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pTH (1-37) (human)

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

pTH (1-37) (human) is a native bioactive fragment of pTH (1-84) (human) in circulation. Pulsatile rather than continuous administration of pTH (1-37) (human) can increase growth, bone calcium content and bone mineral density in uremic animals.

Category

Functional Peptides

Catalog number

BAT-015315

CAS number

136799-54-7

Molecular Formula

C195H316N58O54S2

Molecular Weight

4401.15

Specification
Reference Reading

IUPAC Name

(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(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-5-yl)propanoyl]amino]-4-oxobutanoyl]amino]-4-methylpentanoyl]amino]acetyl]amino]hexanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-4-methylpentanoyl]amino]-4-oxobutanoyl]amino]-3-hydroxypropanoyl]amino]-4-methylsulfanylbutanoyl]amino]-4-carboxybutanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-methylbutanoyl]amino]-4-carboxybutanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]hexanoyl]amino]hexanoyl]amino]-4-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-carboxypropanoyl]amino]-3-methylbutanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-4-oxobutanoyl]amino]-3-phenylpropanoyl]amino]-3-methylbutanoyl]amino]propanoyl]amino]-4-methylpentanoic acid

Synonyms

Parathyrin (1-37) (human); H-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-Val-Ala-Leu-OH; L-seryl-L-valyl-L-seryl-L-alpha-glutamyl-L-isoleucyl-L-glutaminyl-L-leucyl-L-methionyl-L-histidyl-L-asparagyl-L-leucyl-glycyl-L-lysyl-L-histidyl-L-leucyl-L-asparagyl-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-phenylalanyl-L-valyl-L-alanyl-L-leucine

Appearance

White Powder

Purity

95%

Sequence

SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNFVAL

Storage

Store at -20°C

Solubility

Soluble in Acetic Acid, DMSO, Water

InChI

InChI=1S/C195H316N58O54S2/c1-26-104(22)157(253-172(285)123(53-58-151(267)268)227-187(300)142(90-256)248-191(304)154(101(16)17)249-159(272)112(199)88-254)192(305)231-120(50-55-144(201)258)167(280)234-128(70-96(6)7)175(288)228-125(60-67-309-25)170(283)240-134(77-109-85-210-92-217-109)179(292)242-136(79-145(202)259)181(294)232-126(68-94(2)3)160(273)215-87-148(262)220-114(44-32-35-61-196)161(274)239-133(76-108-84-209-91-216-108)178(291)236-130(72-98(10)11)176(289)241-138(81-147(204)261)183(296)247-141(89-255)186(299)229-124(59-66-308-24)169(282)225-121(51-56-149(263)264)165(278)223-118(48-39-65-213-195(207)208)171(284)250-155(102(18)19)189(302)230-122(52-57-150(265)266)168(281)238-132(75-107-83-214-113-43-31-30-42-111(107)113)177(290)235-129(71-97(8)9)173(286)224-117(47-38-64-212-194(205)206)163(276)221-115(45-33-36-62-197)162(275)222-116(46-34-37-63-198)164(277)233-127(69-95(4)5)174(287)226-119(49-54-143(200)257)166(279)244-139(82-152(269)270)185(298)252-156(103(20)21)190(303)245-135(78-110-86-211-93-218-110)180(293)243-137(80-146(203)260)182(295)237-131(74-106-40-28-27-29-41-106)184(297)251-153(100(14)15)188(301)219-105(23)158(271)246-140(193(306)307)73-99(12)13/h27-31,40-43,83-86,91-105,112,114-142,153-157,214,254-256H,26,32-39,44-82,87-90,196-199H2,1-25H3,(H2,200,257)(H2,201,258)(H2,202,259)(H2,203,260)(H2,204,261)(H,209,216)(H,210,217)(H,211,218)(H,215,273)(H,219,301)(H,220,262)(H,221,276)(H,222,275)(H,223,278)(H,224,286)(H,225,282)(H,226,287)(H,227,300)(H,228,288)(H,229,299)(H,230,302)(H,231,305)(H,232,294)(H,233,277)(H,234,280)(H,235,290)(H,236,291)(H,237,295)(H,238,281)(H,239,274)(H,240,283)(H,241,289)(H,242,292)(H,243,293)(H,244,279)(H,245,303)(H,246,271)(H,247,296)(H,248,304)(H,249,272)(H,250,284)(H,251,297)(H,252,298)(H,253,285)(H,263,264)(H,265,266)(H,267,268)(H,269,270)(H,306,307)(H4,205,206,212)(H4,207,208,213)/t104-,105-,112-,114-,115-,116-,117-,118-,119-,120-,121-,122-,123-,124-,125-,126-,127-,128-,129-,130-,131-,132-,133-,134-,135-,136-,137-,138-,139-,140-,141-,142-,153-,154-,155-,156-,157-/m0/s1

InChI Key

ZEKQAUSYRLLYQY-QBKSNYRVSA-N

Canonical SMILES

CCC(C)C(C(=O)NC(CCC(=O)N)C(=O)NC(CC(C)C)C(=O)NC(CCSC)C(=O)NC(CC1=CN=CN1)C(=O)NC(CC(=O)N)C(=O)NC(CC(C)C)C(=O)NCC(=O)NC(CCCCN)C(=O)NC(CC2=CN=CN2)C(=O)NC(CC(C)C)C(=O)NC(CC(=O)N)C(=O)NC(CO)C(=O)NC(CCSC)C(=O)NC(CCC(=O)O)C(=O)NC(CCCNC(=N)N)C(=O)NC(C(C)C)C(=O)NC(CCC(=O)O)C(=O)NC(CC3=CNC4=CC=CC=C43)C(=O)NC(CC(C)C)C(=O)NC(CCCNC(=N)N)C(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)NC(CC(C)C)C(=O)NC(CCC(=O)N)C(=O)NC(CC(=O)O)C(=O)NC(C(C)C)C(=O)NC(CC5=CN=CN5)C(=O)NC(CC(=O)N)C(=O)NC(CC6=CC=CC=C6)C(=O)NC(C(C)C)C(=O)NC(C)C(=O)NC(CC(C)C)C(=O)O)NC(=O)C(CCC(=O)O)NC(=O)C(CO)NC(=O)C(C(C)C)NC(=O)C(CO)N

1. Biomarkers of Kidney Tubule Health, CKD Progression, and Acute Kidney Injury in SPRINT (Systolic Blood Pressure Intervention Trial) Participants

Pranav S Garimella, Michelle M Estrella, Michael G Shlipak, Alexander L Bullen, Alexandra K Lee, Vasantha Jotwani, Ronit Katz, Joachim H Ix Am J Kidney Dis . 2021 Sep;78(3):361-368.e1. doi: 10.1053/j.ajkd.2021.01.021.

Rationale & objective:The Systolic Blood Pressure Intervention Trial (SPRINT) compared the effect of intensive versus standard systolic blood pressure targets on cardiovascular morbidity and mortality. In this ancillary study, we evaluated the use of exploratory factor analysis (EFA) to combine biomarkers of kidney tubule health in urine and plasma and then study their role in longitudinal estimated glomerular filtration rate (eGFR) change and risk of acute kidney injury (AKI).Study design:Observational cohort nested in a clinical trial.Setting & participants:2,351 SPRINT participants with eGFR < 60 mL/min/1.73 m2at baseline.Exposure:Levels of neutrophil gelatinase-associated lipocalin (NGAL), interleukin 18 (IL-18), chitinase-3-like protein (YKL-40), kidney injury molecule 1 (KIM-1), monocyte chemoattractant protein 1 (MCP-1), α1-microglobulin (A1M) and β2-microglobulin (B2M), uromodulin (UMOD), fibroblast growth factor 23 (FGF-23), and intact parathyroid hormone (PTH).Outcome:Longitudinal changes in eGFR and risk of AKI.Analytical approach:We performed EFA to capture different tubule pathophysiologic processes. We used linear mixed effects models to evaluate the association of each factor with longitudinal changes in eGFR. We evaluated the association of the tubular factors scores with AKI using Cox proportional hazards regression.Results:From 10 biomarkers, EFA generated 4 factors reflecting tubule injury/repair (NGAL, IL-18, and YKL-40), tubule injury/fibrosis (KIM-1 and MCP-1), tubule reabsorption (A1M and B2M), and tubule reserve/mineral metabolism (UMOD, FGF-23, and PTH). Each 1-SD higher tubule reserve/mineral metabolism factor score was associated with a 0.58% (95% CI, 0.39%-0.67%) faster eGFR decline independent of baseline eGFR and albuminuria. Both the tubule injury/repair and tubule injury/fibrosis factors were independently associated with future risk of AKI (per 1 SD higher, HRs of 1.18 [95% CI, 1.10-1.37] and 1.23 [95% CI, 1.02-1.48], respectively).Limitations:The factors require validation in other settings.Conclusions:EFA allows parsimonious subgrouping of biomarkers into factors that are differentially associated with progressive eGFR decline and AKI. These subgroups may provide insights into the pathological processes driving adverse kidney outcomes.

2. Isolation and characterization of the bioactive circulating human parathyroid hormone, hPTH-1-37

G Heine, W G Forssmann, P P Ochlich, D Hock, M Mägerlein FEBS Lett . 1997 Jan 3;400(2):221-5. doi: 10.1016/s0014-5793(96)01390-7.

The occurrence of hPTH-1-37 as the native bioactive circulating form of PTH-1-84 has now been obtained using a specific purification procedure for circulating parathyroid hormone, which involves a newly developed immunoenzymetric assay for N-terminally intact hPTH. In combination with two different methods of mass spectrometry, the molecular weight of the isolated immunoreactive peptide was shown to be 4401 Da, which corresponds to hPTH-1-37. Synthetic hPTH-1-37 material was tested in the chick bioassay and produced a clearcut increase in serum calcium concentration. We conclude that hPTH-1-37 is the native bioactive fragment of hPTH-1-84 in circulation.

3. Phosphate homeostasis in Bartter syndrome: a case-control study

Silvana Tedeschi, Mario G Bianchetti, Alessandra Albisetti, Alberto Bettinelli, Maria Cristina Provero, Barbara Scicchitano, Francesco Barretta, Cristina Viganò Pediatr Nephrol . 2014 Nov;29(11):2133-8. doi: 10.1007/s00467-014-2846-z.

Background:Bartter patients may be hypercalciuric. Additional abnormalities in the metabolism of calcium, phosphate, and calciotropic hormones have occasionally been reported.Methods:The metabolism of calcium, phosphate, and calciotropic hormones was investigated in 15 patients with Bartter syndrome and 15 healthy subjects.Results:Compared to the controls, Bartter patients had significantly reduced plasma phosphate {mean [interquartile range]:1.29 [1.16-1.46] vs. 1.61 [1.54-1.67] mmol/L} and maximal tubular phosphate reabsorption (1.16 [1.00-1.35] vs. 1.41 [1.37-1.47] mmol/L) and significantly increased parathyroid hormone (PTH) level (6.1 [4.5-7.7] vs. 2.8 [2.2-4.4] pmol/L). However, patients and controls did not differ in blood calcium, 25-hydroxyvitamin D, alkaline phosphatase, and osteocalcin levels. In patients, an inverse correlation (P < 0.05) was noted between total plasma calcium or glomerular filtration rate and PTH concentration. A positive correlation was also noted between PTH and osteocalcin concentrations (P < 0.005), as well as between chloriduria or natriuria and phosphaturia (P < 0.001). No correlation was noted between calciuria and PTH concentration or between urinary or circulating phosphate and PTH.Conclusions:The results of this study demonstrate a tendency towards renal phosphate wasting and elevated circulating PTH levels in Bartter patients.