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BMP-7 (osteogenic protein-1, OP-1) is not a peptide but a recombinant disulfide-linked homodimeric glycoprotein of ~35 kDa from the TGF-β superfamily. It signals through Smad1/5/8 and, in preclinical fibrosis models, counter-regulates the TGF-β1/Smad3 axis.
Size: 100 mcg
No published analyses yet.
Titration schedule · reference
The information below is provided from public sources for reference only. It is not advice or instructions for use; products are intended for laboratory research only and not for human consumption.
| Period / condition | Dose | Escalation |
|---|---|---|
| Phase 1, knee (intra-articular, single dose) | 0.1 mg | Starting dose |
| Phase 1, higher level (intra-articular, single dose) | 0.3 mg | Increase if needed |
| Surgical implant (OP-1, on collagen, local) | 3.5 mg | Maximum in this schedule |
| Preclinical systemic reference (animal) | 30 mcg/kg, twice weekly | , |
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BMP-7 stands apart from most of this catalogue in two ways. First, it is not a peptide: the molecule is a recombinant homodimeric glycoprotein of roughly 35 kDa, its two subunits joined by an interchain disulfide and folded around the cystine knot typical of the TGF-β superfamily. A 5–30 residue synthetic peptide and a recombinant protein of this size differ in manufacture, stability and solution behaviour. Second, BMP-7 is one of the few compounds in this category that actually reached clinical use and then left it — for reasons only partly related to efficacy.
TGF-β1 and BMP-7 belong to the same superfamily but engage different receptor complexes and different R-Smads. TGF-β1 signals through ALK5 to phosphorylate Smad2/3, the profibrotic branch. BMP-7 signals through type I receptors (ALK2/ALK3/ALK6) to phosphorylate Smad1/5/8. Both branches compete for the shared co-mediator Smad4, so in kidney injury models raising BMP-7 signalling shifts the balance against the TGF-β1-driven fibrotic programme. It is this counter-regulatory mechanism, rather than a simple growth-factor effect, that made BMP-7 an antifibrotic research subject.
Orthopaedic. As OP-1 on a collagen carrier, the protein received in the US not full approval but a Humanitarian Device Exemption — a restricted pathway for tibial nonunion and revision posterolateral fusion. The commercial story ended before the scientific one: assets moved from Stryker Biotech to Olympus Biotech in 2010, and manufacturing was halted in 2014.
Renal. BMP-7 is most highly expressed in the adult kidney, and its knockout in mice produces severe renal dysplasia. Preclinical work from 1998–2004 showed attenuated injury in ischaemia models and antagonism of TGF-β1-induced epithelial-to-mesenchymal transition. No clinical trial of BMP-7 in human kidney disease has been conducted. This branch has remained entirely preclinical for over twenty years.
The principal obstacle is pharmacokinetic: soluble recombinant BMPs are cleared from circulation within minutes, so a systemic antifibrotic cannot be built from the naked protein. Orthopaedic use sidestepped this by local implantation on a carrier — a fundamentally different pharmacology from the systemic hypothesis. Attempts to overcome the limitation (albumin fusion, micellar constructs, BMP-signal enhancers) remain experimental.
A full treatment of mechanism, evidence and limitations is in the BMP-7 reference monograph. Related items sit under Tissue Repair and Anti-fibrosis.
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