pTH (1-34) selectively targets and activates the type-1 parathyroid hormone receptor (PTH1R), a class B G protein-coupled receptor expressed in various tissues including bone, kidney, and the central nervous system. Upon binding to PTH1R, pTH (1-34) activates multiple downstream signaling pathways, including stimulation of adenylyl cyclase via Gs protein to produce cAMP, and activation of phospholipase C via Gq protein to generate inositol phosphates. Cryo-electron microscopy structural studies have revealed that the N-terminus of pTH (1-34) engages the transmembrane domain of the receptor, while the C-terminus interacts with the extracellular domain.
bovine PTH-(1-34) acts on the parathyroid hormone receptor (PTH1R) in bone and kidney [2]

When added to the culture medium, bovine hormone (0.1-100 ng/mL; 2-20 days) and parathyroid hormone (1-34) suppressed osteoblast growth in a dose-dependent manner. In a different group, bPTH was added to the culture medium from day 1 to day 10, but it was not added from day 11 to day 20. Following the removal of bPTH, a proliferative rebound was seen in the PTH day 1–10 group [1]. There are different effects of bovine parathyroid hormone (1-34) (0.1-100 ng/mL; 2-20 days) on the amount of calcium and phosphorus in the culture medium. The PTH-C 100 ng/mL group's culture media had greater calcium and phosphorus concentrations than the control group's [1].

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In vitro, pTH (1-34) exerts its biological activity through activation of PTH1R. In LLC-PK1 cells stably expressing human PTH1R, pTH (1-34) activates adenylyl cyclase with an EC₅₀ of approximately 1-2 nM. Studies have shown that pTH (1-34) not only activates the cAMP signaling pathway but also fully stimulates phospholipase C activity. In UMR-106 rat osteosarcoma cells, pTH (1-34) treatment induces a dose-dependent increase in intracellular cAMP levels. Furthermore, in HEK293 cells expressing PTH1R, pTH (1-34) effectively recruits both β-arrestin-1 and β-arrestin-2.

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bovine PTH-(1-34) (1 × 10⁻⁷ M) added to cultured rabbit costal growth cartilage chondrocytes for 24 hr significantly increased ³⁵SO₄²⁻ incorporation into glycosaminoglycans (GAG) by 62% compared to PBS control (from 4,166 ± 43 to 6,757 ± 61 dpm/well, p<0.05). [2]
bovine PTH-(1-34) (1 × 10⁻⁷ M) increased GAG synthesis in mandibular condylar cartilage chondrocytes by 137% (from 4,238 ± 54 to 5,809 ± 22 dpm/well). [2]
bovine PTH-(1-34) (1 × 10⁻⁷ M) increased GAG synthesis in nasal septal cartilage chondrocytes by 138% (from 2,394 ± 67 to 2,744 ± 98 dpm/well). [2]
bovine PTH-(1-34) (1 × 10⁻⁷ M) increased GAG synthesis in spheno-occipital synchondrosis chondrocytes by 133% (from 2,687 ± 216 to 3,366 ± 123 dpm/well). [2]

In both groups of old animals, parathyroid hormone (1-34) (s.c.; 80 μg/kg; 5 days) raised blood osteocalcin concentrations but did not change serum levels of calcium or inorganic phosphate. When compared to sex-matched vehicle-treated controls, older female rats treated with PTH had considerably greater serum 1,25-dihydroxyvitamin D concentrations [1].

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In vivo, pTH (1-34) is a critical regulator of bone metabolism. In young male Fisher rats, daily subcutaneous administration of pTH (1-34) (10 or 40 μg/kg for 1-4 weeks) produces dose- and time-dependent increases in volumetric bone mineral density and bone mineral content of the proximal tibia, as well as increased bone mass in the distal femur and lumbar vertebrae. Intermittent administration of pTH (1-34) exhibits bone anabolic effects, promoting bone formation and increasing bone density. In healthy human subjects, following a single subcutaneous injection of 20 μg recombinant human pTH (1-34), the drug is rapidly absorbed, reaching peak concentration at approximately 20-30 minutes, and is rapidly cleared with a half-life of approximately 47-60 minutes.

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In senile (23-month-old) male rats, intermittent subcutaneous administration of bovine PTH-(1-34) at 80 μg/kg/day for 5 consecutive days per week over 3 weeks (total 15 doses) prevented the fall in spinal bone mineral content (BMC) and significantly increased spinal bone mineral density (BMD) compared to vehicle-treated controls (BMD change: +0.03 ± 0.006 g/cm² in PTH-treated vs -0.01 ± 0.006 g/cm² in controls, p<0.05). In young (3-month-old) male rats, the same treatment amplified the increase in BMC and BMD (BMD change: +0.055 ± 0.003 g/cm² in PTH-treated vs +0.036 ± 0.003 g/cm² in controls, p<0.05). [1]
In senile male rats, bovine PTH-(1-34) treatment significantly increased serum 1,25-dihydroxyvitamin D concentrations from baseline (12 ± 10 pg/ml pretreatment to 68 ± 9 pg/ml post-treatment, p<0.05) and the final mean level was not different from that in young PTH-treated animals (85 ± 6 pg/ml). The change in spinal BMC was significantly associated with final 1,25-dihydroxyvitamin D concentration (r² = 0.53, p = 0.01). [1]
In senile male rats, bovine PTH-(1-34) increased serum osteocalcin concentrations (change: +8.8 ± 2 ng/ml vs -8.2 ± 3 ng/ml in controls, p<0.05) without significantly changing serum calcium, inorganic phosphate, or alkaline phosphatase. [1]
In senile female rats (24-month-old), bovine PTH-(1-34) (80 μg/kg/day, same schedule) significantly increased spinal BMD (0.291 ± 0.008 g/cm² in PTH-treated vs 0.250 ± 0.009 g/cm² in controls, p<0.01), serum osteocalcin (27.6 ± 1.7 vs 14.7 ± 1.7 ng/ml, p<0.05), and serum 1,25-dihydroxyvitamin D (100 ± 15 vs 31 ± 7 pg/ml, p<0.05). [1]

The binding affinity of pTH (1-34) to PTH1R can be determined using competitive binding assays. A common approach utilizes radiolabeled tracers such as [¹²⁵I][Nle8,18,Tyr34] human PTH(1-34) incubated with membrane preparations expressing recombinant PTH1R. In competitive binding experiments, varying concentrations of unlabeled pTH (1-34) compete with a fixed concentration of radiolabeled tracer for receptor binding, and IC₅₀ values are calculated by measuring the reduction in bound radioactivity. Alternatively, bioluminescence resonance energy transfer technology using fluorescently labeled PTH(1-34) derivatives can be employed to measure competitive binding in live cells.

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Cell Proliferation Assay[1]
Cell Types: MC3T3-E1 Cell
Tested Concentrations: 0.1-100 ng/mL
Incubation Duration: 2-20 Days
Experimental Results: Resulted in a concentration-dependent decrease in osteoblast proliferation. Proliferation rebounds when PTH is discontinued.

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Cell-based bioactivity assays are typically performed using the UMR-106 rat osteosarcoma cell line. The procedure involves seeding UMR-106 cells at 1,000 cells per well in 384-well plates, followed by treatment with serially diluted pTH (1-34) samples prepared in assay medium (starting concentration approximately 4,000 ng/mL) for 30 minutes at 25°C in the dark. After adding cAMP detection reagents and incubating for an additional 60 minutes in the dark, intracellular cAMP levels are measured using time-resolved fluoroimmunoassay. The relative potency of samples is calculated using four-parameter fitting analysis, and this method demonstrates good specificity, accuracy, and precision (geometric coefficient of variation ranging from 2.0 to 3.5%).

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Chondrocytes were isolated from rabbit mandibular condylar cartilage, nasal septal cartilage, spheno-occipital synchondrosis, and costal growth cartilage by sequential digestion with EDTA (0.1% for 20 min), trypsin (0.2% for 1 hr), and collagenase (0.1-0.2% for 1-3 hr). Cells were plated in Dulbecco's modified Eagle's medium with 10% fetal calf serum, ascorbic acid (50 μg/ml), penicillin (32,000 mU/ml), and streptomycin (40 μg/ml). For GAG synthesis assay, sub-confluent cells were incubated with bovine PTH-(1-34) (1 × 10⁻⁷ M) for 24 hr, then labeled with Na₂³⁵SO₄ (3 μCi/ml) in balanced salt solution for 3 hr. ³⁵SO₄²⁻ incorporation into GAG was measured by cetylpyridinium chloride precipitation. [2]

In vivo activity of pTH (1-34) is typically evaluated in osteoporosis animal models. Using young male Fisher rats as an example, animals receive daily subcutaneous injections of pTH (1-34) at doses of 10 or 40 μg/kg for 1 to 4 weeks. Blood calcium and phosphate levels are monitored periodically during the study. At study termination, volumetric bone mineral density and bone mineral content of the proximal tibia are measured by peripheral quantitative computed tomography, the distal femur is analyzed for calcium content and dry weight, and lumbar vertebrae are subjected to bone histomorphometry analysis. Results demonstrate dose- and time-dependent increases in bone mass in treated animals compared to controls.

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Human pharmacokinetic studies demonstrate that pTH (1-34) is rapidly absorbed following subcutaneous injection, with a time to peak concentration (Tmax) of 20-30 minutes in healthy Chinese subjects. The elimination half-life (t½) is approximately 47.2-60.6 minutes, indicating rapid clearance. Within the dose range of 10-60 μg, Cmax, AUC0-t, and AUC0-∞ increase proportionally with dose, while t½, total clearance, and Tmax are dose-independent, exhibiting linear pharmacokinetic characteristics. Oral administration of pTH (1-34) (1.8 mg) is also rapidly absorbed but results in lower AUC compared to subcutaneous administration. No significant differences in pharmacokinetic parameters are observed between sexes.

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In clinical studies, pTH (1-34) is generally well tolerated in healthy subjects. The most commonly reported adverse events are erythema at the injection site and gastrointestinal reactions. Within the studied dose ranges (single doses of 10-60 μg and multiple doses of 10-20 μg once daily for 7 consecutive days), no dose-related significant effects on serum calcium and phosphate levels are observed compared to baseline. As the active ingredient of teriparatide, the long-term safety profile of pTH (1-34) is consistent with that of the approved osteoporosis therapeutic agent.

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No significant changes in serum calcium, inorganic phosphate, or creatinine were observed in senile male rats treated with bovine PTH-(1-34) (serum calcium: 9.5 ± 0.14 mg/dl in PTH-treated vs 9.4 ± 0.15 in controls; phosphorus: 5.9 ± 0.3 vs 6.1 ± 0.3 mg/dl; creatinine: 0.5 ± 0.13 vs 0.7 ± 0.15 mg/dl), indicating no nephrotoxicity. Serum alkaline phosphatase activity showed a slight non-significant increase (64 ± 20 IU/liter increase in PTH-treated vs -1 ± 22 in controls, p=0.06). [1]
In young male rats, bovine PTH-(1-34) significantly increased serum calcium (10.23 ± 0.1 vs 9.93 ± 0.1 mg/dl, p<0.05) and inorganic phosphate (8.73 ± 0.18 vs 7.58 ± 0.18 mg/dl, p<0.05) but values remained within normal range. [1]

[1]. Intermittent administration of bovine PTH-(1-34) increases serum 1,25-dihydroxyvitamin D concentrations and spinal bone density in senile (23 month) rats. J Bone Miner Res. 1992 May;7(5):479-84.

[2]. Studies on chondrocytes from mandibular condylar cartilage, nasal septal cartilage, and spheno-occipital synchondrosis in culture. I. Morphology, growth, glycosaminoglycan synthesis, and responsiveness to bovine parathyroid hormone (1-34). J Dent Res. 1984 Jan;63(1):19-22.

bovine PTH-(1-34) is an anabolic agent for bone when administered intermittently, contrasting with its catabolic effects when given continuously. The anabolic effect depends on timing and dose. In senile rats, it increases serum 1,25-dihydroxyvitamin D concentrations to levels seen in young PTH-treated animals, suggesting reversal of age-related vitamin D axis impairment. The study supports co-administration of PTH with 1,25-dihydroxyvitamin D in elderly osteoporotic patients. [1]
bovine PTH-(1-34) stimulates glycosaminoglycan synthesis and ornithine decarboxylase activity in chondrocytes, serving as a marker of differentiated chondrocytes. Different craniofacial cartilages (mandibular condyle, nasal septum, spheno-occipital synchondrosis) respond to PTH but show different growth characteristics in culture. [2]

C183H288N54O50S2

3970.49976

3973.039

12583-68-5

Parathyroid Hormone (1-34), bovine TFA

16132279

H-Gly-Val-Ser-Glu-Ile-Gln-Gly-Met-His-Asn-Leu-Gly-Lys-His-Leu-Gly-Ser-Met-Glu-Arg-Val-Glu-Trp-Leu-Arg-Lys-Lys-Leu-Gln-Asp-Val-His-Asn-Phe-OH
glycyl-L-valyl-L-seryl-L-alpha-glutamyl-L-isoleucyl-L-glutaminyl-glycyl-L-methionyl-L-histidyl-L-asparagyl-L-leucyl-glycyl-L-lysyl-L-histidyl-L-leucyl-glycyl-L-seryl-L-methionyl-L-alpha-glutamyl-L-arginyl-L-valyl-L-alpha-glutamyl-L-tryptophyl-L-leucyl-L-arginyl-L-lysyl-L-lysyl-L-leucyl-L-glutaminyl-L-alpha-aspartyl-L-valyl-L-histidyl-L-asparagyl-L-phenylalanine

GVSEIQGMHNLGKHLGSMERVEWLRKKLQDVHNF

White to off-white solid powder

-18.6

58

60

141

279

9360

31

NCCCCC(C(NC(C(NC(C(NCC(NC(C(NC(C(NC(C(NC(C(NC(C(NC(C(NC(CC1=CNC2=CC=CC=C12)C(NC(C(NC(C(NC(C(NC(C(NC(C(NC(C(NC(C(NC(C(NC(C(NC(C(NC(CC1=CC=CC=C1)C(=O)O)=O)CC(=O)N)=O)CC1=CN=CN1)=O)C(C)C)=O)CC(=O)O)=O)CCC(=O)N)=O)CC(C)C)=O)CCCCN)=O)CCCCN)=O)CCCNC(=N)N)=O)CC(C)C)=O)=O)CCC(=O)O)=O)C(C)C)=O)CCCNC(=N)N)=O)CCC(=O)O)=O)CCSC)=O)CO)=O)=O)CC(C)C)=O)CC1=CN=CN1)=O)NC(CNC(C(NC(C(NC(C(NC(C(NC(CNC(C(NC(C(NC(C(NC(C(NC(C(C(C)C)NC(CN)=O)=O)CO)=O)CCC(=O)O)=O)C(CC)C)=O)CCC(=O)N)=O)=O)CCSC)=O)CC1=CN=CN1)=O)CC(=O)N)=O)CC(C)C)=O)=O

BHCZZGBILISWFT-KANWXXSKSA-N

InChI=1S/C174H278N54O49S2/c1-19-93(16)142(228-156(260)110(46-51-137(243)244)208-167(271)126(82-230)224-168(272)139(90(10)11)225-131(235)73-178)171(275)210-106(42-47-127(179)231)143(247)193-78-133(237)200-111(52-59-278-17)153(257)218-119(68-97-76-188-84-197-97)161(265)219-121(70-129(181)233)163(267)213-114(62-87(4)5)145(249)194-79-132(236)199-101(37-25-28-54-175)146(250)217-118(67-96-75-187-83-196-96)160(264)212-113(61-86(2)3)144(248)195-80-134(238)201-125(81-229)166(270)209-112(53-60-279-18)154(258)206-108(44-49-135(239)240)150(254)204-105(41-32-58-191-174(185)186)155(259)226-140(91(12)13)169(273)211-109(45-50-136(241)242)152(256)216-117(66-95-74-192-100-36-24-23-35-99(95)100)159(263)215-116(64-89(8)9)157(261)205-104(40-31-57-190-173(183)184)148(252)202-102(38-26-29-55-176)147(251)203-103(39-27-30-56-177)149(253)214-115(63-88(6)7)158(262)207-107(43-48-128(180)232)151(255)221-123(72-138(245)246)165(269)227-141(92(14)15)170(274)222-120(69-98-77-189-85-198-98)162(266)220-122(71-130(182)234)164(268)223-124(172(276)277)65-94-33-21-20-22-34-94/h20-24,33-36,74-77,83-93,101-126,139-142,192,229-230H,19,25-32,37-73,78-82,175-178H2,1-18H3,(H2,179,231)(H2,180,232)(H2,181,233)(H2,182,234)(H,187,196)(H,188,197)(H,189,198)(H,193,247)(H,194,249)(H,195,248)(H,199,236)(H,200,237)(H,201,238)(H,202,252)(H,203,251)(H,204,254)(H,205,261)(H,206,258)(H,207,262)(H,208,271)(H,209,270)(H,210,275)(H,211,273)(H,212,264)(H,213,267)(H,214,253)(H,215,263)(H,216,256)(H,217,250)(H,218,257)(H,219,265)(H,220,266)(H,221,255)(H,222,274)(H,223,268)(H,224,272)(H,225,235)(H,226,259)(H,227,269)(H,228,260)(H,239,240)(H,241,242)(H,243,244)(H,245,246)(H,276,277)(H4,183,184,190)(H4,185,186,191)/t93-,101-,102-,103-,104-,105-,106-,107-,108-,109-,110-,111-,112-,113-,114-,115-,116-,117-,118-,119-,120-,121-,122-,123-,124-,125-,126-,139-,140-,141-,142-/m0/s1

(4S)-4-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-5-amino-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-3-methylpentanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-4-methylsulfanylbutanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-4-oxobutanoyl]amino]-4-methylpentanoyl]amino]acetyl]amino]hexanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-4-methylpentanoyl]amino]acetyl]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-5-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

Bpth (1-34); BPTH(1-34); RefChem:170012; 12583-68-5; L-Phenylalanine, L-alanyl-L-valyl-L-seryl-L-alpha-glutamyl-L-isoleucyl-L-glutaminyl-L-phenylalanyl-L-methionyl-L-histidyl-L-asparaginyl-L-leucylglycyl-L-lysyl-L-histidyl-L-leucyl-L-seryl-L-seryl-L-methionyl-L-alpha-glutamyl-L-arginyl-L-valyl-L-alpha-glutamyl-L-tryptophyl-L-leucyl-L-arginyl-L-lysyl-L-lysyl-L-leucyl-L-glutaminyl-L-alpha-aspartyl-L-valyl-L-histidyl-L-asparaginyl-;

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)

H2O : ~50 mg/mL (~12.17 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.)