory T cell numbers by approximately 2-3 fold; blocking this Treg increase prevented PTH-induced bone formation and trabecular bone volume improvement. Teriparatide (10 or 40 mg/kg for 4 weeks) significantly increased trabecular bone calcium content by approximately 70% and 123%. In human clinical trials, teriparatide treatment for 6 months significantly increased both absolute and relative numbers of circulating regulatory T cells, along with elevated TGFβ1 mRNA levels in Tregs.

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In ovariectomized (OVX) rat models of estrogen-deficiency-induced osteopenia, daily subcutaneous administration of teriparatide (5-15 μg/kg) dose-dependently increases bone formation marker gene expression, trabecular bone area, cortical thickness, bone mineral content (BMC), bone mineral density (BMD), and bone strength, confirming its bone anabolic efficacy.

Radioligand binding assays are commonly used to evaluate the binding affinity of teriparatide to PTH1R in cell-free systems. Using ¹²⁵I-labeled PTH(1-34) analog as a tracer, the compound competes with the radioligand for binding to cell membrane preparations expressing PTH1R. After incubation, bound and free radioligands are separated by filtration or centrifugation, and radioactivity is measured to calculate the half-maximal inhibitory concentration (IC₅₀) or dissociation constant (Kd), assessing the binding affinity of teriparatide to the receptor.

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The binding activity of teriparatide to PTH1R is typically measured using a functional enzyme-linked immunosorbent assay (ELISA) with immobilized PTH1R. Alternatively, bioluminescence resonance energy transfer (BRET)-based assays employing tetramethylrhodamine-labeled agonist peptides enable direct kinetic and thermodynamic characterization of ligand-receptor interactions. In competitive ELISA formats, a 96-well plate pre-coated with anti-teriparatide antibody is incubated with standards/samples and biotin-labeled teriparatide, which competitively bind to the antibody. Unbound material is removed by washing, followed by addition of streptavidin-HRP and substrate, with color development inversely proportional to teriparatide concentration.

To evaluate the direct effect of teriparatide on regulatory T cells, human peripheral blood CD4⁺CD25⁺ T cells are cultured in vitro for 6 days in the presence of anti-CD3 antibody and IL-2. Teriparatide or vehicle is added every 2 days for 1 or 24 hours. Following culture, the proportion of CD4⁺CD25⁺Foxp3⁺ cells is assessed by flow cytometry to evaluate Treg number, and TGFβ mRNA expression levels are measured to assess Treg function. Results demonstrate that teriparatide does not directly increase Treg number or function in vitro.

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A rat osteosarcoma cell line (UMR-106) expressing PTH1R is treated with various concentrations of teriparatide. Following incubation, intracellular cyclic adenosine monophosphate (cAMP) levels are quantitatively measured using a time-resolved fluoroimmunoassay (TRFIA). A four-parameter logistic regression analysis is then used to calculate the relative biological potency of teriparatide samples. Optimized conditions and validated parameters, including specificity, relative accuracy (bias -0.8% to +1.4%), precision (geometric CV 2.0-3.5%), and linearity (R² = 0.9953 over range 50-150% of target concentration), ensure the method is suitable for quality control and lot release testing.

Animal/Disease Models: Female New Zealand White Rabbit[1]
Doses: 20 μg/kg
Route of Administration: subcutaneous injection; one time/day for 4 weeks
Experimental Results: Increased porosity, number and density as well as cortical area, thickness and bone mineral content ( BMC), but had no significant effect on volumetric bone mineral density (BMD).

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Forty-two female New Zealand white rabbits (17–21 weeks old) were housed in an animal room (temperature, 19 °C; humidity, 50 %; and a 12-h on/off light cycle) with free access to water. Rabbits were fed a chow diet (RC-4, 120 g/day). After 10 days of adaptation to their new environment, the rabbits (18–22 weeks old) were randomized into six groups of 7 animals each using the stratified weight method, as follows: 4-week vehicle administration group (4W-Veh), 4-week Teriparatide (TPTD) administration group (4W-TPTD: 20 μg/kg, subcutaneously [s.c.], daily), 12-week vehicle administration group (12W-Veh), 4-week TPTD administration + 8-week vehicle administration group (4W-TPTD + 8W-Veh), 4-week TPTD administration + 8-week lower-dose IBN administration group (4W-TPTD + 8W-IBN(L): 20 μg/kg of IBN, s.c., every 4 weeks), and 4-week TPTD administration + 8-week higher-dose IBN administration group (4W-TPTD + 8W-IBN(H): 100 μg/kg of IBN, s.c., every 4 weeks). The TPTD (human recombinant teriparatide) dose was selected based on the results of a previous rabbit study. The IBN doses were determined based on the results of previous ovariectomized monkey studies. Body weight was monitored weekly.[1]

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To evaluate the effect of teriparatide on peri-implant bone repair, an orchiectomized Wistar rat model is employed. Animals are divided into 3 groups: sham-operated control (SHAM), orchiectomized (ORQ), and orchiectomized with teriparatide treatment (TERI). Eight animals per group receive implants in the right and left tibial metaphysis. The TERI group receives daily subcutaneous injections of PTH 1-34 (0.5 μg/kg). After 60 days, animals are euthanized, and bone parameters including bone volume fraction (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), and trabecular separation (Tb.Sp) are evaluated by micro-computed tomography. Mineral apposition rate and neoformed bone area are assessed by laser confocal microscopy, and histological evaluation is performed using Stevenel blue and alizarin red staining.

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In a typical efficacy study, six-month-old female rats undergo bilateral ovariectomy (OVX) and are allowed to lose bone for two months to establish established osteopenia. Teriparatide or vehicle is then administered by daily subcutaneous injection (5 or 15 μg/kg/day) for 3 to 12 weeks. Bone formation gene expression in the distal femur metaphysis is analyzed by RT-PCR after 3 weeks. After 12 weeks, histomorphometric analysis of the proximal tibial metaphysis and biomechanical testing of the lumbar vertebrae and femur are performed to assess bone formation, bone mass, architecture, and strength. Body weight is monitored regularly, and blood and urine samples are collected for biochemical marker analysis.

Absorption, Distribution, and Excretion
Teriparatide's systemic clearance (approximately 62 L/hr for women and 94 L/hr for men) exceeds normal hepatic plasma flow, consistent with hepatic and extrahepatic clearance pathways. Following intravenous injection, the volume of distribution is approximately 0.12 L/kg. Inter-individual variability in systemic clearance and volume of distribution ranges from 25% to 50%.
Following subcutaneous injection, teriparatide is extensively absorbed; based on pooled data from the 20 μg, 40 μg, and 80 μg dose groups, its absolute bioavailability is approximately 95%. Both absorption and elimination rates are rapid. Peak serum concentrations of the peptide are reached approximately 30 minutes after subcutaneous injection of a 20 μg dose and decrease to unquantifiable concentrations within 3 hours.
Biological Half-Life
The half-life of teriparatide in serum is 5 minutes after intravenous injection and approximately 1 hour after subcutaneous injection. The longer half-life after subcutaneous injection reflects the time required for drug absorption from the injection site.

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In rats, teriparatide acetate is rapidly absorbed into the circulation following subcutaneous administration and is immediately eliminated. In vivo and in vitro studies indicate that the kidneys play a particularly important role in the distribution and metabolism of teriparatide, with kidney radioactivity concentrations exceeding liver concentrations by more than 3-fold. Renal failure affects the pharmacokinetics of teriparatide, resulting in decreased clearance, whereas hepatic failure shows no significant effect. In human volunteers with severe renal impairment (eGFR 15.0-29.9 mL/min/1.73 m²), following a single subcutaneous injection of teriparatide 56.5 μg, the elimination half-life (t₁/₂) is significantly prolonged to 5.0 hours, compared with 1.5 hours in normal-to-mild impairment and 1.2 hours in moderate impairment groups. However, virtually no intact drug is detectable in blood after 24 hours in all subjects. Given the once-weekly administration schedule, drug accumulation in the body is highly unlikely even with repeated dosing.

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Following subcutaneous administration, teriparatide is rapidly absorbed with an absolute bioavailability of approximately 95%. Peak serum concentrations (Cmax) are reached at approximately 30 minutes (median Tmax 0.25 h, range 0.12-1.08 h), with a Cmax of 109.5 ± 62.8 pg/mL and an AUC₀₋ᵢₙf of 149.8 ± 68.1 pg·h/mL. The terminal elimination half-life (t₁/₂) is approximately 0.79 ± 0.35 hours, and concentrations decline to non-quantifiable levels within 3 hours post-dose. Systemic clearance is faster in men (∼94 L/h) than in women (∼62 L/h), suggesting both hepatic and extra-hepatic elimination via non-specific enzymatic proteolysis, followed by renal excretion of fragments. Volume of distribution (Vd) is approximately 0.12 L/kg. Patients with severe renal impairment (CrCl <30 mL/min) show increased AUC and t₁/₂, but no dosing adjustment is recommended based on available data.

Effects during pregnancy and lactation
◉ Overview of medication use during lactation
An infant with congenital hyperparathyroidism was breastfed while the mother was using teriparatide. Breastfeeding appeared to protect the infant from hypoparathyroidism. Serum calcium levels in breastfed infants should be monitored regularly while the mother is receiving teriparatide treatment.
◉ Effects on breastfed infants
A woman with autosomal dominant hypoparathyroidism type 1 (ADH1) received teriparatide treatment during pregnancy at 28 mcg daily via continuous intravenous infusion. She also took 1000 IU of vitamin D3 daily, 400 mg of magnesium oxide twice daily, and 0 to 3 g of calcium carbonate orally based on serum calcium levels. Eight months postpartum, the infusion continued at 27 to 30 mcg daily, and calcitriol was switched to twice daily at 0.5 mcg. She exclusively breastfed her infant for 6 months, then introduced complementary foods until 1 year of age. When the mother started taking calcitriol, the infant's serum calcium levels did not change. The mother began weaning the infant at 11 months of age, and after weaning was completed at 1 year of age, the infant developed hypocalcemia and was diagnosed with ADH1, sharing the same gene mutation as the mother and other family members. During the first year of lactation, the infant's serum parathyroid hormone-related protein levels were within the median of the normal range. A sample taken after weaning showed a significant decrease in these levels. Breastfed infants appear to be protected from severe hypocalcemia during the first year of life by breast milk. At 1.5 years of age, the infant's growth and development were normal.
◉ Effects on breastfeeding and breast milk
As of the revision date, no relevant published information was found.

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In a 6-month human clinical trial, teriparatide treatment was well tolerated with no specific safety concerns reported. However, in real-world clinical applications for osteoporosis patients, adverse events are common. In a cohort study of a twice-weekly dosing regimen (163 patients), gastrointestinal side effects such as heartburn, nausea, and vomiting were the most frequently reported adverse events. The overall treatment discontinuation rate was 47.9%, with 48 patients discontinuing due to adverse events. Other reported adverse events included palpitations or hypotension (9 cases), headache or dizziness (9 cases), anxiety (1 case), and chills (1 case). Treatment discontinuation predominantly occurred within 0-3 months of initiation (accounting for 72.9% of all discontinuations).

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In 2-year carcinogenicity studies in Fischer 344 rats, daily subcutaneous teriparatide produced a marked dose- and duration-dependent increase in the incidence of osteosarcoma (a rare malignant bone tumor), osteoblastoma, and osteoma. At the highest dose (75 mcg/kg/day, achieving 60-fold greater systemic exposure than the human clinical dose), osteosarcoma incidence reached 40-50%. However, teriparatide was not genotoxic in standard mutagenicity assays, including the Ames test, mouse lymphoma assay, Chinese hamster ovary cell chromosomal aberration assay, or in vivo mouse micronucleus test. No bone tumors were observed in long-term monkey studies. Fertility was not impaired in rats at doses up to 300 mcg/kg/day. Common clinical adverse events from FAERS analysis include pain in extremity (PRR 4.54), muscle spasm (PRR 5.11), fracture (PRR 17.67-552.95), hypercalcemia (PRR 50.73), and nausea (5.1%).

[1]. Influence of Teriparatide and Ibandronate on Cortical Bone in New Zealand White Rabbits: A HR-QCT Study. Calcif Tissue Int. 2016 Nov;99(5):535-542.

Teriparatide (TPTD) is known to increase cortical bone thickness and porosity. This study aimed to investigate whether replacing TPTD with ibandronate (IBN) in an adult rabbit model could improve cortical bone parameters, which were evaluated using high-resolution quantitative computed tomography (HR-QCT). Forty-two female New Zealand white rabbits (18-22 weeks old) were randomly divided into six groups of seven each: a 4-week vector control group, a 4-week TPTD administration group (20 μg/kg, subcutaneous injection, once daily), a 12-week vector control group, a 4-week TPTD administration group + an 8-week vector control group, a 4-week TPTD administration group + an 8-week low-dose IBN administration group (20 μg/kg, subcutaneous injection, every 4 weeks), and a 4-week TPTD administration group + an 8-week high-dose IBN administration group (100 μg/kg, subcutaneous injection, every 4 weeks). After the 4-week or 12-week experiment, cortical bone from the distal femur was harvested for high-resolution quantitative CT (HR-QCT) analysis. Four weeks of TPTD administration increased bone porosity, number, and density, as well as cortical area, thickness, and bone mineral content (BMC), but had no significant effect on volumetric bone mineral density (BMD). Compared to four weeks of TPTD administration, four weeks of TPTD administration followed by eight weeks of excipient administration decreased bone porosity, number, and density, as well as cortical area and thickness, but its bone porosity, cortical area, and thickness were still higher than those of 12 weeks of excipient administration. Compared to four weeks of TPTD administration followed by eight weeks of excipient administration, four weeks of TPTD administration followed by eight weeks of high-dose IBN administration (rather than four weeks of TPTD administration followed by eight weeks of low-dose IBN administration) increased cortical area, thickness, BMC, and volumetric BMD, and decreased bone porosity, but did not decrease bone porosity or density. These results indicate that administration of higher doses of IBN after TPTD treatment is beneficial for bone mineral content (BMC), volumetric bone mineral density (BMD), cortical area, thickness, and porosity in adult rabbits. [1]

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Therapeutic Use: Bone Mineral Degradation Protectant
Forteo is indicated for the treatment of postmenopausal women with osteoporosis at high risk of fracture. These women include those with a history of osteoporotic fractures, multiple fracture risk factors, or those who have failed or are intolerant of previous osteoporosis treatments, subject to physician evaluation. In postmenopausal women with osteoporosis, Forteo can increase bone mineral density and reduce the risk of vertebral and nonvertebral fractures.
Forteo is also indicated for increasing bone mass in men with primary or hypogonadal osteoporosis at high risk of fracture. These men include those with a history of osteoporotic fractures, multiple fracture risk factors, or those who have failed or are intolerant of previous osteoporosis treatments, as assessed by a physician. For men with primary or hypogonadal osteoporosis, Forteo can increase bone mineral density. The effect of Forteo on fracture risk in men has not been studied.

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Drug Warning: In male and female rats, teriparatide increases the incidence of osteosarcoma (a malignant bone tumor), and the degree of increase is related to dose and duration of treatment. This effect was observed at systemic exposures to teriparatide at doses 3 to 60 times higher than the human exposure to a 20 μg dose. Because the relevance of the rat osteosarcoma finding to humans is uncertain, teriparatide should only be prescribed to patients for whom the potential benefit outweighs the potential risk.

Teriparatide should not be prescribed to patients at increased baseline risk for osteosarcoma (including those with Paget's disease or unexplained elevation of alkaline phosphatase, unclosed epiphyses, or a history of external beam radiation therapy or implant-based radiation therapy involving the bone).
Adverse reactions reported as an increase in teriparatide treatment in clinical trials include leg cramps and dizziness. Adverse reactions reported in at least 2% of patients receiving teriparatide, at a higher incidence than in the placebo group, but without established causality, include pain, arthralgia, rhinitis, fatigue, nausea, dizziness, headache, hypertension, exacerbated cough, pharyngitis, constipation, indigestion, diarrhea, rash, insomnia, depression, pneumonia, vertigo, dyspnea, neck pain, vomiting, syncope, leg cramps, angina, gastrointestinal disorders, sweating, or dental problems.
Transient episodes of symptomatic orthostatic hypotension have been occasionally observed in short-term clinical pharmacology studies of teriparatide. Typically, such events occur within 4 hours of administration and resolve spontaneously within minutes to hours. Transient orthostatic hypotension usually occurs after the first few doses and is relieved by the patient adopting a reclining position, without affecting continued treatment. The safety and efficacy of Forteo have not been evaluated in treatment exceeding 2 years. Therefore, use of this drug for more than 2 years is not recommended. In clinical trials, the incidence of urinary tract stones was similar in the Forteo treatment group and the placebo group. However, Forteo has not been studied in patients with active urinary tract stones. If active urinary tract stones or a history of hypercalciuria are suspected, urinary calcium excretion should be measured. Because Forteo may exacerbate active or recent urinary tract stones, it should be used with caution in patients with active or recent urinary tract stones. Physician's Desk Reference, 60th edition, Thomson PDR, Montvale, NJ, 2006, p. 119. 1741

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Mechanism of action: The effects of teriparatide on bone depend on its systemic exposure pattern. Teriparatide, administered once daily, promotes new bone formation on the surface of cancellous and cortical bone (periosteum and/or endosteum) by preferentially stimulating osteoblast activity over osteoclast activity. In monkey studies, teriparatide improved trabecular microstructure and increased bone mass and strength by stimulating new bone formation in cancellous and cortical bone. In humans, the anabolic effects of teriparatide are manifested as increased bone mass, elevated markers of bone formation and resorption, and enhanced bone strength. Conversely, persistent excess of endogenous parathyroid hormone (PTH) (such as in hyperparathyroidism) may be detrimental to bone health because bone resorption may be more stimulated than bone formation. Endogenous parathyroid hormone (PTH), composed of 84 amino acids, is a major regulator of calcium and phosphorus metabolism in bone and kidneys. The physiological functions of PTH include regulating bone metabolism, renal tubular reabsorption of calcium and phosphorus, and intestinal calcium absorption. The biological effects of PTH and teriparatide are mediated by binding to specific high-affinity cell surface receptors. Teriparatide and PTH bind to these receptors with the same affinity for their 34 N-terminal amino acids and have the same physiological effects on bone and kidney. Teriparatide is not expected to accumulate in bone or other tissues.

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C183H297N55O54S2

4196.0

C, 52.61; H, 7.12; N, 18.44; O, 20.30; S, 1.53

99294-94-7

Teriparatide;52232-67-4

Ser-Val-Ser-Glu-Ile-Gln-Leu-Met-His-Asn-Leu-Gly-Lys-His-Leu-Asn-Ser-Met-Glu-Arg-Val-Glu-Trp-Leu-Arg-Lys-Lys-Leu-Gln-Asp-Val-His-Asn-Phe

SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNF

Typically exists as solid at room temperature

CC[C@H](C)[C@@H](C(=O)N[C@@H](CCC(=O)N)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCSC)C(=O)N[C@@H](CC1=CNC=N1)C(=O)N[C@@H](CC(=O)N)C(=O)N[C@@H](CC(C)C)C(=O)NCC(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC2=CNC=N2)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CC(=O)N)C(=O)N[C@@H](CO)C(=O)N[C@@H](CCSC)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CCC(=O)O)C(=O)N[C@@H](CC3=CNC4=CC=CC=C43)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCC(=O)N)C(=O)N[C@@H](CC(=O)O)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CC5=CNC=N5)C(=O)N[C@@H](CC(=O)N)C(=O)N[C@@H](CC6=CC=CC=C6)C(=O)O)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CO)NC(=O)[C@H](C(C)C)NC(=O)[C@H](CO)N.CC(=O)O.O

acetic acid;(4S)-4-[[(2S)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-5-amino-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-hydroxypropanoyl]amino]-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-3-methylpentanoyl]amino]-5-oxopentanoyl]amino]-4-methylpentanoyl]amino]-4-methylsulfanylbutanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-4-oxobutanoyl]amino]-4-methylpentanoyl]amino]acetyl]amino]hexanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-4-methylpentanoyl]amino]-4-oxobutanoyl]amino]-3-hydroxypropanoyl]amino]-4-methylsulfanylbutanoyl]amino]-5-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S)-1-carboxy-2-phenylethyl]amino]-1,4-dioxobutan-2-yl]amino]-3-(1H-imidazol-4-yl)-1-oxopropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-5-oxopentanoic acid;hydrate

Parathar acetate; hPTH 1-34; Teriparatide acetate hydrate; 99294-94-7; HPTH 1-34 (ACETATE SALT); 9959P4V12N; Teriparatide acetate; Forteo

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

H2O : ~100 mg/mL (~24 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.)