Embryotoxic effects of thalidomide-derivatives in the non-human primate Callithrix jacchus

Merker, H. J.; Heger, Wolfgang; Sames, K.; Stürje, Helga; Neubert, Diether

doi:10.1007/bf00316631

Cited by 47 publications

(11 citation statements)

References 32 publications

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“…Early exposure resulted in severely truncated limbs, even Amelia, whereas later exposure caused less severe damage, for example loss of a digit or digit tips. In fact the damage caused by CPS49 in chicken embryos was consistent with damage seen in other studies using thalidomide (Somers, 1962; Boylen et al, 1963; Merker et al, 1988; Tamilarasan et al, 2006; Therapontos et al, 2009; Vargesson, 2009, 2013; Ema et al, 2010). …”

Section: Thalidomide Is Antiangiogenicsupporting

confidence: 87%

“…Mice, traditionally used to screen for drug action, are less sensitive to thalidomide than other species like non‐human primates, rabbits, etc. (Merker et al, 1988; Stephens et al, 2000; Vargesson, 2013). Why mice are less sensitive to the drug remains unclear.…”

Section: Part One: History and Thalidomide Embryopathymentioning

confidence: 99%

“…Animal studies, particularly in nonhuman primates, show that following thalidomide exposure a range of damage is induced, which can vary between each of the litter‐mates (Merker et al, 1988; Ema et al, 2010; Vargesson, 2013). For example, one littermate could exhibit varying damage to all 4 limbs, another to one limb, and another just a tail anomaly (Merker et al, 1988; Ema et al, 2010; Vargesson, 2013).…”

Section: When Does Thalidomide Cause Damage To the Embryo?mentioning

confidence: 99%

“…For example, one littermate could exhibit varying damage to all 4 limbs, another to one limb, and another just a tail anomaly (Merker et al, 1988; Ema et al, 2010; Vargesson, 2013). The mechanism underlying this variance in damage is unknown, but also hints that thalidomide damage in humans could be broader.…”

Section: When Does Thalidomide Cause Damage To the Embryo?mentioning

confidence: 99%

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Thalidomide‐induced teratogenesis: History and mechanisms

Vargesson

2015

Birth Defects Research Pt C

710

557

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Nearly 60 years ago thalidomide was prescribed to treat morning sickness in pregnant women. What followed was the biggest man‐made medical disaster ever, where over 10,000 children were born with a range of severe and debilitating malformations. Despite this, the drug is now used successfully to treat a range of adult conditions, including multiple myeloma and complications of leprosy. Tragically, a new generation of thalidomide damaged children has been identified in Brazil. Yet, how thalidomide caused its devastating effects in the forming embryo remains unclear. However, studies in the past few years have greatly enhanced our understanding of the molecular mechanisms the drug. This review will look at the history of the drug, and the range and type of damage the drug caused, and outline the mechanisms of action the drug uses including recent molecular advances and new findings. Some of the remaining challenges facing thalidomide biologists are also discussed. Birth Defects Research (Part C) 105:140–156, 2015. © 2015 The Authors Birth Defects Research Part C: Embryo Today: Reviews Published by Wiley Periodicals, Inc.

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Section: Thalidomide Is Antiangiogenicsupporting

confidence: 87%

Section: Part One: History and Thalidomide Embryopathymentioning

confidence: 99%

Section: When Does Thalidomide Cause Damage To the Embryo?mentioning

confidence: 99%

Section: When Does Thalidomide Cause Damage To the Embryo?mentioning

confidence: 99%

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Thalidomide‐induced teratogenesis: History and mechanisms

Vargesson

2015

Birth Defects Research Pt C

710

557

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“…The teratogenic effects of some compounds have been shown to differ significantly between rodent and primate species. For example, whereas rodents are not sensitive to the teratogenic action of thalidomide analogues, the common marmoset is sensitive to these compounds [7]–[9].…”

Section: Introductionmentioning

confidence: 99%

Qualitative De Novo Analysis of Full Length cDNA and Quantitative Analysis of Gene Expression for Common Marmoset (Callithrix jacchus) Transcriptomes Using Parallel Long-Read Technology and Short-Read Sequencing

et al. 2014

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The common marmoset (Callithrix jacchus) is a non-human primate that could prove useful as human pharmacokinetic and biomedical research models. The cytochromes P450 (P450s) are a superfamily of enzymes that have critical roles in drug metabolism and disposition via monooxygenation of a broad range of xenobiotics; however, information on some marmoset P450s is currently limited. Therefore, identification and quantitative analysis of tissue-specific mRNA transcripts, including those of P450s and flavin-containing monooxygenases (FMO, another monooxygenase family), need to be carried out in detail before the marmoset can be used as an animal model in drug development. De novo assembly and expression analysis of marmoset transcripts were conducted with pooled liver, intestine, kidney, and brain samples from three male and three female marmosets. After unique sequences were automatically aligned by assembling software, the mean contig length was 718 bp (with a standard deviation of 457 bp) among a total of 47,883 transcripts. Approximately 30% of the total transcripts were matched to known marmoset sequences. Gene expression in 18 marmoset P450- and 4 FMO-like genes displayed some tissue-specific patterns. Of these, the three most highly expressed in marmoset liver were P450 2D-, 2E-, and 3A-like genes. In extrahepatic tissues, including brain, gene expressions of these monooxygenases were lower than those in liver, although P450 3A4 (previously P450 3A21) in intestine and P450 4A11- and FMO1-like genes in kidney were relatively highly expressed. By means of massive parallel long-read sequencing and short-read technology applied to marmoset liver, intestine, kidney, and brain, the combined next-generation sequencing analyses reported here were able to identify novel marmoset drug-metabolizing P450 transcripts that have until now been little reported. These results provide a foundation for mechanistic studies and pave the way for the use of marmosets as model animals for drug development in the future.

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Reproductive/Developmental Toxicity Assessment of Biopharmaceuticals in Nonhuman Primates

Weinbauer

Frings

Fuchs

et al. 2010

Pharmaceutical Sciences Encyclopedia

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Developmental and reproductive toxicity (DART) evaluation of biopharmaceuticals frequently necessitates the use of nonhuman primate models (NHPs) owing to species specificity. NHPs offer several advantages over rodents and rabbits with regard to DART because of similarity to human. This article provides a state‐of‐the‐art account on the feasibility and limitations of using NHPs for DART evaluation in the context of preclinical development of biopharmaceuticals.

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Embryotoxic effects of thalidomide-derivatives in the non-human primate Callithrix jacchus

Cited by 47 publications

References 32 publications

Thalidomide‐induced teratogenesis: History and mechanisms

Thalidomide‐induced teratogenesis: History and mechanisms

Qualitative De Novo Analysis of Full Length cDNA and Quantitative Analysis of Gene Expression for Common Marmoset (Callithrix jacchus) Transcriptomes Using Parallel Long-Read Technology and Short-Read Sequencing

Reproductive/Developmental Toxicity Assessment of Biopharmaceuticals in Nonhuman Primates

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