Leptin API Manufacturers & Suppliers

0 verified results

When insight is your advantage

Full data, full access, full negotiation power

Total market transparency

Supplier trade data access

Buyer / supplier flow comparison

Commercial-scale Suppliers

Sorry, there are currently no suppliers listed for this ingredient. Hopefully we can help you with other ingredients.

Want to be the first to find out when a supplier for Leptin is listed?

Join our notification list by following this page.

Are you a supplier of Leptin or other APIs and are you looking to list your company on Pharmaoffer?

Click the button below to find out more

LEARN MORE

Looking for a CDMO/CMO that can help you with your pharmaceutical needs?

Click the button below to switch over to the contract services area of Pharmaoffer.

LEARN MORE

When insight is your advantage

Full data, full access, full negotiation power

Total market transparency

Supplier trade data access

Buyer / supplier flow comparison

Trusted by 30,000+ registered pharma professionals:

Reach multinationals, SMEs, compounding pharmacies & more!

Leptin | CAS No: 169494-85-3 | GMP-certified suppliers

A medication that supports treatment of lipodystrophy and obesity by regulating energy balance and appetite through hormonal signaling pathways.

Therapeutic categories

AdipokinesAmino Acids, Peptides, and ProteinsBiological FactorsHormonesHormones, Hormone Substitutes, and Hormone AntagonistsIntercellular Signaling Peptides and Proteins

Generic name

Leptin

Molecule type

small molecule

CAS number

169494-85-3

DrugBank ID

DB05098

Approval status

Investigational drug

Primary indications

Investigated for use/treatment in lipodystrophy and obesity

Product Snapshot

Leptin is a recombinant protein formulation primarily utilized as an injectable peptide
It is investigated for therapeutic applications in lipodystrophy and obesity management
The product remains in the investigational phase without current FDA or EMA approval

Clinical Overview

Leptin (CAS Number 169494-85-3) is an endogenous peptide hormone primarily produced by adipose tissue. It functions as a key regulator of energy balance by signaling satiety to the central nervous system and reducing appetite. Despite circulating as an appetite-suppressing factor, individuals with obesity commonly exhibit elevated leptin levels alongside a state of leptin resistance, analogous to insulin resistance observed in type 2 diabetes. This resistance compromises leptin’s effectiveness in appetite regulation, contributing to sustained energy intake exceeding expenditure and consequent weight gain.

Clinically, leptin is under investigation for therapeutic applications in conditions such as lipodystrophy and obesity. Its precise pharmacodynamics remain incompletely defined. Leptin’s mechanism of action involves binding to the Ob-Rb receptor isoform, primarily located in the hypothalamus. This interaction activates intracellular signaling cascades including Stat3 phosphorylation, which modulates gene expression to suppress orexigenic neuropeptides such as endocannabinoids, thereby decreasing appetite. The entry of leptin into the central nervous system may occur via the circumventricular organs, such as the median eminence or choroid plexus, where the blood-brain barrier is permeable or specialized leptin transporters are expressed, though the exact transport mechanisms are not fully characterized.

Leptin also plays a critical role beyond appetite regulation, including modulation of reproductive function and angiogenesis through upregulation of vascular endothelial growth factor (VEGF). Deficiency in leptin disrupts pubertal development and fertility, linking fat stores to reproductive capacity.

Pharmacokinetic parameters such as absorption, distribution, metabolism, and excretion of exogenous leptin remain under study, with the majority of knowledge derived from animal models and early clinical trials. Safety considerations focus on immunogenicity and the potential for adverse metabolic effects given leptin’s pleiotropic functions.

From an API sourcing perspective, leptin’s complex peptide structure necessitates stringent quality controls. Manufacturing must ensure peptide purity, correct folding, and absence of contaminants to maintain biological activity and safety. Regulatory compliance with biologics standards is essential for clinical and commercial supply.

Identification & chemistry

Generic name	Leptin
Molecule type	Small molecule
CAS	169494-85-3
UNII	Q09SXY6BFI
DrugBank ID	DB05098

Pharmacology

Summary	Leptin acts primarily on leptin receptors (Ob-Rb) in the hypothalamus, where it modulates appetite by activating intracellular signaling pathways such as STAT3, leading to changes in gene expression that suppress endocannabinoid-mediated feeding behavior. Its pharmacodynamics involve neuronal remodeling and regulatory effects on energy balance, though receptor desensitization in obesity results in leptin resistance. Leptin signaling also influences reproductive function and vascular processes, including angiogenesis via VEGF modulation.
Mechanism of action	It is unknown whether leptin can cross the blood-brain barrier to access receptor neurons, because the blood-brain barrier is somewhat absent in the area of the median eminence, close to where the NPY neurons of the arcuate nucleus are. If it does cross the blood-brain barrier, it is unknown whether this occurs via an active or passive process. It is generally thought that leptin might enter the brain at the choroid plexus, where there is intense expression of a form of leptin receptor molecule that might act as a transport mechanism. Once leptin has bound to the Ob-Rb receptor, it activates the molecule stat3, which is phosphorylated and travels to the nucleus, it is presumed, to effect changes in gene expression. One of the main effects on gene expression is the down-regulation of the expression of endocannabinoids, responsible—among their many other functions—for increasing appetite. There are other intracellular pathways activated by leptin, but less is known about how they function in this system. Neuronal receptors remodel in response to leptin to have a different number and different types of synapses. Although leptin is a circulating signal that reduces appetite, in general, obese people have an unusually high circulating concentration of leptin.[3] These people are said to be resistant to the effects of leptin, in much the same way that people with type 2 diabetes are resistant to the effects of insulin. Thus, obesity develops when people take in more energy than they use over a prolonged period of time, and this excess food intake is not driven by hunger signals, occurring in spite of the anti-appetite signals from circulating leptin. The high sustained concentrations of leptin from the enlarged fat stores result in the cells that respond to leptin becoming desensitized. In mice, leptin is also required for male and female fertility. In mammals generally, and in humans in particular, puberty in females is linked to a critical level of body fat. When fat levels fall below this threshold (as in anorexia), the ovarian cycle stops and females stop menstruating. Leptin is also strongly linked with angiogenesis, increasing VEGF levels.

Summary

Leptin acts primarily on leptin receptors (Ob-Rb) in the hypothalamus, where it modulates appetite by activating intracellular signaling pathways such as STAT3, leading to changes in gene expression that suppress endocannabinoid-mediated feeding behavior. Its pharmacodynamics involve neuronal remodeling and regulatory effects on energy balance, though receptor desensitization in obesity results in leptin resistance. Leptin signaling also influences reproductive function and vascular processes, including angiogenesis via VEGF modulation.

Mechanism of action

It is unknown whether leptin can cross the blood-brain barrier to access receptor neurons, because the blood-brain barrier is somewhat absent in the area of the median eminence, close to where the NPY neurons of the arcuate nucleus are. If it does cross the blood-brain barrier, it is unknown whether this occurs via an active or passive process. It is generally thought that leptin might enter the brain at the choroid plexus, where there is intense expression of a form of leptin receptor molecule that might act as a transport mechanism. Once leptin has bound to the Ob-Rb receptor, it activates the molecule stat3, which is phosphorylated and travels to the nucleus, it is presumed, to effect changes in gene expression. One of the main effects on gene expression is the down-regulation of the expression of endocannabinoids, responsible—among their many other functions—for increasing appetite. There are other intracellular pathways activated by leptin, but less is known about how they function in this system. Neuronal receptors remodel in response to leptin to have a different number and different types of synapses. Although leptin is a circulating signal that reduces appetite, in general, obese people have an unusually high circulating concentration of leptin.[3] These people are said to be resistant to the effects of leptin, in much the same way that people with type 2 diabetes are resistant to the effects of insulin. Thus, obesity develops when people take in more energy than they use over a prolonged period of time, and this excess food intake is not driven by hunger signals, occurring in spite of the anti-appetite signals from circulating leptin. The high sustained concentrations of leptin from the enlarged fat stores result in the cells that respond to leptin becoming desensitized. In mice, leptin is also required for male and female fertility. In mammals generally, and in humans in particular, puberty in females is linked to a critical level of body fat. When fat levels fall below this threshold (as in anorexia), the ovarian cycle stops and females stop menstruating. Leptin is also strongly linked with angiogenesis, increasing VEGF levels.

Targets

Target	Organism	Actions
Leptin receptor	Humans

ADME / PK

Half-life	24.9+/-4.4 min

Formulation & handling

Leptin is a small molecule in solid form suitable for oral formulation development.
Stability considerations include protection from moisture and temperature extremes during storage.
Investigational status requires controlled handling and compliance with regulatory standards for experimental APIs.