Checkpoint &
B7 Family
ELISA
Soluble checkpoint biomarker ELISA across the full B7-CD28 superfamily, TIM family, and next-gen inhibitory receptors - paired with KRIBIOLISA- mAb drug monitoring assays covering every approved checkpoint inhibitor. PK, quantitative ADA, and world's-only nAb assays for pembrolizumab, nivolumab, and ipilimumab.
mAb Drug Assays Checkpoint BiologyThe Cancer-Immunity Cycle & Checkpoint Regulation
Immune checkpoints are regulatory proteins that prevent autoimmunity by dampening T cell activation - a mechanism tumours exploit to escape immune destruction. Checkpoint inhibitor therapy (anti-PD-1, anti-PD-L1, anti-CTLA-4 and newer targets) works by blocking these inhibitory signals, restoring T cell-mediated anti-tumour immunity. Measuring soluble checkpoint proteins in serum and plasma enables non-invasive monitoring of checkpoint axis activity, therapy-induced immune changes, and biomarker-guided patient stratification.
The cancer-immunity cycle has seven key steps - from tumour antigen release through to T cell-mediated killing. Checkpoint proteins act at specific steps in this cycle as brakes. Understanding which checkpoint is active in a given tumour type, and at which step, determines both biomarker selection and therapeutic strategy.
CTLA-4 blocks here
LAG-3 - TIGIT active
PD-1 / TIM-3 suppress here
| Tumour Type | Primary Checkpoint | Emerging | Approved Therapy |
|---|---|---|---|
| NSCLC | PD-L1 - PD-1 | LAG-3 - TIGIT - TIM-3 | Pembrolizumab - Nivolumab - Atezolizumab |
| Melanoma | PD-1 - CTLA-4 | LAG-3 | Nivolumab + Ipilimumab - Relatlimab + Nivolumab |
| TNBC | PD-L1 - PD-1 | LAG-3 - TIGIT | Atezolizumab + nab-Paclitaxel - Pembrolizumab |
| RCC | PD-1 - CTLA-4 | LAG-3 | Nivolumab + Ipilimumab - Pembrolizumab |
| AML / Hematologic | TIM-3 - PD-1 | CD73 - LAG-3 | Under investigation |
| Ovarian | PD-L1 - PD-1 | TIM-3 - B7-H4 | Under investigation |
| HNSCC | PD-L1 - PD-1 | TIGIT | Pembrolizumab - Nivolumab |
B7-CD28 Superfamily Biomarker ELISA
The B7-CD28 superfamily is the primary therapeutic checkpoint axis. Soluble forms of all ligands and receptors are measurable in serum and plasma and serve as predictive and pharmacodynamic biomarkers for checkpoint inhibitor therapy.
Programmed Death-1 is expressed on activated T cells and upregulated during T cell exhaustion in the tumour. Soluble PD-1 (sPD-1) is shed into circulation. Elevated serum sPD-1 correlates with tumour stage and has been investigated as a predictive biomarker for anti-PD-1 therapy response across NSCLC, melanoma, and RCC.
Programmed Death Ligand-1 is expressed on tumour cells, TAMs, and DCs, delivering an inhibitory signal to PD-1+ T cells. Soluble PD-L1 (sPD-L1) is shed by matrix metalloproteinases and elevated in NSCLC, TNBC, HCC, and urothelial carcinoma. sPD-L1 is a predictive biomarker for atezolizumab, durvalumab, and avelumab response.
Cytotoxic T-Lymphocyte-Associated Protein 4 is expressed on activated T cells and Tregs. It competes with CD28 for CD80/CD86 binding on APCs, delivering an inhibitory signal that dampens T cell priming in the lymph node - the step targeted by ipilimumab and tremelimumab. Soluble CTLA-4 is measurable in serum. Mouse reactivity available for syngeneic models.
The second PD-1 ligand, expressed primarily on DCs and macrophages. PD-L2 binds PD-1 with ~3- higher affinity than PD-L1 and modulates the threshold for PD-1-mediated T cell inhibition. Relevant in certain lung, gastric, and ovarian cancer subtypes. May serve as an alternative or complementary readout alongside sPD-L1 measurement.
CD28 is the primary co-stimulatory receptor for T cell activation, competing with CTLA-4 for CD80/CD86 binding. Unlike CTLA-4, CD28 signalling activates rather than suppresses T cells. Soluble CD28 may serve as a counterpart readout to sCTLA-4, reflecting the balance of inhibitory vs stimulatory signalling at the APC-T cell interface. Available in Human and Rat.
V-domain Ig Suppressor of T cell Activation (VISTA) is an inhibitory receptor and ligand expressed on T cells and APCs. It suppresses T cell activation independently of PD-1 and CTLA-4 - relevant as a resistance mechanism in patients failing anti-PD-1 therapy. VISTA is overexpressed in prostate cancer and is an emerging combination therapy target.
LAG-3, TIGIT, TIM-3 & B7-H4 ELISA
These targets are clinically validated (LAG-3) or in advanced clinical development (TIGIT, TIM-3), frequently studied in combination with PD-1/PD-L1 blockade to overcome resistance or target distinct exhaustion pathways.
Lymphocyte Activation Gene-3 is expressed on exhausted CD4+ and CD8+ T cells and Tregs. Its ligands include MHC-II (on APCs and tumour cells), FGL1, and Galectin-3. LAG-3 delivers a strong inhibitory signal that reduces T cell proliferation and cytokine production. Relatlimab + nivolumab (Opdualag) - the first approved dual checkpoint inhibitor - targets the LAG-3/PD-1 co-exhaustion state in melanoma. Soluble LAG-3 is shed from T cell surfaces and measurable in serum; elevated levels associate with advanced disease stage and therapy resistance. Available in Human and Mouse.
T cell Immunoreceptor with Ig and ITIM domains is expressed on CD8+ T cells, NK cells, and Tregs. It competes with the activating receptor CD226 (DNAM-1) for binding to CD155 (PVR) on tumour cells and APCs. TIGIT ligation suppresses cytokine production and cytotoxic activity. Tiragolumab (anti-TIGIT) is in late-stage development across NSCLC and SCLC in combination with atezolizumab; vibostolimab with pembrolizumab is in development for NSCLC and melanoma. Soluble TIGIT in serum may reflect NK/T cell activation status. Available in Human and Mouse.
T cell Immunoglobulin and Mucin domain-3 is expressed on exhausted CD8+ T cells, Th1 cells, DCs, and NK cells. Its ligands include Galectin-9 (measured by KBH2998 ELISA), HMGB1, and Ceacam-1. TIM-3 is co-expressed with PD-1 on exhausted tumour-infiltrating lymphocytes and marks the most functionally impaired T cell population. Elevated serum sTIM-3 is associated with poor prognosis in AML, NSCLC, and HCC. Available in Human.
B7-H4 suppresses T cell activation, proliferation, and cytokine secretion. Unlike PD-L1, B7-H4 expression is largely restricted to tumours and does not require IFN- induction. It is overexpressed in breast (~25-30%), ovarian (~70%), endometrial, and lung adenocarcinoma. Soluble B7-H4 is detectable in serum and correlates with tumour burden and poor prognosis. Several anti-B7-H4 monoclonal antibodies and ADCs are in early clinical development. Available in Human.
CD73 & Adenosine Axis ELISA
CD73 (ecto-5'-nucleotidase) is a glycosyl-phosphatidylinositol-anchored cell surface enzyme that converts AMP to immunosuppressive adenosine. Adenosine accumulates in the hypoxic TME and impairs T cell, NK cell, and DC function by binding A2A and A2B receptors. The CD73-adenosine axis is a major mechanism of immunosuppression in many solid tumours that fail to respond to PD-1 blockade.
Soluble CD73 is elevated in serum in multiple solid tumour types - including breast, ovarian, NSCLC, and CRC - and correlates with poor prognosis. CD73 ELISA (KBH5056) is validated in Human and Mouse, making it directly applicable to both clinical cohort studies and pre-clinical syngeneic and xenograft models.
Several anti-CD73 antibodies are in clinical development - including oleclumab (AstraZeneca, Phase II/III), ulocuplumab, and CPI-006 - often in combination with durvalumab or pembrolizumab. CD73 ELISA enables target engagement monitoring and patient stratification in these combination IO trials.
KBH5056 - View DatasheetGalectin-9 is the primary ligand for TIM-3, expressed on tumour cells, MDSCs, and Tregs. Galectin-9 binding to TIM-3 triggers T cell apoptosis or anergy and promotes Treg expansion. Elevated serum Galectin-9 is associated with advanced tumour burden in NSCLC, HCC, and haematologic malignancies. Available in Human, Mouse, and Rat - the widest species coverage of any Galectin-9 ELISA commercially available.
From Biomarker to Drug Monitoring - One Integrated Workflow
Every checkpoint inhibitor has a corresponding biomarker ELISA (measuring the soluble target) and a KRIBIOLISA- drug assay suite - PK quantitation, quantitative ADA, and for several agents, a world's-only neutralizing antibody (nAb) to drug assay. The cards below show the complete per-drug workflow. For drugs where nAb is marked World's Only, Krishgen is the sole commercial source globally.
World's Only = Krishgen is the sole commercial source globally for this assay format. | Tremelimumab (anti-CTLA-4) PK / ADA / nAb also available - contact us
All Checkpoint & mAb Drug ELISA - Full Table
Biomarker ELISA and KRIBIOLISA- drug assays. Contact info@krishgen.com for catalogue numbers for drug assays and full validation data.
| Type | Target / Drug | Role / Indication | Species / Format | Cat No. / Status |
|---|---|---|---|---|
| Biomarker | PD-1 (sPD-1) PDCD1 - CD279 | Anti-PD-1 therapy biomarker - T cell exhaustion | Human - Mouse | KBBA50 |
| Biomarker | PD-L1 (sPD-L1) B7-H1 - CD274 | Anti-PD-L1 therapy biomarker - Tumour expression | Human | KBBA52 |
| Biomarker | PD-L2 B7-DC - CD273 | PD-1 ligand axis - Lung - Gastric | Human | KBH4206 |
| Biomarker | CTLA-4 (sCTLA-4) CD152 | Anti-CTLA-4 biomarker - Treg function | Human - Mouse | KBH0277 |
| Biomarker | VISTA PD-1H - B7-H5 | Emerging checkpoint - PD-1 resistance | Human | KBH2153 |
| Biomarker | B7-H4 VTCN1 | Breast - Ovarian - ADC target | Human | KBH6532 |
| Biomarker | TIM-3 HAVCR2 - CD366 | AML - NSCLC - HCC prognosis | Human | KBH5390 |
| Biomarker | Galectin-9 LGALS9 - TIM-3 ligand | TIM-3 axis - Tumour immune evasion | Human - Mouse - Rat | KBH2998 |
| Biomarker | LAG-3 CD223 | Relatlimab target - T cell exhaustion | Human - Mouse | Contact us |
| Biomarker | TIGIT VSIG9 - VSTM3 | Tiragolumab target - NK/T cell suppression | Human - Mouse | Contact us |
| Biomarker | CD28 Co-stimulatory receptor | T cell activation counterpart to CTLA-4 | Human - Rat | KBH3033 |
| Biomarker | CD73 NT5E - Ecto-5'-nucleotidase | Adenosine pathway - Oleclumab target | Human - Mouse | KBH5056 |
| PKADA nAb | Pembrolizumab KEYTRUDA- | Anti-PD-1 - 1st line NSCLC, Melanoma, dMMR | Serum - Plasma | KBI1084 (PK) |
| PKADA nAb | Nivolumab OPDIVO- | Anti-PD-1 - NSCLC - Melanoma - RCC - HCC | Serum - Plasma | Available |
| PKADA nAb | Ipilimumab YERVOY- | Anti-CTLA-4 - Melanoma - RCC (+ nivo) | Serum - Plasma | Available |
| PKADA | Atezolizumab TECENTRIQ- | Anti-PD-L1 - NSCLC - TNBC - Urothelial | Serum - Plasma | Available |
| PKADA | Durvalumab IMFINZI- | Anti-PD-L1 - Stage III NSCLC - SCLC | Serum - Plasma | Available |
| PKADA | Avelumab BAVENCIO- | Anti-PD-L1 - Merkel cell - Urothelial | Serum - Plasma | Available |
| PKADA | Cemiplimab LIBTAYO- | Anti-PD-1 - CSCC - BCC - NSCLC | Serum - Plasma | Available |
| PKADA | Tremelimumab IMJUDO- | Anti-CTLA-4 - NSCLC (+ durvalumab) - HCC | Serum - Plasma | Available |
nAbWorld's Only nAb assay commercially available - PKDrug quantitation - ADAQuantitative anti-drug antibody
Common Questions - Checkpoint ELISA & Drug Assays
Need the Complete PK / ADA / nAb Workflow?
Contact our technical team for catalogue numbers, validation guides, and availability for your checkpoint inhibitor of interest. Custom development available for pipeline agents.
