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Purity: ≥98%
Abaloparatide (Trade name Tymlos; formerly known as BA-058; ITM-058; BIM 44058) is a 34 amino acid synthetic analog of parathyroid hormone-related protein (PTHrP) that is used to treat osteoporosis. The Food and Drug Administration (FDA) approved it on April 28, 2017, for the treatment of postmenopausal osteoporosis. Not unlike bisphosphonates, but similar to the related medication teriparatide, it is an anabolic (bone-growing) agent. The drug's subcutaneous injection formulation has finished a Phase III osteoporosis trial. Only this one study revealed a decline in fractures. Parathyroid hormone (PTH) (1-34) and parathyroid hormone-related protein (PTHrP) (1-34) share 76% and 41% homology, respectively, with abaloparatide. By selectively activating the parathyroid hormone 1 receptor (PTH1R), a G protein-coupled receptor (GPCR) expressed in osteoblasts and osteocytes, it functions as an anabolic agent for bone. Abaloparatide preferentially binds the PTH1R's RG conformational state, which causes a brief downstream cyclic AMP signaling response that points in the direction of a more anabolic signaling pathway.
Targets |
PTHR1/parathyroid hormone receptor 1
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ln Vitro |
Abaloparatide (0-100 nM; 40 min) increases β-arrestin recruitment and Gs/cAMP signaling in MC3T3-E1 cells[1].
Abaloparatide (0-100 nM) effectively and dose-dependently induces PTHR1 internalization in U2OS cells, with an EC50 value of 0.8 nM[1]. |
ln Vivo |
In mice, abelaparatide (20–80 µg/kg; s.c.; daily for 30 days) improves cortical structure and bone formation[1].
Teriparatide and abaloparatide are parathyroid hormone receptor 1 (PTHR1) analogs with unexplained differential efficacy for the treatment of osteoporosis. Therefore, we compared the effects of abaloparatide and teriparatide on bone structure, turnover, and levels of receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG). Wild-type (WT) female mice were injected daily with vehicle or 20-80 µg/kg/day of teriparatide or abaloparatide for 30 days. Femurs and spines were examined by microcomputed tomography scanning and serum levels of bone turnover markers, RANKL, and OPG, were measured by ELISA. Both analogs similarly increased the distal femoral fractional trabecular bone volume, connectivity, and number, and reduced the structure model index (SMI) at 20-80 µg/kg/day doses. However, only abaloparatide exhibited a significant increase (13%) in trabecular thickness at 20 µg/kg/day dose. Femoral cortical evaluation showed that abaloparatide caused a greater dose-dependent increase in cortical thickness than teriparatide. Both teriparatide and abaloparatide increased lumbar 5 vertebral trabecular connectivity but had no or modest effect on other indices. Biochemical analysis demonstrated that abaloparatide promoted greater elevation of procollagen type 1 intact N-terminal propeptide, a bone formation marker, and tartrate-resistant acid phosphatase 5b levels, a bone resorption marker, and lowered the RANKL/OPG ratio. Furthermore, PTHR1 signaling was compared in cells treated with 0-100 nmol/L analog. Interestingly, abaloparatide had a markedly lower EC50 for cAMP formation (2.3-fold) and β-arrestin recruitment (1.6-fold) than teriparatide. Therefore, abaloparatide-improved efficacy can be attributed to enhanced bone formation and cortical structure, reduced RANKL/OPG ratio, and amplified Gs-cAMP and β-arrestin signaling.[1] Abaloparatide is a novel 34-amino acid peptide selected to be a potent and selective activator of the parathyroid hormone receptor (PTH1R) signaling pathway with 41% homology to PTH(1-34) and 76% homology to PTHrP(1-34). A 12-month treatment study was conducted in osteopenic ovariectomized (OVX) rats to characterize the mechanisms by which abaloparatide increases bone mass. Sprague-Dawley (SD) rats were subjected to OVX or sham surgery at age 6 months and left untreated for 3 months to allow OVX-induced bone loss. Ten OVX rats were euthanized after this bone depletion period, and the remaining OVX rats received daily subcutaneous injections of vehicle (n = 18) or abaloparatide at 1, 5, or 25 μg/kg/d (n = 18/dose level) for 12 months. Sham controls (n = 18) received vehicle daily. Bone densitometry and biochemical markers of bone formation and resorption were assessed longitudinally, and L3 vertebra and tibia were collected at necropsy for histomorphometry. Abaloparatide increased biochemical bone formation markers without increasing bone resorption markers or causing hypercalcemia. Abaloparatide increased histomorphometric indices of bone formation on trabecular, endocortical, and periosteal surfaces without increasing osteoclasts or eroded surfaces. Abaloparatide induced substantial increases in trabecular bone volume and density and improvements in trabecular microarchitecture. Abaloparatide stimulated periosteal expansion and endocortical bone apposition at the tibial diaphysis, leading to marked increases in cortical bone volume and density. Whole-body bone mineral density (BMD) remained stable in OVX-Vehicle controls while increasing 25% after 12 months of abaloparatide (25 μg/kg). Histomorphometry and biomarker data suggest that gains in cortical and trabecular bone mass were attributable to selective anabolic effects of abaloparatide, without evidence for stimulated bone resorption. © 2016 American Society for Bone and Mineral Research.[2] |
Enzyme Assay |
PathHunter® eXpress PTHR1 CHO‐K1 β‐arrestin GPCR assay[1]
To assess the effects of Abaloparatide and teriparatide stimulation of PTHR1 on β‐arrestin recruitment to the cell membrane, a PathHunter eXpress PTHR1 Chinese Hamster Ovary‐K1 (CHO‐K1) β‐arrestin GPCR Assay was used. The assay takes advantage of Enzyme Fragment Complementation technology. The PTHR1 is fused in frame with a small enzyme donor fragment ProLink™ (PK) and co‐expressed in CHO‐K1 cells stably expressing a fusion protein of β‐arrestin and the larger, N‐terminal deletion mutant of β‐galactosidase (called enzyme acceptor or EA). Activation of the PTHR1 stimulates binding of β‐arrestin to the PK‐tagged GPCR and forces complementation of the two enzyme fragments, resulting in the formation of an active β‐galactosidase enzyme. An increase in enzyme activity is then measured using chemiluminescent PathHunter Detection Reagents. Cell seeding, incubation, and detection were performed as instructed by the manufacturer. Briefly, cells were seeded in a clear bottom white 96‐well plate and incubated for 48 h at 37°C CO2 incubator. Cells were treated with vehicle, teriparatide, or Abaloparatide for 60 min at 37°C in a CO2 incubator. At the end of the incubation, β‐gal enzyme substrate was added for 60 min at room temperature in the dark. Light generation (Relative Light Units, RLU), an indication of β‐gal enzyme fragment complementation and β‐Arrestin/ PTHR1 interaction, was measured using BMG Labtech PHERAstar FS luminescence plate reader.[1] PathHunter® eXpress PTHR1 activated GPCR internalization assay[1] To determine PTHR1 internalization, we used PathHunter eXpress PTHR1 U2OS Activated GPCR Internalization Assay. PathHunter® PTHR1 Activated GPCR Internalization U2OS cell lines are engineered to co‐express an untagged PTHR1, an EA‐tagged β‐arrestin, and a PK tag localized to the endosomes. Activation of the untagged PTHR1 induces β‐arrestin recruitment, followed by internalization of the GPCR‐β‐arrestin‐EA complex in PK‐tagged endosomes. Similar to the β‐arrestin assay format, this internalization forces complementation of the two β‐gal enzyme fragments, forming functional enzyme that hydrolyzes substrate to generate a chemiluminescent signal. U2OS osteoblastic cell line seeding, incubation, and detection were performed as instructed by the manufacturer. Cells were treated with vehicle, teriparatide, or Abaloparatide for 60 min at 37°C in a CO2 incubator. At the end of the incubation, β‐gal enzyme substrate was added for 60 min at room temperature in the dark. Light generation (RLU), an indication of β‐gal enzyme fragment complementation and β‐arrestin/endosome/PTHR1 formation, was measured using BMG Labtech PHERAstar FS luminescence plate reader. |
Cell Assay |
Measurement of intracellular cAMP generation[1]
MC3T3‐E1 cells were seeded at 40,000 cells/well of a 24‐well plate containing 500‐µL alpha‐MEM supplemented with 10% FBS and 1% PS. After culture for 1 week, the medium was removed and replaced with 250 µL of stimulation medium (alpha‐MEM containing 0.05% FBS, 0.1% BSA, 5 mmol/L hepes buffer, and 0.5 mmol/L IBMX) for 15 min. IBMX is a phosphodiesterase inhibitor that prevents degradation of the generated cAMP. Vehicle, Abaloparatide, and teriparatide were then added in 250 µL stimulation medium to achieve final concentrations of 0, 0.01, 0.1, 1, 10, and 100 nmol/L/well. Incubation continued for 40 min at 37°C before the medium was removed and the plates were snap frozen in liquid N3 and stored at −80°C. For extraction of intracellular cAMP, 100 mmol/L Hcl was added and cells were incubated at room temperature for 1 h. Intracellular cAMP was assayed using a cAMP competitive ELISA kit and following the manufacturer protocol and instructions. |
Animal Protocol |
16-week-old wild-type (WT) female C57BL/6J mice[1]
20-80 µg/kg S.c.; daily for 30 days All experiments were conducted on 16‐week‐old wild‐type (WT) female C57BL/6J mice (Stock number 664). Vehicle (0.9% NaCl/10 mmol/L acetic acid) or 20–80 µg/kg/day teriparatide or abaloparatide was injected subcutaneously (SC) daily (except Sunday) and continued for 30 days. No peptide injection was performed on the day of animal sacrifice.[1] A total of 13 rats were euthanized or found dead between study days 117 to 358 before study termination: 6 in the sham control group, 2 in the OVX-Veh group, 3 in the OVX + abaloparatide 1 μg/kg/d group, 1 in the OVX + abaloparatide 5 μg/kg/d group, and 1 in the OVX + abaloparatide 25 μg/kg/d group. For these animals’ data, absolute values were reported if collected, and data based on % change from baseline were censored as required. Five deaths were likely secondary to complications from blood collection, whereas the remaining deaths were attributed to incidental age-related pathologies.[1] Study design and dose selection[1] After a 13-week postsurgical bone depletion period, one group of untreated OVX rats was euthanized as a pretreatment baseline group for histomorphometry data. The remaining groups were given daily s.c. injections of vehicle (Vehicle; 0.9% sodium chloride) or one of three dose levels of abaloparatide in a 0.1 mL/kg volume. Abaloparatide dose levels were 1 μg/kg/d (OVX-ABL1), 5 μg/kg/d (OVX-ABL5), and 25 μg/kg/d (OVX-ABL25), with dosing guided by weekly body weight measurements. Preliminary results from another rat study indicated that 6 weeks of abaloparatide at 1.25 μg/kg/d completely reversed OVX-induced bone loss (Radius Health, Inc., Waltham, MA, USA). This led to selection of 1 μg/kg as the low dose, and also 5- and 25-fold multiples of this dose to provide safety margins.[1] |
ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
The absolute bioavailability of abaloparatide in healthy women after subcutaneous administration of an 80 mcg dose was 36%. Following subcutaneous administration of 80 mcg abaloparatide in postmenopausal women with osteoporosis for seven days, the mean (SD) Cmax was 812 (118) pg/mL and the AUC0-24 was 1622 (641) pgxhr/mL. The median Tmax was 0.51 hours, with a range from 0.25 to 0.52 hours. The peptide fragments of abaloparatide are primarily eliminated through renal excretion. The volume of distribution was approximately 50 L. The mean apparent total plasma clearance for subcutaneous administration is 168 L/h in healthy subjects. Metabolism / Metabolites Abaloparatide is metabolized into smaller peptide fragments via non-specific proteolytic degradation. Biological Half-Life The mean half-life of abaloparatide is approximately one hour. |
Toxicity/Toxicokinetics |
Protein Binding
_In vitro_, abaloparatide was approximately 70% bound to plasma proteins. |
References |
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Additional Infomation |
Abaloparatide is an N-terminal analog of parathyroid hormone-related protein (PTHrP) and an agonist at the parathyroid hormone type 1 (PTH1) receptor. It is a synthetic 34 amino acid peptide with 41% homology to human parathyroid hormone 1-34 and human PTHrP 1-34. Abaloparatide and PTHrP share the first 21 amino acids and the receptor-activating domain. Abaloparatide is an osteoanabolic agent that stimulates bone formation. It was first approved by the FDA on April 28, 2017, for the treatment of osteoporosis in postmenopausal women and is also used to increase bone density in men with osteoporosis. In October 2022, the EMA's Committee for Medicinal Products for Human Use (CHMP) recommended abaloparatide be granted marketing authorization in Europe and the drug was fully authorized by the European Commission on December 19, 2022.
Abaloparatide is a 34 amino acid synthetic analog of human parathyroid hormone-related protein (PTHrP) (PTHrP(1-34) analog), with bone-growing and bone density conserving activities. Upon subcutaneous administration, abaloparatide acts similar to PTHrP and targets, binds to and activates parathyroid hormone 1 (PTH1) receptor (PTH1R), a G protein-coupled receptor (GPCR) expressed in osteoblasts and bone stromal cells. PTH1R activates the cyclic AMP (cAMP) signaling pathway and the bone anabolic signaling pathway, leading to bone growth, increased bone mineral density (BMD) and volume. This correlates with increased bone mass and strength and prevents or treats osteoporosis and decreases fractures. Drug Indication Abaloparatide is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture (defined as a history of osteoporotic fracture or multiple risk factors for fracture) or patients who have failed or are intolerant to other available osteoporosis therapy. In postmenopausal women with osteoporosis, abaloparatide reduces the risk of vertebral and nonvertebral fractures. Abaloparatide is also indicated to increase bone density in men with osteoporosis at high risk for fracture (defined as a history of osteoporotic fracture or multiple risk factors for fracture) or patients who have failed or are intolerant to other available osteoporosis therapy. Treatment of osteoporosis in postmenopausal women at increased risk of fracture. Treatment of osteoporosis. Treatment of osteoporosis Mechanism of Action Abaloparatide is an agonist at the PTH1 receptor (PTH1R), a G-protein-coupled receptor (GPCR) that regulates bone formation and bone turnover, as well as mineral ion homeostasis. The PTH1R couples to Gs and Gq, which stimulates adenylyl cyclase (AC), which activates the cAMP/PKA signalling cascade, and phospholipase C (PLC), which activates the IP/PKC signalling cascade. Abaloparatide binds to the PTH1R in target cells to activate the Gs-protein-mediated cAMP signalling pathway, thereby stimulating osteoblastic activity. Abaloparatide also activates Gq and β-arrestin-1 pathway downstream of PTH1R as off-targets in target cells such as the testis and epididymis, which have been associated with anti-inflammatory effects and alleviation of epididymitis and orchitis symptoms. The PTH1R has two conformations with distinct ligand binding profiles. The R0 conformation is a G protein–independent high-affinity conformation, and upon binding, the ligand induces a longer-lasting signalling response that gradually increases cAMP. Due to the prolonged signalling response, ligands selectively binding to the R0 conformation are associated with a risk for increased calcium mobilization and hypercalcemia. Conversely, the RG conformation is G-protein–dependent (GTPγS-sensitive) with a shorter signalling response. Abaloparatide binds to the RG conformation with greater selectivity: it induces more transient signalling responses and favours net bone formation over bone resorption. The drug's relatively low risk for hypercalcemia and osteoclast resorption compared to [teriparatide] is attributed to the preferential binding of abaloparatide to the RG conformation. |
Molecular Formula |
C174H300N56O49
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Molecular Weight |
3960.58963775635
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Exact Mass |
3959.273
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Elemental Analysis |
C, 52.58; H, 7.62; N, 19.51; O, 20.29
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CAS # |
247062-33-5
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Related CAS # |
Abaloparatide TFA
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PubChem CID |
145705876
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Sequence |
H-DL-Ala-DL-Val-DL-Ser-DL-Glu-DL-His-DL-Gln-DL-Leu-DL-Leu-DL-His-DL-Asp-DL-Lys-Gly-DL-Lys-DL-Ser-DL-xiIle-DL-Gln-DL-Asp-DL-Leu-DL-Arg-DL-Arg-DL-Arg-DL-Glu-DL-Leu-DL-Leu-DL-Glu-DL-Lys-DL-Leu-DL-Leu-Aib-DL-Lys-DL-Leu-DL-His-DL-xiThr-DL-Ala-NH2
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SequenceShortening |
AVSEHQLLHDKGKSXQDLRRRELLEKLLXKLHXA; AVSEHQLLHDKGKSIQDLRRRELLEKLL-{Aib}-KLHTA-NH2
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Appearance |
White to off-white solid powder
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LogP |
-20.9
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Hydrogen Bond Donor Count |
61
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Hydrogen Bond Acceptor Count |
60
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Rotatable Bond Count |
145
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Heavy Atom Count |
279
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Complexity |
9310
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Defined Atom Stereocenter Count |
0
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InChi Key |
BVISQZFBLRSESR-UHFFFAOYSA-N
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InChi Code |
InChI=1S/C174H300N56O49/c1-26-93(20)136(228-165(274)126(80-232)224-141(250)101(39-28-32-56-176)200-129(236)78-195-140(249)100(38-27-31-55-175)201-161(270)123(73-133(243)244)223-160(269)121(71-98-76-190-82-197-98)220-158(267)118(68-90(14)15)216-155(264)114(64-86(6)7)213-148(257)107(45-50-127(180)234)207-159(268)120(70-97-75-189-81-196-97)219-151(260)111(49-54-132(241)242)209-164(273)125(79-231)225-167(276)135(92(18)19)227-139(248)94(21)179)168(277)210-108(46-51-128(181)235)149(258)222-124(74-134(245)246)162(271)217-112(62-84(2)3)152(261)205-105(44-37-61-194-173(187)188)143(252)203-103(42-35-59-192-171(183)184)142(251)204-104(43-36-60-193-172(185)186)144(253)206-110(48-53-131(239)240)150(259)214-115(65-87(8)9)154(263)215-113(63-85(4)5)153(262)208-109(47-52-130(237)238)147(256)202-102(40-29-33-57-177)145(254)211-116(66-88(10)11)156(265)218-119(69-91(16)17)166(275)230-174(24,25)170(279)226-106(41-30-34-58-178)146(255)212-117(67-89(12)13)157(266)221-122(72-99-77-191-83-198-99)163(272)229-137(96(23)233)169(278)199-95(22)138(182)247/h75-77,81-96,100-126,135-137,231-233H,26-74,78-80,175-179H2,1-25H3,(H2,180,234)(H2,181,235)(H2,182,247)(H,189,196)(H,190,197)(H,191,198)(H,195,249)(H,199,278)(H,200,236)(H,201,270)(H,202,256)(H,203,252)(H,204,251)(H,205,261)(H,206,253)(H,207,268)(H,208,262)(H,209,273)(H,210,277)(H,211,254)(H,212,255)(H,213,257)(H,214,259)(H,215,263)(H,216,264)(H,217,271)(H,218,265)(H,219,260)(H,220,267)(H,221,266)(H,222,258)(H,223,269)(H,224,250)(H,225,276)(H,226,279)(H,227,248)(H,228,274)(H,229,272)(H,230,275)(H,237,238)(H,239,240)(H,241,242)(H,243,244)(H,245,246)(H4,183,184,192)(H4,185,186,193)(H4,187,188,194)
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Chemical Name |
Ala-Val-Ser-Glu-His-Gln-Leu-Leu-His-Asp-Lys-Gly-Lys-Ser-Ile-Gln-Asp-Leu-Arg-ArgArg-Glu-Leu-Leu-Glu-Lys-Leu-Leu-Aib-Lys-Leu-His-Thr-Ala-NH2
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Synonyms |
BIM-44058; Abaloparatide acetate; BA-058; ITM-058; BIM 44058; BA 058;ITM 058; BIM44058; BA058;ITM058; H-DL-Ala-DL-Val-DL-Ser-DL-Glu-DL-His-DL-Gln-DL-Leu-DL-Leu-DL-His-DL-Asp-DL-Lys-Gly-DL-Lys-DL-Ser-DL-xiIle-DL-Gln-DL-Asp-DL-Leu-DL-Arg-DL-Arg-DL-Arg-DL-Glu-DL-Leu-DL-Leu-DL-Glu-DL-Lys-DL-Leu-DL-Leu-Aib-DL-Lys-DL-Leu-DL-His-DL-xiThr-DL-Ala-NH2; trade name: Tymlos
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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 Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
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) |
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Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (0.63 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (0.63 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (0.63 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 0.2525 mL | 1.2624 mL | 2.5249 mL | |
5 mM | 0.0505 mL | 0.2525 mL | 0.5050 mL | |
10 mM | 0.0252 mL | 0.1262 mL | 0.2525 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
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.
NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
NCT03841058 | Recruiting | Drug: Abaloparatide Drug: Placebo |
Spinal Fusion | Hospital for Special Surgery, New York |
August 14, 2019 | Phase 2 |
NCT04626141 | Not yet recruiting | Drug: Abaloparatide Drug: Placebo |
Femoral Fractures | Daniel Horwitz | September 2023 | Phase 4 |
NCT04167163 | Recruiting | Drug: Abaloparatide | Osteoporosis Arthroplasties, Knee Replacement |
University of Wisconsin, Madison | January 10, 2020 | Phase 4 |
NCT04760782 | Recruiting | Drug: Abaloparatide Device: Hard collar immobilization |
Odontoid Fracture | David Lunardini | May 18, 2022 | Phase 2 |
NCT03710889 | Completed | Drug: Abaloparatide | Osteoporosis Osteoporosis Risk |
Radius Health, Inc. | September 20, 2018 | Phase 3 |
Effects of abaloparatide and teriparatide administration on vertebral trabecular bone architecture: Female C57BL/6J WT mice were SC injected daily, except Sunday, with vehicle or 20–80 µg/kg/day teriparatide or abaloparatide for 30 days. Physiol Rep . 2019 Oct;7(19):e14225. td> |
Effects of daily abaloparatide and teriparatide on serum Ca2+ and Pi: Female C57BL/6 WT mice were injected SC daily, except Sunday, with vehicle or 20–80 µg/kg/day teriparatide or abaloparatide for 30 days. Physiol Rep . 2019 Oct;7(19):e14225. td> |
Anabolic windows during 12 months of abaloparatide administration. J Bone Miner Res . 2017 Jan;32(1):24-33. td> |